The Conundrum of Spinal Compression [PDF]

Energy failure plays a key role, with loss of blood flow leading to failure of the sodium pumps in cell membranes. .....

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BVOA BRITISH VETERINARY ORTHOPAEDIC ASSOCIATION

The Conundrum of Spinal Compression 23rd - 25th November 2007 McDonald Holyrood Hotel Edinburgh

AUTUMN SCIENTIFIC MEETING 23rd - 25th November 2007 McDonald Holyrood Hotel, Edinburgh The BVOA thank all our sponsors for supporting this meeting: Boehringer Ingelheim Hills Orthomed Pfizer Synthes Idexx Freelance Surgical Schering Plough Veterinary Instrumentation

The Committee extend special thanks to Schering Plough for their very generous sponsorship of the champagne reception aboard the Royal Yacht Britannia

The BVOA and editor are not responsible for information provided on dosages, methods of application of drugs or the use of any unlicensed drugs mentioned in these proceedings. Details of this kind should be verified by individual users from the appropriate literature.

Proceedings editor: Andy Moores Programme organiser: John Ferguson

Contents

Pathology of spinal cord compression Nick Jeffery ………………………………………. 1 Prognosis after spinal cord compression Jacques Penderis …………………….……… 4 Spinal cord recovery Nick Jeffery ……………………………………………………….…… 8 Optimising imaging in spinal compression Jacques Penderis ………….………………. 10 Comparative imaging in spinal compression Donald Collie ……………………….……. 16 Cervical spondylomyelopathy: An overview Laurent Garosi …………………………… 17 Type II disc associated Cervical spondylomyelopathy: How I treat and why: The role of decompressive techniques Nick Jeffery …………………………….. 23 The role of intervertebral spacers Malcolm McKee ……………………………… 25 The role of pins/screws and PMMA Luisa de Risio ……………………………... 33 The use of AO implants Rita Goncalves ……………………………………..…….. 38 The role of conservative management Laurent Garosi ………………..………… 41 Thoracolumbar type II disc protrusion: An overview Carlos Macias ………….….……. 42 Thoracolumbar type II disc protrusion: Lateral Corpectomy Pierre Moissonnier….…. 46 Thoracolumbar type II disc protrusion: Vertebral stabilisation Malcolm McKee ….… 50 A pain in the neck! Cervical spinal cord compression in man Patrick Statham ……... 58 Surgical management of developmental anomalies of the spine Jacques Penderls…. 59 Lumbosacral disease: Pathology Laurent Garosi …………………………………………. 65 Treatment for LS disease: The role of conservative management: The surgeon’s view Steven Butterworth ……………………………..….………… 71 The veterinary physiotherapist’s view Lowri Davies ……………………………. 74 Treatment for LS disease: The role of surgery Luisa de Risio ………………………..… 78 Management of chronic low back pain in man Patrick Statham ………………………… 86

PATHOLOGY OF SPINAL CORD COMPRESSION Nick Jeffery Dept Veterinary Medicine, University of Cambridge

An important aspect of spinal cord injury (SCI) is that there are (almost always) two components: Contusion

and

Compression

Contusion refers to a transient deformation of the spinal cord whereas compression implies a persistent deformation. This conceptual differentiation is important because the causes, distribution of tissue damage, treatment and prognosis are different.

1. Contusion Contusive injury to the spinal cord is better understood than compression because it has been the subject of very many experimental studies. The first experiments were carried out at the beginning of the 20th century, using weight-drop models – since then the methods have been considerably refined. Contusive injury produces tissue damage through two mechanisms, firstly there is the primary injury caused by mechanical disruption and direct injury to the neurons, axons and glia, plus tearing the blood vessels, leading to areas of haemorrhage and infarction. However, this primary injury is generally very mild, even after major impacts. The primary injury triggers a cascade of secondary injury events that are responsible for most of the tissue loss. Energy failure plays a key role, with loss of blood flow leading to failure of the sodium pumps in cell membranes. Depolarisation of the cell causes release of neurotransmitters, some of which (glutamate, aspartate) are toxic in high concentration, and activates the sodium / calcium transporter in reverse, allowing calcium into the cell. Calcium entry is a central mechanism of cell death, since is activates a vast range of enzymes within the cell, notably caspases, that cause apoptosis (programmed cell death), xanthine oxidase, that produces free radicals and phospholipase, producing prostaglandins. Oxygen and nitrogen free radicals are highly toxic to cells, since they damage cell membranes, allowing unrestricted ion fluxes, and are a prominent cause of cell death. These mechanisms form a vicious cycle since the vasoactive products will cause thrombosis or vascular leakage thereby increasing the chain of events from the beginning. All cell types can be affected - leading to neuron, axon and glial destruction.

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2. Compression Few studies have examined the mechanisms underlying the pathological effects of chronic compression in the spinal cord. However, it is generally assumed that the mechanisms are similar to those applying in contusive injury, but occurring in ‘slow motion’; the available data suggest that there is decreased blood flow that then leads to death of neurons in particular. Lesions resulting from compression are centred at the ‘watershed’ area between blood supplies derived from the central artery and the peripheral arteries. Chronic compression is certainly also associated with demyelination and axon loss, which can be appreciated grossly as cord atrophy.

Causes of compression and contusion Although conceptually it is important to make a distinction between the two, in many clinical diseases there is a mixed compressive / contusive lesion. For instance, a type I disc extrusion often occurs explosively, thus resulting in a contusion, but the extruded material may then constitute a compressive lesion. Examples of: Causes of contusion:

Causes of compression:

Type I disc extrusion

Type II disc extrusion

‘Type III’ disc extrusion

Tumour

Hyperextension at type II disc

Extruded type I disc material Hemivertebrae / anomalies

Treatment 1. Compression Persistent compression clearly can be alleviated by surgical decompression – the rationale for almost all veterinary neurosurgery. However, the question then arises as to how much compression of the spinal cord makes decompression mandatory. Experimental data suggest that less than 50% compression of the area of the spinal cord has an insignificant effect on conduction through the affected area, at least in the short term. There is also plenty of clinical evidence to suggest that very severe long-term compression of the thoracic spinal cord is compatible with satisfactory locomotion. Therefore, decompressive surgery would be most valuable for relatively severe, or dynamic, compression. It is also important to recognise that there are competing methods of decompression for compressive lesions (e.g. ‘direct’ and ‘indirect’ decompression for ‘wobbler’ syndrome). What other treatment options exist? The effects of CNS compression can often be alleviated very substantially by corticosteroid drugs, since they can reduce the vascular permeability and vasoconstriction associated with inflammatory mediators and VEGF and therefore improve poor perfusion. Of course, they have many undesirable long term side effects.

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2. Contusion A very large number of treatments have been investigated for their ability to reduce the consequences of spinal cord contusion. At present there are no drugs that have been satisfactorily proven to improve outcome. Methylprednisolone sodium succinate, used at high dosage, was for a period of time thought to be efficacious in treating human SCI. However, recent re-analysis of the relevant clinical trial data suggests that the apparent beneficial effect resulted from flawed randomisation. On the other hand, it is known that abnormal blood pressure after SCI (both too high and too low) will worsen the tissue damage in experimental injuries; similarly, in human stroke and head trauma patients it has been shown that maintenance of a normal pO2 will ameliorate functional loss. Therefore it appears sensible to treat these patients by maintaining normotension and normal oxygen tension.

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PROGNOSIS AFTER SPINAL CORD COMPRESSION Jacques Penderis University of Glasgow

How is the Neurological Examination Useful in Clinical Decision Making? The main aim of the neurological examination is to localise lesions affecting the nervous system. However, in lesions affecting the spinal cord, there are a number of other factors we can determine as part of the neurological examination, namely: • Establish the severity: most simply as the 5 point scale, originally developed by Ian Griffiths, but modified by Wheeler and Sharp. The more advanced 14-point scale subsequently developed by Natasha Olby allows finer discrimination of recovery, but is less suited to rapid clinical assessment. • Serial examinations: is there progression? • Does the lesion interrupt the local spinal reflexes to the limbs (specifically the cervical or lumbar intumescences)? • How extensive is the lesion? • Unfavourable underlying causes? For example the identification of gradual progression of the lesion localised to the mid-thoracic region would be more consistent with neoplasia than intervertebral disc disease. Establishment of the Prognosis as Part of the Neurological Examination The most important clinical feature affecting the prognosis or outcome following spinal cord injury is still the initial severity grading at the time of presentation. Severity grading in animals is complicated by difficulty in assessing a number of the sensory pathways within the spinal cord, including temperature discrimination, pressure, touch, etc. However, there are still enough spinal cord pathways of varying susceptibility that we can assess to allow us to accurately grade spinal cord injuries. The critical prognostic feature is the presence or absence of conscious perception of a painful stimulus applied to the affected limbs. Unfortunately, accurate discrimination of a conscious response to pain is often still poorly distinguished from the withdrawal (or pedal) reflex by many veterinarians in practice and it is therefore often difficult to give accurate prognostic advice over the telephone in many of these cases. 5 point scale: originally developed by Ian Griffiths, but modified by Wheeler and Sharp: Grade: 0 Normal 1 Pain: not severe enough to result in any neurological dysfunction. 2 Paresis with or without pain: as the lesion becomes more severe the degree of paresis and/or proprioceptive deficits become more severe. 3 Plegia: total loss of voluntary movement in the affected limbs (and/or tail). 4 Plegia with loss of voluntary urinary function. 5 Plegia with loss of voluntary urinary function and loss of deep pain in the affected limbs (and/or tail). In particular, the 5-point grading system is useful for predicting the outcome following intervertebral disc disease. The table modified from Wheeler and Sharp summarises the major outcome predictors.

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Severity Score 1 2 3 4 5

Disc Š Conservative 100% 84% 100% 50% 7%

Disc Hemilaminectomy 100% 100% 95% 90% 50% (48h)

Aligned Fracture

10% ( or = to 70 years of age) the 1-year mortality rate is 27.7% as compared to 3.2% in younger patients.



Duration of the clinical signs prior to treatment. Although the contribution of duration of signs has already been discussed in relation to deep pain absent dogs with intervertebral disc disease, this factor also plays a role in less severe spinal cord injury. In an experimental model of spinal cord injury in the dog (J Bone Joint Surg Am 1995;77:1042-1049) there was a direct correlation with the speed of decompression and clinical outcome (measured either as a return to ambulation or by means of somatosensory evoked potentials), and a similar situation has been demonstrated in the rat (Spine 1999;24:1623-1633). Even in the short-term the duration of spinal cord compression has an effect in the dog, with dogs having spinal cord compression of only 90 minutes having a less severe severity score and better functional recovery than dogs having spinal cord compression of 180 minutes duration (J Bone Joint Surg Am 2—3;85:86-94). However, in the Olby study (Journal of Neurotrauma 2003;21:49-59) and an additional study (JSAP 2002;43:158-163) the outcome in dogs with a less severe severity was good irrespective of the duration of the clinical signs, although a longer duration did correlate with a longer recovery period. The rate of onset of clinical signs was correlated with a worse outcome. In a separate retrospective study of thoracolumbar disc extrusion there was no correlation between the duration of clinical signs and outcome (JAVMA 2005;227:1454-1460).

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SPINAL CORD RECOVERY Nick Jeffery Dept Veterinary Medicine, University of Cambridge

Contusive spinal cord injury (SCI) will almost inevitably be associated with tissue destruction and loss of certain of the cellular components of the injured region. Despite recent evidence of the existence of stem cells within the CNS, there is no effective replacement of lost neurons or severed axons. Nevertheless, we know that very substantial functional recovery does occur; the mechanisms can be sub-divided into: i) regression of injurious processes and ii) reparative processes. Recovery after compression follows similar mechanisms, although the intensity of the injurious processes is much less.

1. Regression of injurious processes The pathological processes that occur after SCI lead to widespread inflammation within the spinal cord, incorporating elevation of cytokines and a cellular infiltrate producing a range of toxic molecules and immune-mediated damage. Many inflammatory products are directly detrimental to normal neural function (e.g. IL-1 and TNF-a cause axon conduction block) and others indirectly affect neural function through reducing blood flow through the damaged region. Decreased blood flow causes difficulties in maintaining a normal membrane potential and therefore loss of the ability to communicate through depolarisation. Whilst some tissue will be destroyed through this process, nearby regions can survive, despite a period in which they are inexcitable, or inappropriately excitable. This is similar to the well-developed concept of the ‘penumbra’ surrounding strokes in human patients. Therefore during the first three weeks, reduction in severity of the clinical signs can in large part be attributed to the gradual resolution of the acute inflammatory response. Recovery after compression can be similarly attributed to the restoration of adequate blood flow to the affected tissue.

2. Repair processes Although replacement of nerve cells and axons does not occur to any appreciable extent, glial cells are highly responsive to injury and able to rapidly proliferate in response to insult. Thus, after any type of SCI there will be astrocyte activation and proliferation which results in sealing of the CNS from the remainder of the body, and especially from any pathogen. This in itself is not generally a beneficial response in terms of function, but does protect the CNS from further invasion by pathogens. The loss of oligodendrocytes (ODC) that occurs after SCI, and during compression, will lead to demyelination of axons; when demyelinated the axons will not conduct properly and this may also contribute to functional loss soon after injury. However, replacement ODC are widely available in the CNS and the repair process of remyelination is very efficient (at least it is when the blood supply is adequate). Therefore remyelination constitutes one further method by which recovery of function can occur – and probably would be most prominent at around 4-6 weeks after the initial insult.

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Finally, and probably most importantly, the CNS is able to respond by means of ‘plasticity’. This is a general term to encompass all the various methods by which circuitry of the CNS can be ‘re-wired’. Recent research has emphasised the very plastic nature of the CNS – a necessary property if it is to remain flexibly responsive to the external and internal environment. Plasticity thus incorporates events at microscopic and sub-microscopic levels, including axonal sprouting, dendritic tree alterations and variability in synaptic number and weighting.

New approaches Ultimately of course, plasticity is limited since it cannot mediate recovery of function in a spinal cord that has been anatomically transected, since there will be NO remaining pathways across the damaged region. The development of novel approaches to therapy for humans and animals with this type of extremely severe injury has been the focus of research interest in many laboratories around the world, especially during the 1990s ‘decade of the brain’ and stimulated by the well-publicised injury to Christopher Reeve. The problem in this type of very severe SCI is that there is a need to encourage axons to regenerate across the damaged region – because, predominantly, such lesions cause clinical signs through loss of white matter. In evolution, mammals have lost the ability to regenerate the spinal cord, whereas ‘lower’ animals are able to do this. It would appear that there are several barriers to be overcome if widespread axonal regeneration is to be successful – most notably myelin or myelin debris and the products of activated astrocytes. There are many methods that have been devised to overcome these obstacles, involving both cell transplants and injection of chemicals to neutralise the effects of the numerous molecules that inhibit axonal regeneration (such as chondoitin sulphate proteoglycans, nogo and MBP). Many approaches have been shown to be effective in the laboratory but none have yet been successfully translated into the clinic. In our Department we have been investigating the possible application of autologous olfactory ensheathing cells (OEC) as a means to provide a pathway for axons to regenerate across the damaged region and therefore improve function in dogs with very severe SCI. OEC are current ‘front runners’ for application in human SCI and the establishment of the dog as a model for novel approaches to SCI treatment means that dogs will be able to rapidly benefit from any of the other laboratory approaches through clinical trials. Our work so far shows that intraspinal OEC transplantation is safe and reliable, and we have some data to suggest that there could well be beneficial effects. However statistical demonstration of beneficial effects is a function of a Phase II clinical trial for which we are currently seeking funding.

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OPTIMISING IMAGING IN SPINAL COMPRESSION Jacques Penderis University of Glasgow

Magnetic resonance imaging (MRI) is a diagnostic tool that is starting to gain more and more familiarity in the veterinary profession. The most important use and one with which most veterinary surgeons are now familiar lies in the diagnosis of intracranial disorders, e.g. tumours and inflammatory lesions. However, increasingly in veterinary neurology the value of MRI in imaging the spine is being recognised and where available it is starting to replace myelography. It has particularly proven to be of value in intramedullary spinal cord disorders and for the evaluation of lumbosacral disease. This lecture provides a brief insight into the use of MRI in disorders of the spine, in addition to the obvious application of MRI in imaging intracranial disorders. The Use of MRI to Replace Myelography: Although the majority of MRI scans performed in veterinary medicine are still to assess intracranial lesions, in those centres where MRI can easily be performed it has largely replaced myelography as the imaging modality of choice for spinal disorders. However, the availability of MRI is still limited and when we examine the similar situation in human medicine 10-years ago when MRI was widely available it is true that MRI was much more frequently used in the investigation of lower back pain, but this was largely as an add-on procedure (Radiology 1997;203:533-538). Indeed, if the neuroimaging trends are examined in human medicine, the use of MRI increased between 1993 and 1998 by 83% in the 10 regions of the USA examined, but then so did the use of myelography by 57% indicating that this technique will remain useful in veterinary medicine. However, when the usefulness of myelography and CT-myelography is assessed in cases where MRI was also performed it becomes apparent that the indications for CT-myelography are limited and it should probably be avoided in routine cases. One particular benefit of the widespread introduction of MRI is that where MRI is widely available in the human population it leads to increased rates of spinal surgery, particular of spinal stenosis (Spine 2003;28:616-620). Advantages of MRI over Myelography: o Non-invasive and less risk to the patient. This is particularly important in cases with severe spinal cord injuries (e.g. intervertebral disc disease with decreased or loss of deep pain sensation) where introducing a potentially irritant contrast medium and the manipulation required for myelography may exacerbate the spinal cord injury beyond the point of recovery. o Differentiates different types of spinal cord swelling (e.g. fluid from soft tissue). o Not affected by severe spinal cord swelling, which could render myelography nondiagnostic. o Detects lesions not causing a mass effect and which would therefore not be apparent on myelography). o Detects early disc degeneration. o Transverse planes give more 3D information. o Is usually quicker and easier (no difficulty of trying to get the spinal needle into the subarachnoid space). o If the neurological localisation is unclear then the brain can be included at the same time if no spinal cord lesion is apparent on the MRI to explain the clinical signs.

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o Good detail of paraspinal soft tissues as well.

MR images from a 6-year old Border collie with suspected myelitis demonstrating minimal mass effect on T1W images and therefore in which myelography would be of little benefit, but significant intra-parenchymal signal changes on T2W images (arrowed) within the mid-thoracic spinal cord.

MR imaging is particularly useful in demonstrating lesions involving the paraspinal tissues in addition to the spinal cord. Discospondylitis in a 7month-old Labrador retriever with evidence of intervertebral disc and vertebral changes (open arrows, top image), but no spinal cord compression, and enlargement of the sub-lumbar lymph nodes on T2W images and contract enhancement within the vertebral bodies and end plates (open arrows, bottom row) and paraspinal soft tissues (closed arrows, bottom row) on T1W contrastenhanced images.

Disadvantages of MRI over Myelography: o More expensive and not often immediately available for acute cases. o Performing stressed and traction views, e.g. in ‘wobbler syndrome’, is harder. o Fine bone detail is reduced. Although performing dynamic studies during MR imaging is less easily achieved, the difficulties in obtaining traction images in the assessment of canine ‘wobbler’ syndrome were largely overcome by a method described in Veterinary Radiology and Ultrasound 2004;45:216-9. In neutral position there is severe compression at the level of C6-C7 intervertebral disc space in this Dobermann, evident on sagittal T2W MR images. Following linear traction to the cervical spine the compression has largely been alleviated, confirming that the compression is dynamic in nature.

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Specific Lesions on MRI: Neoplasia: Tumours usually contrast-enhance and this aids in the ease of their identification. Although many tumour types have characteristic MRI features, MRI will not provide a definitive tissue diagnosis and the final diagnosis of intracranial or spinal neoplasia relies on histopathology. The tissue averaging over the thickness of the slice (usually between 3mm to 5mm) means that precise localisation of spinal cord lesions with respect to the meninges can be difficult. Despite this MRI is especially useful in assessing spinal cord neoplasia in those cases where: • There is little or no spinal cord swelling. • There are multiple lesions. • Where lesions extend outside of the spinal cord (e.g. nerve root tumours and locally invasive tumours). Dorsal and sagittal T2W MR images of an extradural tumour (open arrows) compressing the mid-lumbar spinal cord. What is apparent on the MR images which may not have been immediately apparent on a well-collimated myelogram is the soft tissue mass (closed arrows) within the abdomen. Fine needle aspirate biopsy of the mass confirmed it to be a carcinoma, most likely an adrenal carcinoma.

Intervertebral Disc Disease: MRI is very sensitive for the detection of early intervertebral disc disease, as the intervertebral disc nuclei usually have a high signal intensity on T2-weghted MRI scans and this signal intensity is lost with disc dehydration and degeneration. MRI will also demonstrate intervertebral disc prolapses and spinal cord compression, with lateralisation clearly evident on transverse MRI scans. High velocity/low volume intervertebral disc extrusions and spinal cord infarcts (fibro-cartilaginous emboli) are visible on MRI and may not be detected on myelography. Sagittal T2W MR image of incidental intervertebral disc degeneration in a 6-yearold Labrador retriever. MR is extremely sensitive for the early detection of intervertebral disc disease as is evident in the loss of signal intensity and subtle disc extrusion from the nucleus pulposis indicating disc dehydration and degeneration (closed arrow). The adjacent intervertebral discs still have normal nucleus pulposis signal intensity (open arrows).

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Sagittal and dorsal T2W MR images demonstrating a large, right-sided intervertebral disc prolapse in a 9-year-old Japanese Akita. The signal hyperintensity of the CSF-filled subarachnoid space on T2W images provides good delineation of the spinal cord and allows accurate prediction of the side of the intervertebral disc prolapse without the requirement for injection of a potentially harmful contrast medium into the subarachnoid space.

Trauma: MRI is ideal for assessing the degree of spinal cord trauma and surrounding haemorrhage following traumatic injury to the spinal cord. However, due to the limited bone definition MRI should ideally be combined with radiography or CT of the spine to define the degree of bone involvement. Lateral radiograph of the cervical spine of a 1year-old Borzoi demonstrating a traumatic fracture of C3 vertebrae, involving the dorsal lamina (solid arrow) and caudo-ventral vertebral body (open arrow). While radiography provides good bony detail and may suggest reasonable alignment of the cervical spine, MR imaging allows visualisation of the soft tissue components as well and in this case demonstrates a large haematoma compressing the spinal cord. The dog made a complete recovery following surgical decompression and stabilisation.

Inflammatory Disease: Intracranial and spinal cord inflammatory disease produce lesions detectable on MRI but may be difficult to differentiate from diffuse or multifocal neoplasia (particularly lymphoma). In these cases CSF analysis is often helpful.

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Differentiating between inflammatory disease and neoplasia (particularly infiltrative or multifocal neoplasia) affecting the spinal cord can be extremely difficult. Sagittal gradient echo (T2*W) (top left), sagittal T2W (bottom left), transverse T1W with contrast medium (top right) and transverse T2W MR images (bottom right) of the cervico-thoracic spine of a 2-year-old Cairn Terrier with a mildly contrast-enhancing mass lesion within the spinal canal compressing the spinal cord. Despite the appearance of the lesion being highly suggestive of a neoplastic process, histopathology on material collected during surgical decompression was consistent with steatitis and the dog demonstrated an excellent response to a prolonged course of antibiotics.

Haemorrhage: MRI is particularly helpful in assessing intracranial or spinal cord haemorrhage or infarct (e.g. a fibrocartilaginous embolism), although an underlying neoplasm may be obscured by a large haematoma. Sagittal and transverse T2W MR images of the caudal lumbar spinal cord of a 2-year-old Boxer dog demonstrating the typical clinical signs of a spinal infarct (fibrocartilaginous embolism). There is no evidence of spinal cord compression; however subtle swelling of the caudal lumbar spinal cord is evident. Furthermore, increased signal intensity (consistent with spinal cord oedema) is present throughout the right side of the caudal lumbar spinal cord (arrows).

Cauda Equina Syndrome: MRI is the imaging modality of choice for the assessment of cauda equina syndrome and has replaced radiography and myelography in centres with access to MRI. Dynamic views, including stressed views, are difficult because of the logistical limitations of the equipment. The interpretation of cauda equina MRI scans (as for radiographs, myelograms and epidurograms) should always be treated with caution, as there appears to be a poor correlation between the degree of cauda equina compression and the clinical signs. Many middle-aged, larger-breed dogs have some degree of lumbosacral degeneration in the absence of clinical signs consistent with cauda equina syndrome.

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Sagittal T2W MR image of the caudal lumbar spine and sacrum of an eight-year-old Labrador retriever demonstrating degeneration of the lumbosacral disc with severe attenuation of the vertebral canal at the lumbosacral junction (arrow). Although MRI is the imaging modality of choice for assessment of cauda equina syndrome the interpretation should always be treated with caution, as there appears to be a poor correlation between the degree of compression and the clinical signs.

Syringomyelia and Hydromyelia: Syringohydromyelia is often seen in dogs with Chiari-like malformations (mainly the Cavalier King Charles Spaniel breed) as a result of compression of the normal CSF drainage pathways at the foramen magnum by the abnormally-formed caudal skull. It may also be seen following spinal cord trauma. MRI will clearly demonstrate the fluid accumulation within the spinal cord and resultant thinning of the overlying spinal cord, which is rarely severe enough to produce convincing spinal cord swelling on myelography. Performing a cervical myelogram in cases with suspected Chiari-like malformation has the added danger that the contrast medium is often injected directly into the syringohydromyelia defect – with the consequent danger of catastrophic respiratory failure. Sagittal T2W MR image of the brain and cervical spine of a two and a half-year-old Cavalier King Charles spaniel demonstrating crowding of the caudal fossa by the cerebellum secondary to occipital bone dysplasia (closed arrow) and resulting fluid distension of the cervical spinal cord (syringohydromyelia) (open arrows)

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CERVICAL SPONDYLOMYELOPATHY: AN OVERVIEW Laurent Garosi DVM, Dip ECVN, MRCVS Davies Veterinary Specialists, Hitchin, Bedfordshire

Cervical spondylomyleopathy (CSM) is a multifactorial disease characterised by cervical spinal cord compression secondary to vertebral canal stenosis. The stenosis results from vertebral malformation associated or not with secondary degenerative changes of structures surrounding the spinal cord. The aetiology of CSM is not fully understood. Nutritional factors have been advocated in horses and in Great Dane as well as breed conformation, head weight and carriage in the Doberman pinscher. As it stands, we have a limited understanding of what we are treating. Many questions remain unanswered about the pathogenesis of CSM, the natural progression of the disease, and the role of medical treatment as opposed to the various types of surgical options considered for this condition.

Pathogenesis 1. The role of cervical stenosis An important feature that distinguishes normal from CSM-affected dogs is that CSMaffected dogs have a consistent stenosis of the cervical vertebral column. Two basics groups of CSM-affected dogs are recognised. The first one includes immature or young adult large-breed dogs such as Great Danes or Doberman pinschers which present with vertebral canal malformation, stenosis, or both. These developmental abnormalities are directly responsible for the spinal cord compression and multiple sites of compression are not uncommon. The second category includes middle-aged or older dogs which have degenerative changes of the vertebral column, ligaments structures and joints (articular facet synovial hypertrophy or cyst formation, dorsal longitudinal and ligamentum flavum hypertrophy, osteophytes production, dorsal or lateral disc extrusion or protrusion) with subsequent acquired stenosis of the vertebral canal. These changes can also be added to the above mentioned developmental abnormalities and progressively induce clinical decompensation. The spinal cord compression due to the stenosis can be static (no worsening according to the head position) or dynamic (worsening or diminution of the cord compression according to the neck extension/flexion position). Adult Doberman pinschers seem to be most commonly affected by these degenerative changes characterised by ventral compressive lesions from hypertrophy of the dorsal part of the annulus fibrosus. The dorsal longitudinal ligament contributes slightly to the compressive force. If dorsal compression is present, it results from the ligamentum flavum or synovial facet proliferation. The primary vertebral abnormalities which can be observed in CSM-affected dogs include: 1. Vertebral body malformation found in 25% of CSM-affected Doberman pinschers. The vertebral body appears misshapen with rounding of the cranio-ventral aspect and a prominent cranio-dorsal ridge, which encroach into the ventral funiculi of the spinal cord. In one study, a third of Doberman Pinschers examined had abnormally shaped caudal cervical vertebrae before 16 weeks of age giving credence for the congenital

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hypothesis of cervical stenosis in this breed (Burbidge et al. Aust Vet J 1999). However, no long-term follow-up was available to establish whether those vertebral changes caused clinical signs later in life. 2. Impaired growth of the cranial vertebral pedicles resulting in cranial vertebral stenosis with cranial orifice narrower than the caudal orifice. The cord development is rapidly impaired and clinical signs appear after a few months of life. A recent morphometric ex-vivo study demonstrated that the height of the cranial aspect of the vertebral canal of large breed dogs is significantly smaller than those of small breeds, resulting in a funnel-shaped vertebral canal particularly in the caudal cervical vertebrae; among the large-breed dogs studied, this funnel shaped appearance of the vertebral canal was most pronounced in Doberman Pinschers (Breit et al. J Anat 2001). 3. Malformed articular processes and facets & synovial proliferation resulting in encroachment into the dorso-lateral funiculi of the spinal cord. These alterations in the articular facets are common in Great Danes. 4. Relative stenosis of the cervical vertebral canal has recently been recognised in a morphologic and morphometric MRI study of Doberman Pinschers with and without clinical signs of CSM (da Costa & al. AJVR 2006). The vertebral canal of CSMaffected dogs appears to be stenotic throughout the cervical portion of the vertebral column, and not just at the caudal cervical region were most clinical lesions have been detected. Since this stenosis is not responsible alone for the clinical signs, it is considered as a relative and not absolute stenosis. This relative stenosis associated with a space-occupying lesion such as intervertebral disc disease or articular facet proliferation, could then lead to the appearance of clinical signs. 5. Abnormal orientation of the articular facets has recently been incriminated as a potential underlying cause for the high incidence of disc degeneration in the caudal cervical spine of large breed of dogs with CSM. A recent ex-vivo osteological study in dogs showed a significant higher incidence of concave articular facets in the caudal cervical spine of large breed dogs compared to small dogs (Breit et al. Eur J Morphol 2002). Concave articular facets facilitate axial rotational motion or torsion. These torsional forces are the main forces leading to intervertebral disc degeneration in nonchondrodystrophoid dogs by causing concentric fissures or tears in the outer annular lamellae leading ultimately to fibrocartilaginous degeneration of the nucleus pulposus. However, in vivo kinetic and biomechanic studies of normal and abnormal dogs are needed to investigate if this different anatomic conformation leads to an altered and potentially harmful force distribution on the vertebral column and in particular the intervertebral disc.

2. The role of instability Instability is defined as “the loss of ability of the cervical spine under physiologic loads to maintain relationships between vertebrae in such a way that there is neither initial nor subsequent damage to the spinal cord or nerve roots, and in addition, there is neither development of incapacitating deformity nor severe pain”. The importance and role of vertebral instability associated with the developmental abnormalities is still controversial. Although it has been commonly proposed in the literature as mechanism implicated in the pathogenesis of CSM, no study has objectively examined this

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hypothesis. The evaluation of instability has only been done subjectively based on radiographic or pathological studies. The idea of instability was initially proposed in the pathogenesis of CSM because of the misalignment of the cervical vertebrae or spinal cord compression that was evident on radiographic views of the cervical portions of large-breed dogs’ vertebral columns during flexion and extension. However, this does not mean that instability is present. Further studies indicated that slippage of cervical vertebrae and variation in the degree of spinal cord compression in flexion or extension are evident in all dogs because these represent a natural pattern of motion in dogs and in humans. A primary instability is difficult to evaluate in the presence of compensating secondary degenerative changes including spondylosis and ligament hypertrophy. However, it seems reasonable to consider vertebral body or facet malformation as a possible predisposing factor for the previously mentioned degenerative processes. As it stands, it appears that a restricted rather than an excessive intervertebral motion is more likely to take place at the sites of advance disc degeneration. It has been found in human that the overall and segmental stiffness of the cervical vertebral column increased with increasing severity of disc degeneration (Kumaresan et al J Orthop Res 2001). Data collected in an MR imaging study to investigate the relationship between disc degeneration and the conventional plain radiographic evaluation of cervical segmental instability in 260 humans patients suggested that instability was associated with early intervertebral disc degeneration but normal or moderate to severely degenerated discs were stable (Dai Spine 1998). Finally, experimental study in dogs also suggested that with progressive fibrocartilaginous degeneration of the intervertebral disc, the increased fibrosis of the nuclear region result in progressive stiffening of the disc (and therefore segmental stiffness causing restricted vertebral motion at the site of disc degeneration) which would point again against instability as a mechanism involved in canine CSM (Bray et al. JAAHA 1998). Although the above evidences do not strongly suggest instability in the pathogenesis of CSM, again in vivo kinetic and biomechanical studies of normal and CSM-affected dogs are needed to investigate this controversial issue.

3. The role of dynamic factors The simple pathoanatomic concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment, often fails to explain the entire spectrum of clinical findings observed in CSM. The pathophysiology of CSM likely involves static factors, which result in acquired or developmental stenosis of the cervical canal and dynamic factors, which involve repetitive injury to the cervical spinal cord. These mechanical factors in turn result in direct injury to neurons and glia as well as a secondary cascade of events including ischemia, excitotoxicity, and oligodendrocyte apoptosis (Kim et al. Spine J 2003). A growing body of evidence in human indicates that spondylotic narrowing of the spinal canal and abnormal or excessive motion of the cervical spine results in increased strain and shear forces that cause localized axonal injury within the spinal cord. During normal motion, significant axial strains occur in the cervical spinal cord. In the presence of pathological displacement, strain can exceed the material properties of the spinal cord and cause transient or permanent neurological injury. Stretch and shear forces generated within the spinal cord seem to be important factors in the pathogenesis of cervical spondylotic myelopathy (Henderson et al. Neurosurgery 2005).

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In any cases, constant progressive or recurrent spinal cord compression is responsible for spinal cord parenchymal ischemic lesions (mostly affecting the gray matter) associated with Wallerian-type degeneration affecting the ascending and descending white matter tracts.

Diagnosis The diagnosis of cervical spondylomyelopathy is based on the demonstration of extradural cord compression by diagnostic imaging studies (myelography, computed tomography or MRI). However, signalment (breed, age) and patient history (age of onset, progression) are the first steps of the diagnostic approach. CSM is mainly observed in large or giant breed dogs. Doberman pinschers are overrepresented with a first peak incidence around 7 years. A second peak is observed at 6 months to 1 year old in large or giant breed dogs such as Great Dane as well as Doberman pincher presenting with vertebral malformation. The most common presentation of CSM is a gait disturbance. Truncal ataxia and progressive tetraparesis are classically observed. Initially the forelimbs may appear less severely affected than the hind limbs. A short stride and a stiff gait may appear later. Neurological examination most often is consistent with a C6 – T2 spinal cord segments presentation. Usually the cranial part of the intumescence is involved, inducing lower motorneuron signs of the shoulders. Muscular palpation may reveal atrophy of the supraspinatus, infraspinatus and biceps brachii muscles. When the lesion is localised at C5-C6 intervertebral space in a post-fixed type cervico-thoracic intumescence (segment C5 not contributing to the nerve roots of the brachial plexus), the neurolocalisation may refer to an upper motorneuron C1-C5 presentation with a ‘floating’ thoracic limb gait. Cervical pain is usually mild or absent and tetraplegia is an uncommon presentation. Clinical manifestation is often characterised by paraspinal muscle rigidity and reluctance to extend or laterally flex the neck. In case of nerve roots compression, pain is usually more evident, especially on forelimb extension. Neurological deterioration can also be observed acutely in some animals. Differentials diagnosis for CSM (slowly progressive gait abnormality on all 4 limbs) should include spinal/spinal cord tumour, meningo-myelitis, discospondylitis and epidural abscess, cervical disc herniation, degenerative myelopathy, leukodystrophies, synovial and spinal arachnoid cyst, atlanto-axial subluxation and syringohydromyelia. Survey radiographs Plain radiographs of the cervical spine are useful in order to rule-out other differentials such as discospondylitis, fracture/luxation, vertebral neoplasm. Radiographic changes suggestive of cervical spondylomyelopathy are: - Vertebral body malformation with rounding of the cranio-ventral aspect and prominent cranio-dorsal ridge which encroach on the vertebral canal - Vertebral misalignment secondary to dorsal vertebral body tilting. This abnormality does not always seem to be correlated with the myelographic findings. In some cases the compression is localised to the adjacent caudal intervertebral space

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- Cranial stenosis of the vertebral canal: in general without clinical consequence when difference between the cranial and caudal vertebral canal diameter is less than 3 mm - Narrowing of the inter-vertebral spaces (spaces C5-C6 or C6-C7 in Doberman pinscher), nucleus pulposus calcification (rare) with or without disc herniation, ventral spondylosis - Increased opacity and loss of the joint space between facets which may be associated with extensive new bone formation on the facets (common in Great Danes) In some affected dogs, plain radiographs can be normal despite the fact that myelographic evaluation will reveal significant extra-dural spinal cord lesion. Myelography Myelography should always be preceded by plain radiographic evaluation. In any case, CSF should be collected in order to rule-out myelitis/meningo-myelitis. Myelographic abnormalities that could be seen in CSM include: Ventral extradural compression centred on an intervertebral space suggestive of disc extrusion or protrusion Dorsal extradural compression suggestive of ligamentum flavum hypertrophy Dorso-lateral extradural compression in general associated with abnormally positioned and/or degeneration of the articular facets Annular extradural compression suggestive of cranial vertebral canal stenosis secondary to impaired growth of the pedicles Ventral extradural compression secondary to the dorsally tilted cranial part of the vertebral body Several views of the cervical spine should be obtained after contrast injection: neutral lateral, flexed lateral, extended lateral, lateral with linear traction of the neck and ventro-dorsal. Compressive lesion can be classified as 1) static or positional (degree of compression influenced by the position of the neck in flexion and/or extension) and 2) traction-responsive or traction non-responsive (improve or not with linear traction of the neck). Plain radiographs obtained with flexion of the neck may enhance the appearance of vertebral misalignment. However, these modifications may be observed in normal patients. The flexed post-myelographic views will show a decreased ventral compression because of ligament and dorsal annular distraction. Post-myelographic extension views make ligaments and dorsal annulus redundant; this will increase ventral cord compression. They may be useful in order to detect lesion that could have been overlooked in neutral view (positional lesion). If two lesions are present, extended myelographic views can be used to determine which one of the lesion is the most significant in terms of compression. These views must be performed with caution as cord compression is exacerbated in this position. Traction views are used to classified the lesion as traction-responsive (annulus fibrosus and/or ligamentous hypertrophy) or not (bony malformation, abnormally positioned and/or degeneration of the articular facets) and should therefore be obtained for surgical planning (decompressive versus distraction procedures). It appears that 20% of dog’s weight is enough to produce sufficient traction. Further studies are necessary to establish the distraction efficacy of different weights and traction methods. Myelography is essential to make a definitive diagnosis. It helps to localise accurately the site and the type of compression (static or positional and traction-responsive or not). Each case should be assigned a definite subtype because therapy should be aimed at

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correcting the abnormality in that individual case, rather than treating every case of CSM the same way. CT or MRI It is often difficult to choose between these two techniques, especially when the results of myelography are not conclusive. CT remains the technique of choice in order to evaluate anatomical osseous details (vertebral malformation, abnormally positioned and/or proliferation of the articular facets) allowing transverse views. Postmyelographic CT studies are used to detect spinal cord atrophy (enlargement of the subarachnoid space). This evaluation may be important in term of prognosis in surgical candidates although no study has been done to correlate this finding with the surgical outcome. MRI also offers the advantage of giving better resolution of soft tissue (ligament structures, compression or parenchyma malformation, spinal cord atrophy) as well as 3-dimentional views. One question that remains to be answered in veterinary medicine is the effect of intramedullary signal intensity changes seen in MRI of some CSM-affected dog on the surgical outcome. The evidences in human medicine suggest that the presence of intramedullary signal changes on T1- as well as T2-weighted sequences on MRI in CSM-affected patients indicate a poor prognosis whereas T2-weighted hyperintensity alone reflects pathologically reversible changes (Suri et al. Spine J 2003, Fernandez et al. J Neurosurg Spine 2007). Correlation between these MRI changes and histopathology has been established in humans. Areas of hyperintensity in T2-weighted images alone were characterized by slight loss of nerve cells, gliosis, and edema in the grey matter, as well as demyelination, edema, and Wallerian degeneration in the white matter while the combination of T2 hyperintensity and T1 hypointensity was characterized by severe histologic changes such as necrosis, myelomalacia, and spongiform changes in the gray matter, as well as white matter necrosis (Ohshio et al. 1993).

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DISC-ASSOCIATED WOBBLER SYNDROME: HOW I TREAT AND WHY THE ROLE FOR DECOMPRESSION Nick Jeffery Dept Veterinary Medicine, University of Cambridge

My interpretation of the background: ‘Disc-associated wobbler syndrome’ (DAWS) is by far and away the most common cause of the ‘wobbler’ syndrome in this country and exhibited predominantly by middle aged large breed dogs with type II disc protrusions in the caudal part of the cervical vertebral column. The treatment of these cases causes controversy because there are plainly a number of different competing approaches (unlike, say, the obvious route of bone removal for young Great Danes with overgrown articular facets etc). DAWS produces a compressive lesion that often induces intermittent contusive insults to the spinal cord, particularly during periods when the vertebral column becomes hyperextended (dorsiflexed), but that probably also occur during ‘everyday life’. Since there is compression of the spinal cord one option is obviously decompression. However this can be sub-divided into what could be called ‘direct’ decompression – i.e. removal of the protruding disc, or perhaps removal of the laminae of the neighbouring vertebrae or ‘indirect’ decompression that can be achieved by linear traction across the disc space, leading to flattening of the dorsal annulus, thus removing the compression. My preferred treatment: This is a neurological condition and so I believe the treatment should be focussed on treating the spinal cord. There is a reasonable case for conservative treatment of these cases bearing in mind the recent reports from Da Costa et al, but for optimal treatment of middle aged dogs I would still opt for surgery – since, in view of the pathological processes, the disc-associated compression over a period of years will cause such loss of axons that response to surgery in future will be considerably blunted. For DAWS caused by a single disc I prefer to excise the disc – i.e. use a ventral slot technique. I use a modified technique (inverted cone) and rongeurs that are reserved for soft tissue removal only. The rationale for this approach is that it is directly decompressive – if the disc is removed there is no compression. The results I have had from this technique over many years have been very good (the last 24 of 25 dogs have recovered very satisfactorily) and the complications are predictable and usually simple to treat. For multi-level DAWS I would consider a multilevel laminectomy, although the shortterm morbidity can be quite high. The rationale for multilevel laminectomy is evidence that the recurrence rate is low after this procedure and (somewhat perversely) that laminectomy is associated with stability of the cervical region.

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Arguments regarding these choices The most common arguments advanced against slotting is that: a) there is a risk of serious intraoperative haemorrhage; and b) a significant proportion of operated dogs will get worse or become non-ambulatory after surgery. Whilst both these arguments have some justification, my experience is that neither occurs frequently; furthermore even if dogs do become non-ambulatory they usually recover. A further argument against slotting is that there is a possible higher risk of a second lesion developing at a neighbouring site. This is a risk associated with both slotting and stabilisation procedures and therefore best avoided by either laminectomy or conservative therapy. The argument against multilevel laminectomy is the high morbidity. I agree and only use this technique in cases that would be at high risk of recurrence (i.e. many protruding discs), need both dorsal and ventral decompression or have many levels of stenosis.

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DISC-ASSOCIATED WOBBLER SYNDROME: HOW I TREAT AND WHY THE ROLE OF INTERVERTEBRAL SPACERS Malcolm McKee DSA Willows Referral Service, 78 Tanworth Lane, Solihull, West Midlands

The pathogenesis of cervical spondylopathy is poorly understood. Vertebral instability has been hypothesised as one important factor (Trotter and others 1976, Mason 1977). Abnormal development of the cervical vertebrae (vertebral malformation) or the concomitant abnormal articulation of these vertebrae may directly compress the spinal cord. More commonly, these features produce spinal cord compression by inducing secondary changes, primarily in the soft tissues. These secondary changes arise in the intervertebral disc, the interarcuate ligament, the articular facets, or in any combination of these structures (Seim and Withrow 1982). Myelography enables the degree of spinal cord compression to be evaluated when the cervical vertebral column is placed in traction, flexion or extension. With all three “stressed” positions the terms dynamic and static have been used synonymously to indicate whether or not the degree of compression is affected. Differentiating traction from the normal physiological positions of flexion and extension is important as it aids management decisions. When the cervical spine is evaluated in traction, compression caused by the intervertebral disc and, to a lesser degree the interarcuate ligament, may be classified as being either traction responsive or traction non-responsive. In traction responsive lesions the compression resolves during traction. There is no change in traction non-responsive lesions. This information, in particular, helps the surgeon to decide whether to mimic the effect of traction by performing a distraction and stabilisation procedure (traction responsive lesions) or whether to decompress by ventral slot / dorsal laminectomy (traction non-responsive lesions). A recent report showed that magnetic resonance imaging is more accurate in predicting the site, severity and nature of spinal cord compression compared to myelography (Da Costa and others 2006).

Surgical management of cervical spondylopathy-associated disc protrusion The large number of reported techniques reflects the difficulty of managing this condition. Direct decompression (ventral slot, dorsal laminectomy), indirect decompression (vertebral distraction-stabilisation), vertebral stabilisation without distraction, and intervertebral disc fenestration techniques have been described. It is difficult to compare results because there are no control groups, cases are generally not consecutive and numbers of cases are usually small. Furthermore the historical, clinical, radiographic, surgical, peri-operative, postoperative and long-term follow-up details vary considerably (Jeffery and McKee 2001). However, it would appear that intervertebral disc fenestration is contraindicated since it does not remove the protruding dorsal annulus fibrosus and it may decrease vertebral stability and collapse the disc space (Mason 1977, Lincoln and Pettit 1985, Macy and others 1999). Vertebral stabilisation techniques without concomitant vertebral distraction may provide inadequate spinal cord decompression for dogs with large disc protrusions (McKee and others 1989). 25

The choice of distraction-stabilisation or ventral slot decompression techniques is primarily dependent on the nature of the compression (i.e. traction responsive or traction non-responsive). Additional factors include the number of sites of spinal cord compression, the degree of vertebral malformation and the presence or absence of thoracic limb lameness (nerve root compression). Both approaches have their own potential advantages and disadvantages (McKee and Sharp 2003).

Vertebral distractionstabilisation

Ventral slot decompression

Advantages Degree of vertebral malformation is generally not a factor Immediate decompression of spinal cord Immediate decompression of spinal nerve roots Immediate improvement in stability Low morbidity No long-term implant complications Possibly reduced incidence of additional disc protrusions Immediate decompression of the spinal cord if the surgeon can remove most of the protruded annulus Also allows for removal of any extruded nuclear material Familiar technique for most surgeons

Disadvantages Less appropriate for traction non-responsive lesions Potentially catastrophic implant complications More risk of iatrogenic spinal cord injury Not all techniques are appropriate for multiple lesions May predispose to additional disc protrusions Internal vertebral venous plexus haemorrhage Technically challenging with the potential for inadequate spinal cord decompression Does not address interarcuate ligament lesions Inadequate spinal nerve root decompression Can cause significant postoperative morbidity

Polymethylmethacrylate (PMMA) bone cement plugs have probably been the most commonly used intervertebral spacers used in vertebral distraction-stabilisation techniques over the last decade. The following are examples of other reported intervertebral spacers that are now primarily of historical interest: Screw / bone cement and bone graft technique Ellison and others (1988) reported the use of an interbody corticocancellous iliac crest autograft stabilised with ventral screws and bone cement in 10 dogs. Clinical improvement was observed in eight dogs. Implant loosening developed in three of which two were euthanatised. Screw and bone graft technique Bruecker and others (1989) described the use of a transvertebral screw and interbody cortical tibial allograft in seven dogs. The outcome was considered to be successful in three dogs. In four dogs ventral spinous process fracture occurred with resultant loss of vertebral distraction. Plastic plate and bone graft technique Bruecker and others (1989) reported the use of a ventral plastic plate and interbody cortical tibial allograft or bovine cancellous xenograft in 37 dogs. Twenty-four dogs had a successful neurological recovery. Eight dogs were considered surgical failures. Five dogs died of unrelated causes before surgical success or failure could be determined. Screw and double washer technique McKee and others (1990) reported the results of a prospective study using a transvertebral screw and double interbody washers in 17 Dobermans and three great Danes. Seventeen dogs improved following surgery and of these seven were considered 26

to be normal. One dog died in the early postoperative period and two were euthanatised due to ventral spinous process fracture. One dog had a recurrence of pelvic limb ataxia 10 months following surgery due to screw displacement into the vertebral canal. Other complications included vertebral canal remodelling (n=1) and screw breakage (n=1). Washer subsidence was evident in all cases at follow-up. Screw and 7.5 / 6.0 mm washer technique McKee and others (1999) reported the use of 7.5 mm and 6.0 mm interbody washers and a transvertebral screw in 78 consecutive dogs. The median duration of hospitalisation following surgery was two days. Euthanasia was performed in nine dogs within six months of surgery and fifteen dogs had varying degrees of neck pain during this period. Long-term follow-up information was available on 65 dogs nine to 70 months following surgery (median 32 months). Sixty-three of these dogs improved postoperatively. Neurological function subsequently deteriorated in 17 dogs, 10 to 59 months following surgery (median 34 months). Eight cases had further myelographic investigations and all had additional disc protrusions with no evidence of cord compression at the previous sites of surgery. The remaining nine cases had a deterioration in pelvic limb function but were not investigated further. Complications included vertebral endplate fracture (n=6) and screw displacement into the vertebral canal (n=3). Washer subsidence with loss of vertebral distraction was evident in all cases at follow-up. Radiograph 19 months following surgery showing subsidence of the C6-C7 intervertebral washer and marked new bone formation ventral to the affected space. Despite the loss of vertebral distraction the spinal cord is not compressed

Vertebral distraction-stabilisation using an intervertebral bone cement plug Surgical technique The patient is positioned in dorsal recumbency with the upper jaw secured cranially and the thoracic limbs caudally in traction. The cervicothoracic region is elevated 5 to 10 cm in a trough. Symmetrical positioning is critical. A ventral approach to the cervical vertebrae is performed. Vertebral distraction may be achieved with a distraction instrument (Veterinary Instrumentation, U.K), distraction screw or by manual traction on the cervical spine. The latter is difficult to control and generally not recommended. Distraction techniques involving disc fenestration for placement of the distractors may increase vertebral instability and contribute to the development of additional disc protrusions (Macy and others 1999). Anchoring the tips of the distraction instrument in the vertebral bodies is therefore preferable. A disadvantage of the distraction screw technique is the creation of a stress riser in the intervertebral cement plug, which may then break. The affected disc space is exposed and a partial discectomy performed by removing the ventral annulus fibrosus, nucleus pulposus and vertebral endplate cartilage. The medial aspect of the annulus fibrosus is removed bilaterally with a number 11 scalpel blade to

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leave a narrow rim at the lateral margins. Material in the craniodorsal disc space is the hardest to remove. Care is taken to not penetrate the dorsal annulus fibrosus and so enter the vertebral canal. Either of the following techniques may be employed to obtain vertebral distraction and prevent ventral displacement of the intervertebral bone cement plug. Cement plug with endplate anchor holes (Dixon and others 1996) To prevent ventral displacement of the cement, anchor holes are burred in the vertebral endplates. Burring the caudal endplate of the more cranial vertebra is difficult because of the orientation of the disc spaces in the caudal cervical spine. An angle-tipped bur attachment is particularly advantageous for this task. The necessity of postoperative external support with this technique remains unresolved. Cement plug with retention screws (McKee 2000) In order to prevent ventral displacement of the cement, retention screws are placed in the caudal vertebral body. The point of entry for the cement retention screws is the cranioventral aspect of the vertebral body and the tips of the screws should penetrate the trans-cortex to prevent loosening. In contrast to the anchor hole technique, this technique preserves the vertebral endplates and thus increases the area of contact with the interbody bone cement. Prior to mixing sterile, medical-grade, polymethylmethacrylate bone cement the intervertebral area is lavaged and dried. Bone cement is packed into the distracted disc space either by hand or injection via a catheter-tipped syringe working from dorsal to ventral to ensure maximum filling. As the cement hardens it is irrigated with sterile saline solution in an attempt to dissipate the heat of polymerisation. Numerous small holes are drilled in the ventral aspect of the exposed vertebrae to promote incorporation of a cancellous bone graft. The latter is collected from the proximal aspect of one or both humeri and placed over the foraged vertebrae and bone cement.

Vertebral distractor, C6-C7 interbody cement plug, 2 retention screws & cancellous bone graft

Pre- and postoperative radiographs showing C6-C7 vertebral distraction-stabilisation using an interbody cement plug and two retention screws

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Pre- and postoperative radiographs showing C5-C6 vertebral distraction-stabilisation using an interbody cement plug and two retention screws. Note the small distraction screw

Possible complications include loss of vertebral distraction due to subsidence or endplate fracture, ventral displacement of the cement plug, cement plug breakage, and inadvertent entry of bone cement into the vertebral canal (McKee and Sharp 2003). Some degree of subsidence and loss of vertebral distraction is common with both techniques, although this is usually of no clinical significance. The main advantage of cement plug techniques is that they can be used to distract and stabilise more than one disc space. Addressing the two high-risk sites (C5-C6 and C6-C7) at the same time may prevent the tendency of an untreated disc to cause clinical signs at a later date.

Breakage of cement plugs at C5-C6 and C6-C7 with concomitant subsidence and loss of vertebral distraction

Cement plug technique results Cement plug with vertebral distraction screw McKee and Miller (1996) reported the results of intervertebral cement plug using a 2.7 mm vertebral distraction screw in 13 Dobermans pinschers and five great Danes. Anchor holes or plug retention screws were not used. Eleven dogs improved. Complications were recorded in the remaining seven cases. In five the bone cement fractured through the transvertebral screw hole between day two and day 30 postoperatively (the neurological dysfunction remained unchanged in one dog and deteriorated in four). Due to inadequate interbody cement, fracture of the caudal endplate of C6 occurred in one case on the second day following surgery. One dog deteriorated due to the vertebral distraction causing ventral protrusion of the interarcuate ligament.

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Cement plug with endplate anchor holes Dixon and others (1996) described the use of an interbody cement plug retained with vertebral endplate anchor holes in 22 dogs. Nineteen of 21 dogs for which success/failure could be determined had a successful outcome, and 11 dogs attained normal neurologic status. The two cases that were considered failures involved dogs that were non-ambulatory tetraparetic prior to surgery and failed to improve to a functional status. Complications included ventral displacement of the cement plug without loss of distraction in one dog and discospondylitis at an adjacent disc space in another dog. Evidence of fusion of the affected vertebrae, in the distracted position, was radiographically evident in all dogs. Cement plug with retention screws The preliminary results of the cement plug technique with vertebral body retention screws in 47 Dobermans treated at Willows Referral Service will be presented.

Protrusion of additional intervertebral discs Protrusion of additional intervertebral discs (so-called “domino” lesions) occurs in approximately 20 per cent of dogs at variable times following surgery (Bruecker and others 1989, McKee and others 1999). It has been postulated that these additional disc protrusions result from abnormal stresses imposed on discs by stabilisation or fusion of adjacent vertebrae. However, it is also possible that the degeneration and protrusion of additional discs is directly related to the vertebral malformation rather than the surgery and that as in humans C5-C6 and C6-C7 are both high-risk discs (Hilibrand and others 1999). Whatever the reason, a surgical technique that can address both sites is probably advantageous. It is possible that foraging and cancellous bone grafting the adjacent vertebrae of these discs may increase spinal stability and reduce the possibility of protrusion.

C5-C6 intervertebral disc protrusion that caused a relapse of pelvic limb ataxia three years following C6-C7 cement plug distraction-stabilisation surgery

The future of intervertebral spacers An important requirement for intervertebral spacers / spinal fusion devices is that they provide sufficient stability and have a low subsidence risk. It is unlikely that cement plug techniques will ever achieve this. A recent experimental study in sheep concluded that intervertebral cement plug stabilisation, albeit in combination with ventral slot decompression, did not maintain distraction of the disc space and bony union between vertebrae was not achieved (Fransson and others 2007). Cervical spinal fusion cages are commonly used in people. These interbody cages are hollow and may enable vertebral distraction and bony fusion (Wilke and others 2002). The BioMedtrix tantalum spinal

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fusion block and Synthes-Stratec intervertebral spacers (SynCage-C and Cervios poly ether ether ketone “PEEK”) are worthy of investigation in dogs with cervical spondylopathy-associated disc protrusion. The elastic modulus and bone ingrowth characteristics of some of these fusion devices may be more physiological than PMMA cement and metal washers (Bobyn and others 1999). Total disc replacement may also be an option in the future (Mayer 2005).

Tantalum interbody spinal fusion block at C5-C6 stabilised with two K-wires

References BOBYN, J. D., STACKPOOL, G. J., HACKING, S. A., TANZER, M. & KRYGIER, J. J. (1999) Characteristics of bone ingrowth and interface mechanics of a new porous tantalum biomaterial. Journal of Bone and Joint Surgery 81B, 907-914 BRUECKER, K. A., SEIM, H. B. & WITHROW, S. J. (1989) Clinical evaluation of three surgical methods for treatment of caudal cervical spondylomyelopathy of dogs. Veterinary Surgery 18, 197-203 Da COSTA, R. C., PARENT, J., DOBSON, H., HOLMBERG, D. & PARTLOW, G. (2006) Comparison of magnetic resonance imaging and myelography in 18 Doberman pinscher dogs with cervical spondylomyelopathy. Veterinary Radiology & Ultrasound 47, 523-531 DIXON, B. C., TOMLINSON, J. L. & KRAUS, K. H. (1996) Modified distraction-stabilisation technique using an interbody polymethyl methacrylate plug in dogs with caudal cervical spondylomyelopathy. Journal of the American Veterinary Medical Association 208, 61-68 ELLISON, G. W., SEIM, H. B. & CLEMMONS R. M. (1988) Distracted cervical spinal fusion for management of caudal cervical spondylomyelopathy in large-breed dogs. Journal of the American Veterinary Medical Association 193, 447-453 FRANSSON, B. A., ZHU, Q., BAGLEY, R. S., TUCKER, R. & OXLAND, T. R. (2007) Biomechanical evaluation of cervical intervertebral plug stabilization in an ovine model. Veterinary Surgery 36, 449-457 HILIBRAND, A. S., CARLSON, G. D., PALUMBO, M. A., JONES, P. K. & BOHLMAN, H. H. (1999) Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. Journal of Bone and Joint Surgery 81A, 519-528 JEFFERY, N. D. & McKEE, W. M. (2001) Disc-associated wobbler syndrome in the dog – examination of the controversy. Journal of Small Animal Practice 42, 574-581 LINCOLN, J. D. & PETTIT, G. D. (1985) Evaluation of fenestration for treatment of degenerative disc disease in the caudal cervical region of large dogs. Veterinary Surgery 14, 240-246 MACY, N. B., LES, C. M, STOVER, S. M. & KASS, P. H. (1999) Effect of disk fenestration on sagittal kinematics of the canine C5-C6 intervertebral space. Veterinary Surgery 28, 171-179

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MASON, T. A (1977) Cervical vertebral instability (wobbler syndrome) in the Doberman. Australian Veterinary Journal 53, 440-445 MAYER, H. M. (2005) Total lumbar disc replacement. Journal of Bone and Joint Surgery 87B, 10291037 McKEE, W. M., LAVELLE, R. B. & MASON, T. A. (1989) Vertebral stabilisation for cervical spondylopathy using a screw and washer technique. Journal of Small Animal Practice 30, 337-342 McKEE, W. M., LAVELLE, R. B., RICHARDSON, J. L. & MASON, T. A. (1990) Vertebral distraction-fusion for cervical spondylopathy using a screw and double washer technique. Journal of Small Animal Practice 31, 22-27 McKEE, W. M. & MILLER, A. (1996) Surgical management of canine cervical spondylopathy. Veterinary Record 138, 340 McKEE, W. M., BUTTERWORTH, S. B. & SCOTT, H. W. (1999) Management of cervical spondylopathy-associated intervertebral disc protrusions using 7.5 mm and 6.0 mm intervertebral metal washers in 78 dogs. Journal of Small Animal Practice 40, 465-472 McKEE, W. M. (2000) Intervertebral disc disease in the dog 2. Management options. In Practice 22, 458-471 McKEE, W. M. & SHARP, N. J. H. (2003) Cervical spondylopathy. In: Textbook of Small Animal Surgery. 3rd edition. Ed Slatter, Saunders, Philadelphia, pp 1180-1193 SEIM, H. B. & WITHROW, S. J. (1982) Pathophysiology and diagnosis of caudal cervical spondylomyelopathy with emphasis on the Doberman pinscher. Journal of the American Animal Hospital Association 18, 241-251 TROTTER, E. J., deLAHUNTA, A., GEARY, J. C. & BRASMER, T. H. (1976) Caudal cervical vertebral malformation-malarticulation in great Danes and Doberman pinschers. Journal of the American Veterinary Medical Association 168, 917-930 WILKE, H. J., KETTLER, A. & CLAES, L. (2002) Stabilising effect and sintering tendency of 3 different cages and bone cement for fusion of cervical vertebrae segments. Orthopaedics 31, 472-480

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DISC-ASSOCIATED WOBBLER SYNDROME: HOW I TREAT AND WHY THE ROLE OF PINS/SCREWS AND PMMA Luisa De Risio, DVM, MRCVS, PhD, Dip ECVN Neurology/Neurosurgery Unit, Centre for Small Animal Studies, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk

The use of metal implants and PMMA to achieve vertebral distraction-fusion for the treatment of disc associated cervical stenotic myelopathy (CSM) has first been described by Ellison et al (1) and Bruecker et al (2). Ellison reported the use of cortico-cancellous bone autograft from the ilium, partly threaded 4mm-diameter cancellous bone screws and PMM in 10 dogs, four of which had previous unsuccessful surgery (ventral slot or fenestration). Only 10 mm of the screw length was threaded and penetrated the vertebral body, the unthreaded part was exposed. Distraction was achieved with an assistant applying gentle traction on the neck and maintained by the cortico-cancellous bone autograft that was placed within the ventral slot. A Robert-Jones neck bandage or neck brace was applied postoperatively. Eight of the 10 dogs had a successful outcome with a mean follow-up of 24 months (range, 10 to 36 months). Implant loosening (PMM fracture and/or screw pull-out) developed in 3 dogs (including both dogs that underwent distraction-fusion over 2 consecutive intervertebral disc spaces) and resulted in a poor outcome in 2 of these 3 dogs (1). Bruecker’s retrospective study included 41 dogs with disc associated-CSM at C5-6 and/or C6-7. All dogs underwent a partial ventral slot, linear traction of the cervical spine (with a vertebral spreader), placement of an autologous cancellous bone graft and stabilization with Steinmann pins (2 in each vertebral body, placed at diverging angles, approximately 30-35° from the midline) and PMMA. The success rate was of 90% (37/41) with a mean follow-up of 20 months (range 3-50 months). Mean time to best response was 3 months. Eight of the 37 dogs with a successful outcome initially, had recurrence of clinical signs 5 to 42 months post-operatively; in 3 of these a new lesion at an adjacent intervertebral disc space was confirmed by myelography or post-mortem examination (2). Over the years these techniques have been widely used and partially modified based on individual experience and preference.

PATIENT POSITIONING The patient is positioned in dorsal recumbency with the cervical spine perfectly aligned in a relatively neutral or mildly extended position. Excessive extension should be avoided as it tends to close the dorsal part of the disc space and exacerbate spinal cord compression (3, 4). The upper jaw is secured cranially and the thoracic limbs caudally in traction, symmetrical positioning is critical (3). A standard ventral approach to the cervical spine is performed. A paramedian approach has been suggested to improve exposure to the caudal cervical vertebrae (4).

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VENTRAL SLOT In the technique originally described by Ellison and Bruecker a partial ventral slot was performed (1,2). In Bruecker study the slot was no wider than 1/2 to 3/4 of the width of the vertebra and no longer than 1/4 of the length of the vertebra cranially or caudally. The slot was created to the level of the inner cortical bone only and did not extend into the spinal canal in all but 1 dog (2). The size of the slot used by different surgeons may vary, however it is important to preserve enough of the vertebral body length to allow placement of 2 screws or threaded pins of adequate size (e.g 3.5 mm for a 25-30 kg dobermann). A partial slot has the main purpose to expose the cancellous bone to achieve osseous fusion. In dogs with very sclerotic end-plates and poorly vascularised subcondral bone, multiple forages can be performed within the edges of the slot. Performing a complete slot allows entering the vertebral canal and removing the dorsal annulus and protruded/extruded disc material. This can be particularly useful in those cases in which disc-associated compression improves but not completely following cervical traction. Removing chronically herniated disc material and achieving good visualization of the spinal cord may be difficult in dogs with CSM. Using a head-light, maintaining the vertebrae in a distracted position and performing the inverted cone technique described by Goring (5) may help to improve visualization. The main disadvantages of the complete slot include the risk of hemorrage from the vertebral sinuses, and manipulation of the spinal cord which may result in transient postoperative deterioration. If a complete slot is preformed a collagen sponge (Gelfoam, Lysostip, Spongostan) should be interposed between the exposed spinal cord and the cancellous bone graft that is positioned within the slot to promote fusion. Most surgeons use autologous cancellous bone harvested from one or both proximal humerus/i. Other surgeons use an autologous cortical or cortico-cancellous bone graft harvested from the ilial wing or transverse process of C6 and place it within the partial slot in order to maintain vertebral distraction. The autologous cancellous bone graft is subsequently position to promote bone fusion. A further modification of this technique involves the use a cortical ring allograft (commercially available from Veterinary Transplantation Service, USA) filled in with cancellous bone autograft (6). The cortical ring allograft is packed with autologous cancellous bone and is placed in the intervertebral disc space after linear traction is applied to the spine. This cortical ring allograft maintains distraction and decreases load on the metal-bone implant until fusion occurs. In this latter technique a ventral slot is not performed (6). The annulus fibrosus, nucleus pulposus and end-plate cartilage are removed in order to prepare a smooth surface for good contact with the cortical ring allograft. The centre of both endplates should be foraged to expose cancellous bone and promote vascular ingrowth (6).

DISTRACTION Distraction has been achieved with a number of different instrumental distractors, with screws positioned in a way to produce intervertebral distraction, and with an unscrubbed assistant pulling on the head of the dog to provide linear traction of the cervical spine. In the technique originally described by Bruecker the tips of a modified Gelpi were placed within the intervertebral disc spaces cranial and caudal to the one to distract (2). This is not longer advisable as it might enhance intervertebral disc degeneration, protrusion, collapse and instability at the spaces adjacent to the one undergoing distraction-fusion (7). The tips of the distractor can be placed within the vertebral body of the vertebrae cranial and caudal to the 2 vertebrae to distract. Regardless of the type of instrumental distractor used it is important to position the tips

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as deep as possible within the vertebral body in order to avoid traction on the ventral aspect of the vertebral body only. This may produce wedging of the intervertebral disc space with further collapse of its dorsal part and exacerbation of the buckling of the dorsal annulus fibrosus. Another method to achieve distraction is the use 2 “distraction screws” directed from the ventral aspect of the cranial vertebra to be distracted, through the intervertebral disc space, to rest against the end plate of the caudal vertebra to be distracted (3, 4). With this latter method it is very important to position the screws correctly and to achieve a symmetrical distraction. If one of the 2 screws is aimed too laterally or too ventrally this can result in lateral or dorsal (respectively) wedging of the disc space and asymmetrical distraction (4). If distraction is provided by an un-scrubbed assistant pulling on the head of the dog it is important that the operator is knowledgeable of spinal anatomy and dog’s positioning in order to achieve linear distraction of the vertebrae avoiding cervical extension and subsequent dorsal wedging of the intervertebral disc space. The surgeon should monitor closely the adequacy of the distraction. In addition, the adequate degree manual distraction needs to be maintained until the cement has fully hardened. Orthopaedic cement that hardens in 3-4 minutes may help. When applying distraction it is also important to be careful not to overdistract the intervertebral disc space, especially if the anaesthetist has used neuromuscular blocking agents, as this may result in excessive postoperative load on the implant and increase the risks of in implant failure.

PINS/ SCREWS In the technique originally described by Bruecker (2) Steimann pins were positioned at diverging angles, approximately 30-35° from the midline, with the aim to engage two cortices with each pin. Penetrating 2 cortices increases the pull-out strength of the implant. However, aiming at penetrating the far cortex is associated with higher risks of iatrogenic damage to the spinal arteries, nerve roots and the spinal cord even when the recommended angle of 30-35° is used (8). Advanced diagnostic imaging such as CT and MRI help to plan accurately the ideal angle and depth of insertion of each pin/ screw in each individual. These angles and depth of implant insertion can be calculated preoperatively in order to maximize bone purchase and minimize the risks of iatrogenic lesion. The screws/ pins should be placed in a convergent orientation in order to improve pull-out strength. Positive profile fully threaded pins should be used instead of smooth ones if pins are preferred to screws. The pins/ screws should enter the vertebral body close to the mid-line and then be driven towards the contralateral aspect of the vertebra, away from the vertebral canal (4). Two implants are placed in the vertebrae on each side of the lesion (4). Cortical (or cancellous) fully threaded bone screws can be placed in a monocortical fashion as long as they are placed correctly (nice tread, good purchase in the bone, no over tightening) and as deep as possible (based on accurate CT/MRI preoperative planning) in order to maximize pullout strength. Using 3 monocortical screws instead of 2 in each vertebra will strengthen the implant is screw size is maintained adequate. In general, only the outer cortical bone is tapped. Tapping of the cancellous bone is not recommended as it might reduce pullout strength (9, 10). In general, in an averaged-sized dobermann pinscher, the screws (3.5 to 4.5 mm diameter) should penetrate at least 1.2 cm in the vertebral body, leaving 1.2-1.4 cm exposed to be incorporated in the PMMA. Once all screws are in place their head can be filled with bone wax. This will help in case they need to be pulled out in the future.

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PMMA The PMMA is placed along the ventral aspect of the vertebrae incorporating all the screws. Screws and PMMA should be placed in a fashion that minimizes interference with the trachea and/ or oesophagus. While the cement hardens it should be irrigated constantly to dissipate the heat of polymerization.

TREATMENT OF TWO SITES It has been recommended that the use of metal implants in combination with PMMA to achieve distraction-fusion be limited to only one level, due to the potential failure of implants associated with multilevel fusions (1-4). The main complications associated with 2 level fusions in the limited case reports available has been fracture of the PMMA (1) and loosening of the pin/s or the screw/s with loss of vertebral distraction (1, 2). Stabilization of 2 consecutive intervertebral disc sites using PMMA and bi-cortical pins has been described (11). To improve the strength of the implant when bridging 2 consecutive intervertebral disc spaces, 2 or 3 screws should be placed in each vertebra and the cement should be reinforced with 1 or 2 Steinmann pin/s (4). The use of the cortical ring allograft placed under compression after distraction of the intervertebral disc space, may also help in increasing the overall stability until bony fusion occurs (6).

POST OPERATIVE MONITORING AND COMPLICATIONS Postoperative management includes analgesia, anti-inflammatory and antibiotic treatment, nursing care, physiotherapy, confinement and gradual reintroduction to normal exercise level. Most surgeons do not apply a cervical brace. The first 6-8 weeks are most critical with regard to movement at the site of desired fusion since this is the time a weak callus forms and subsequent ossification develops (12). Sufficient strength develops by 3-6 months (12). Fusion criteria in humans include complete trabecular bridging of the graft-bone interface and a lack of motion on dynamic images (13). The mean time for maximum improvement of neurological function following successful distraction and fusion in dogs has been reported to be 3 months (2). Some improve much more quickly (48 hours) and some take up to 13 months (2). Potential complications using this procedure include pin/ screw penetration of the spinal canal, iatrogenic spinal cord, nerve root or vascular injury, pin/ screw loosening, pin/ screw breakage, PMMA fracture, cortical bone graft collapse/movement, and infection of the endplates or implants. Pseudoarthrosis and domino lesion are potential long-term complications.

DOMINO LESIONS One of the main disadvantages of distraction-fusion techniques for CSM is the risk of “domino lesion” at adjacent intervertebral disc space/s. It has been reported than normal disc spaces can tolerate increased biomechanical stressed following fusion of an adjacent intervertebral disc space (2, 14). On the contrary, degenerated discs may suffer a high incidence of domino lesions (2, 14). MRI allows assessment of the hydration of intervertebral discs and is very sensitive in detecting mild protrusions. In case of degenerated and slightly protruding intervertebral disc/s adjacent to the one to undergo

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distraction-fusion a prophylactic procedure can be performed in order to minimize the risk of domino lesions. This can be performed by forage of the cortical bone of the ventral aspect of 2 adjacent vertebrae (without damaging the intervertebral disc) and applying cancellous bone over the exposed vertebral cancellous bone (4).

References 1. 2.

3. 4. 5.

6. 7. 8.

9. 10. 11. 12. 13. 14.

Ellison GW, Seim HB, Clemmons RM. Distracted cervical spinal fusion for management of caudal cervical spondylomyelopathy in large-breed dogs. JAVMA 1988; 194:447-453. Bruecker KA, Seim HB III, Blass CE. Caudal cervical spondylomyelopathy: decompression by linear traction and stabilization with Steinmann pins and polymethyl methacrylate. JAAHA; 1989, 25:677-683. McKee WM, Sharp NJH. Cervical spondylopathy. In: Slatter DH, ed. Textbook of small animal surgery. 3rd ed. Philadelphia: Saunders, 2003;1180–1193. Sharp NJ, Wheeler SJ (2005) Cervical spondylomyelopathy. In; Small Animal Spinal Disorders. 2nd ed. Mosby Goring RL, Beale BS, Faulkner RF. The inverted cone decompression technique: a surgical treatment for cervical vertebral instability “Wobbler syndrome” in Doberman pinshcers. JAAHA, 1991; 27: 403-409. Bergman RL. Modification of spinal fusion techniques for canine cervical spondylomyelopathy. Proceedings of ACVIM Annual Symposium 2007 Macy NB, et al. Effect of disc fenestration on sgittal kinematics of the canine C5-C6 intervertebral space. Vet Surg 28:171, 1999. Corlazzoli D. Safe corridors for implant insertion in caudal cervical spondylomyelopathy: a computed tomography study in affected dobermann pinscehrs. Proceedings of 2006 ECVN annual congress; p 60. Dickman CA and FF Marciano. Operative Tech of Cervical Spine, RF Spetzler, Ed.1998, Saunders: Philadelphia. p. 123-139. Schatzker J, F Meutstege, and WD Prieur, in Man Int Fixation in Small Animals, WO Brinker, et al., Eds. 1998, Springer: Berlin. p. 57-96. Seim HB, in CVT XIII Small An Prac, JD Bonagura, Ed 2000, Saunders: Philadelphia. Kalfas. Neurosurg Focus, 2002.12(1). Kaiser MG, et al., Neurosurgery, 2002. 50(2):229. Hilbrand A, Carlson G, Palumbo M, et al. Radiculopathy and myelopathy at segments adjacent to the site of a previous anterior cervical arthrodesis. The Journal of bone and joint surgery-American volume. 1999; 81:519-528.

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DISC-ASSOCIATED WOBBLER SYNDROME: HOW I TREAT AND WHY THE USE OF AO IMPLANTS Rita Gonçalves Institute of Comparative Medicine, Division of Companion Animal Sciences, Faculty of Veterinary Medicine, University of Glasgow

Over the past years, a proliferation of plate devices for anterior (ventral) cervical fusion in human orthopaedic practice has occurred.1,2 These plates have been reported to improve both fusion rates and outcome in human patients and are therefore routinely used in the management of many pathological conditions affecting the human cervical spine.2,3 The use of spinal locking plate systems offers specific advantages over the other distraction-stabilisation methods. These plates allow the use of monocortical screws, thus significantly reducing the risk of iatrogenic damage to the spinal cord. Due to the locking system screw loosening and backout are less likely. The locking mechanism minimises the compressive forces exerted by the plate on the bone, which means that the plate does not need to have intimate contact with the underlying bone. This not only facilitates application but also preserves periosteal blood supply at the fusion site. Also, some disadvantages of the other surgical techniques can be avoided (e.g. increased risk of infection, possibility of pin migration and of compression of adjacent structures when using pins/screws and bone cement).4

Synthes Cervical Spine Locking Plate (CSLP) System: The CSLP system (Synthes Spine, Paoli, PA) has been used in veterinary medicine from 1995 with little change in the recommended surgical technique. However, to date, experience in its application is limited to short communications rather than formal clinical trials.5,6,7 The Synthes CSLP is available in 3 models (Classic, Narrow and Variable Angle). One level and multiple level plates are available at different lengths from 20 to 109mm. This system uses monocortical self tapping or self drilling screws with expansion heads which are locked with a locking screw, thus ensuring stable locking of the screws in the plate.

Figure 1. The CSLP Systems: CSLP Classic, CLSP Narrow and CSLP Variable Angle

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Surgical technique: The standard ventral approach to the cervical spine is used. After identification of the affected intervertebral disc space, distraction of the segment (linear traction, Caspar distractor, modified Gelpi retractors, Synthes Cervical distractor) is used to expand the disc space. A complete discectomy is performed and the cartilage from the endplates is removed. Bone cement, a cancellous autograft within an interbody cage or within a cortical ring allograft is then introduced in the disc space. Once the preferred intervertebral disc substitute is placed, the distraction is relieved and the plate can be applied. The plate is contoured to fit the ventral surface of the vertebral bodies, which in turn are shaped to allow the plate to fit by removing any osteophytes and irregularities. However, as much of the cortical bone layer as possible should be preserved, as it contributes substantially to the screws resistance to pulling out (very important in systems that rely on monocortical bone purchase). Temporary fixation pins can be used during drilling and screw insertion. A locking drill guide as well as drill bits with safety stop help correct insertion of the screws and prevent iatrogenic damage to the spinal cord. Finally, locking screws are placed within the screw expansion heads, locking these to the plate.

Options for intervertebral disc replacement: 1. Bone cement – if used, preparation of the endplates should include a few drill holes to increase bone-cement interface. In human medicine, it is reported to achieve less bone fusion around the implant than other techniques but does not seem to affect long-term outcome.8 2. Bone grafts: 1. cancellous autografts lend little mechanical stabilization and if used alone may predispose to collapse of the intervertebral space. These grafts possess osteoconductive, osteogenic and weak osteoinductive properties.9 2. the Veterinary Transplant Services, Inc (Kent, Washington) offers several different cortical allograft options for spinal fusion, including cortical blocks and dowels. The use of cortical allografts may provide increased mechanical strength and help maintain distraction. These grafts only possess osteoconductive and weak osteoinductive properties but can be used in conjunction with cancellous autografts to promote increased fusion rates.9 3. 3. Cages – interbody fusion cages are hollow implants that restore physiological disc height, allowing bone growth within and around them, thus stimulating bone fusion. The cages can be filled with an allograft (e.g. Osteo-AllograftTM, Veterinary Transplant Services) or with a cancellous autograft. An example is the SynCage-C (Synthes), which has been used in veterinary medicine in conjunction with the CSLP.5 It is available in 4 sizes and both in curved and wedged shapes to facilitate adaptation to individual anatomical circumstances (Fig 2).

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Figure 2. Wedge-shaped and curved SynCage-C (SYNTHES Spine, Paoli, PA)

Complications that may arise from this surgery relate to graft collapse and subsidence, implant problems, pseudoathrosis and possible development of instability at other levels. The most significant disadvantages are the cost and fact that these plates were designed for the human cervical spine, resulting in time-consuming shaping of the ventral aspect of the cervical vertebrae and of the spinal plate for adequate fit.7 In summary, the use of spinal locking plates has emerged as a viable alternative in the surgical management of cervical spondylomyelopathy in dogs. Although further experience is necessary, the preliminary results divulged by those using this technique present it as a safe and reliable method for distraction-stabilisation of the cervical spine.

References: 1. 2. 3. 4. 5. 6. 7.

8. 9.

Haid RW, Foley KT, Rodts GE, et al: The Cervical Spine Study Group anterior cervical plate nomenclature. Neurosurg Focus 12:1-6, 2002 Baskin JJ, Vishteh AG, Dickman CA, et al: Techniques of Anterior Cervical Plating. Operative Techniques in Neurosurgery 1:90-102, 1998 Kaiser MG, Haid RW, Subach BR, et al. Anterior cervical plating enhances arthrodesis after discectomy and fusion with cortical allograft. Neurosurgery 50: 229-238, 2002 Wheeler SJ, Sharp NJH: Caudal cervical spondylomyelopathy, in: Wheeler SJ, Sharp NJH (eds): Small Animal Spinal Disorders. London, Mosby, 2000 pp 135-154 Matis U: AO spinal implants for canine Wobbler syndrome. Proceedings, 1st World Orthopaedic Veterinary Congress, Munich, pp 137-138, 2002 Shores A: The use of cervical locking plates in spinal surgery. Proceedings, 24th Annual American College of Veterinary Internal Medicine Forum, Louisville, pp 295-296, 2006 Bergman RL: Spinal fusion techniques for canine cervical spondylomyelopathy: past experience. Proceedings, 25th Annual American College of Veterinary Internal Medicine Forum, Seattle, pp 321-323, 2007 Schröder J, Grosse-Dresselhaus F, Schul C, et al. PMMA versus titanium cage after anterior cervical discectomy - a prospective randomized trial. Zentralbl Neurochir 68:2-7, 2007 Pilitsis JG, Lucas DR, Rengachary SR. Bone healing and spinal fusion. Neurosurg Focus 13:1-6, 2002

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DISC-ASSOCIATED WOBBLER SYNDROME: HOW I TREAT AND WHY THE ROLE OF CONSERVATIVE TREATMENT?

Laurent Garosi DVM, Dip ECVN, MRCVS Davies Veterinary Specialists, Hitchin, Bedfordshire Currently, there are multiple procedures that are used clinically in dogs, and the recommended therapy is dependent on the type of compression present and the experiences and opinions of the attending veterinarian. Two basic types of surgical intervention are decompression and distraction/fusion techniques. While each of these techniques may be effective, each method is not without problems. Despite having a high short-term success, all of the surgical methods of treatment have unacceptable rates of failure with recurrence rate of clinical signs estimated at about 20%. However, the cause of such deterioration is usually not investigated. Many questions remain unanswered about the natural progression of CSM. Until this issue is resolved, the long-term benefits of the various surgical techniques that have been proposed for CSM are difficult to evaluate. Ideally, a prospective randomized controlled study involving a very large number of dogs with the same type of CSM and similar neurological grading undergoing either conservative or the same surgical treatment and long-term MRI and clinical follow-up could help us to resolve this question.

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AN OVERVIEW OF THORACOLUMBAR ANNULAR PROTRUSIONS IN DOGS. WHY ARE THEY SO CHALLENGING? Carlos Macias DSAS(Orth) MRCVS Centro Veterinario de Referencia Bahía de Málaga, Parque Empresarial Laurotorre 25, Alhaurín de la Torre. Málaga, Spain

An overview Degenerative disc disease is the most common neurological disorder affecting the canine thoracolumbar spine. Intervertebral discs degenerate in one of two ways, namely by chondroid or fibroid metaplasia. Fibroid degeneration may lead to protrusion of the annulus fibrosus leading to clinical signs.1,2 Thoracolumbar annular protrusions were first described in 19521, although it is not until 1997 were the first clinical details of five cases are reported3. A review of the published literature reveals only 48 dogs with annular protrusions3,4,5. Pathogenesis Degenerative annular protrusion occurs following hyperplasia, hypertrophy and partial rupture of the annulus fibrosus with bulging of the dorsal annulus into the vertebral canal. This is thought to be a very slow process, especially compared with nuclear extrusions. The spinal cord injury and therefore the associated clinical signs are the result of the degree of spinal cord compression, that leads to focal ischemia, demyelination, loss of axons and focal areas of malacia. Chronic spinal cord compression can lead to irreversible cord atrophy6. Clinical Data Annular protrusions usually affect large, non-chondrodystrophoid dogs. In the largest survey published to date that include 36 dogs, the German shepherd dog was the most commonly affected breed by far, representing more than half of all cases (20)4. Other reported breeds include the Labrador retriever, the basset hound, the Staffordshire bull terrier and the Weimaraner4. Annular protrusions are not reported in the small chondrodystrophoid dogs although it has been seen by the author in the Pekingese and the Jack Russell terrier. Affected dogs are usually over 7 years of age, in contrast with nuclear extrusions were younger dogs are usually reported in the literature4. Male dogs tend to be overrepresented. Affected animals present with variable degrees of neurological dysfunction, being dogs with ambulatory paraparesis the most frequent clinical presentation4. Because of the slow progression of clinical signs, affected dogs are rarely non-ambulatory at the time of clinical presentation and of those reported cases that presented as non-ambulatory, there are no cases that were paraplegic or presented with urinary incontinence4,5. The rate of onset of neurological signs can vary from peracute to chronic4. This may only represent the ultimate event that lead to a significant deterioration which prompts the owner to seek veterinary attention and may not reflect the degree of spinal cord compression, the duration of such spinal cord compression nor the degree of spinal cord atrophy.

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As with thoracolumbar nuclear extrusions, the majority of protruded discs are between T12 and L33,4,5. Almost half of the reported cases have two or more protrusions at the time of diagnosis4,5. Radiographic findings that will alert the clinician towards the diagnosis include vertebral endplate sclerosis, spondylosis deformans and narrowing of the intervertebral disc space. The final diagnosis needs advanced imaging, either by myelography, CT or MRI. The myelographic pattern can help towards differentiate annular protrusions of nuclear extrusions as there is a different pattern of contrast distribution4 (see table).

Nuclear extrusion

Annular protrusion

Thinning and dorsal or lateral deviation Thinning and dorsal or dorsolateral deviation of the contrast columns of the contrast columns Thinning of the contrast columns is mild Thinning of the contrast columns is mild to severe or contrast columns are discontinuous Thinning of the contrast column is diffuse Thinning of the contrast column is focal and centred on the affected disc and beyond the affected disc

Asymmetric distribution of contrast Symmetric distribution of contrast column thinning cranial or caudal to the column thinning cranial and caudal to the affected disc affected disc

Management options Dogs with annular protrusions have been managed by conservative treatment management or by decompressive surgery alone or in combination with vertebral stabilisation 3,4,5,7,8. Reported outcomes for conservative management suggest that this is a non-effective way of preventing further deterioration as almost 50 % of reported cases treated nonsurgically were euthanatized within a year due to further progression of clinical signs. However there was no difference in outcome in those reported cases when compared to those managed by surgical decompression alone or in combination with vertebral stabilisation4. Decompressive surgical techniques described for the management of thoracolumbar annular protrusions include standard hemilaminectomy with or without annulectomy of protruded material alone or in combination with vertebral plate stabilisation4,7,8 and a lateral corpectomy with excision of protruded material5. Published results suggests that surgical management can be effective in the treatment of thoracolumbar annular protrusions3,4,5,7,8. 43

The challenges. From the diagnosis point of view, one of the main issues is the early recognition of the disease prior to the onset of irreversible changes that are likely to influence the outcome. Information is lacking regarding the natural evolution of the disease, from the onset of protruded material to the development of clinical signs. Another important issue is the presence of multiple affected sites within the same patient, do they occur simultaneously? perhaps associated with vertebral instability or physical exercise? or do they occur following nature´s attempt of increasing stability after the development of the first protrusion?. Conservative management may not be adequate in preventing further deterioration of the disease but may be the best management option in some patients when multiple affected sites are present, the clinical signs are very mild, or the expected deterioration rate will be so slow that it is accepted despite the inevitable progression of clinical signs, especially if surgical intervention carries a guarded prognosis or the dog´s life expectancy is limited due to aging or other concomitant disease. The unsuccessful reported cases were neurological deterioration was observed and euthanasia was chosen4, may not be truly representative as these dogs could have or develop other neurological disease (e.g. degenerative myelopathy) and no attempts were made to obtain a final diagnosis once the initial investigations and a presumptive diagnosis was made4. Standard surgical decompression techniques are not capable of adequately decompressing the spinal cord as the ventral midline or ventrolateral location of the protruded disc means that at best, only partial decompression can be adequately performed7,8. Difficulties include the limited access to the ventral aspect of the vertebral canal as well as the wrapping effect of the spinal cord over the protruded annulus5,7,8. These are reasons that some authors have used to propose surgical stabilisation of the affected vertebrae, in order to promote atrophy of hypertrophic dorsal annulus and therefore achieve long-term spinal cord decompression7,8 (as it is described in the management of cervical caudal spondylomyelopathy related to annular protrusions)7,8. There is limited information to date to support that surgical stabilisation is superior to decompressive surgery alone (providing this is adequately achieved) nor evidence that atrophy of the protruded annulus fibrosus does indeed occur. In addition, there is no information available that suggests that multiple vertebral stabilisation can be safely performed without long-term consequences to the spine biomechanics. Lateral corpectomy has been described as a surgical technique that allows effective access to the vertebral canal in order to achieve radical and successful decompression5. Excellent results have been reported but with limited case numbers (only seven). Details of the authors´ inclusion criteria (or more important, the exclusion criteria) are not available so these results are very likely to be biased. In addition, none of these cases were treated at multiple sites so the effect of this technique if performed simultaneously in multiple sites is unknown. There should be no doubt that this condition is a difficult and challenging disease and that more information regarding many aspects of the disease process as well as the management options will be required if we want to provide adequate care to dogs presenting with this condition. Until more information becomes available the surgeon

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will be faced with many unanswered questions that will difficult a clinical decision regarding the management of these cases. REFERENCES . 1. 2. 3.

4. 5.

6. 7. 8.

Hansen, H. (1952) Pathological-anatomical study on disc generation in dog. Acta Orthopaedica Scandinavica n. XI. Braund, K.G. (1993) Intervertebral disc disease. In Bojrab’s Disease mechanisms of small animal surgery. Philadelphia. Lea & Febiger pp 960-970. Cudia, S.P., & Duval, J.M. (1997) Thoracolumbar intervertebral disk disease in large, nonchondrodystrophic dogs: a retrospective study. Journal of the American Animal Hospital Association 33, 456-460. Macias, C. McKee, W.M., May, C. & Innes, J.F (2002) Thoracolumbar disc disease in large dogs: a study of 99 cases. Journal of Small Animal Practice 43:439-446. Moissonier, P. Meheust, P. & Carozzo, C (2004) Thoracolumbar lateral corpectomy for treatment of Chronic Disk Herniation: Technique description and Use in 15 dogs. Veterinary Surgery 33, 620-628 McKee, W.M. (2000a) Intervertebral disc disease in the dog: Pathophysiology and diagnosis. In Practice 22, 355-369. McKee, W.M. (2000b) Intervertebral disc disease in the dog: Management options. In Practice 22, 458-471. Jeffery, N.D. (1995) Degenerative conditions. In Handbook of Small Animal Surgery. London. Molsby pp 85-200.

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THORACOLUMBAR LATERAL CORPECTOMY A TECHNIQUE TO ACHIEVE RADICAL SPINAL CORD DECOMPRESSION Pierre Moissonnier, DVM, MS, PhD, DipECVS Department of Surgery, Vet School of Maisons Alfort, Paris, France

BACKGROUND We support the hypothesis that the result of the surgical treatment of disc herniation depends directly on the complete removal of disc material. In chronic thoracolumbar disc herniation, disc removal is technically demanding due to its hard, encapsulated nature, ventrolateral location, and adhesions to the dura matter or to venous sinuses. This often leads to incomplete removal of extruded-protruded disc material or carries a high risk of iatrogenic spinal cord trauma during the attempt to remove the disc, leading to post-operative deterioration in the dog’s neurological status. Thus, an optimal approach to the removal of herniated disc material requires improved access to the disc without the need for spinal cord manipulation. The thoraco-lumbar lateral corpectomy (TLLC) provides assess for disc removal, ventral to the spinal cord, with minimal or no cord trauma,

DESCRIPTION OF THE TECHNIQUE Definition: Thoraco-lumbar lateral corpectomy can be defined as the creation of a lateral slot through the vertebral epiphyses of two adjacent vertebral bodies and the inter-vertebral disc. Creation of this slot, centered on the inter-vertebral space, is preceded by lateral disc fenestration. Surgical approach to the spine: In cases of ventrolateral disc protrusion, the surgical approach is performed on the side of herniation. With a ventral midline protrusion, the lateral corpectomy is arbitrarily performed on the left side for a right-handed surgeon. A lateral (our preference) or a dorsal approach can be performed. Lateral corpectomy: The lateral aspect of the annulus fibrosus and the lateral aspects of the adjacent vertebral bodies are identified deep to the spinal nerve (and associated blood vessels), which is gently retracted cranially with a blunt nerve hook. Special care is taken when in close proximity to the lumbosacral plexus spinal nerves. Lateral fenestration of the disc is carried out and a lateral slot is then obtained, centered on the inter-vertebral disc space. The amount of bone removed is as follows: -The cranial and caudal limits are determined for each individual case -The ventral margin should allow almost complete removal of the non-herniated nucleus pulposus. -The dorsal margin is the floor of the vertebral canal. -The depth of the slot is the median plane of the vertebral body in cases of ventrolateral disc protrusion or two-thirds of the vertebral canal in cases of ventral midline disc protrusion.

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Diagram showing the usual limits of the ventro-lateral slot in the vertebral body

Burring is performed in a frontal plane perpendicular to the long axis of the spine (horizontal plane for a dog placed in sternal recumbency or vertical plane for a dog placed in lateral recumbency) until the floor of the vertebral canal is reached. The burr initially penetrates the lateral cortical bone of the vertebral body and then the cancellous bone. It is necessary to stop burring regularly to clean the site and to accurately assess the strength of the dorsal cortical bone of the body in order to avoid penetration of the vertebral canal by the burr. The burr is continuously irrigated with saline solution and the site kept free of debris. Hemorrhage from the cancellous bone is controlled with bone wax (Bone Wax ® Ethicon). Once the cortical bone is sufficiently thin, the vertebral canal is entered. Burring stops when the dorsal longitudinal ligament is reached, so that this ligament is situated between the instrument and the vertebral sinus, avoiding severe hemorrhage from the sinus and preventing iatrogenic trauma to the spinal cord. Any hemorrhage from the venous sinus is controlled with hemostatic sponges (Surgicel Johnson & Johnson). The protruding disc annulus is gently retracted to the level of the slot. When present, the extruded material is grasped with rongeurs and extracted ventrally within the slot. Excision of the protruded disc is considered to be complete when no further material can be harvested from the site.

RESULTS OF THE TECHNIQUE We have retrospectively evaluated TLLC in 40 dogs; 25 giant, large or small, nonchondrodystrophic dogs as well as 15 chondrodystrophic dogs. The German shepherd dog was the most commonly affected breed. Main results can be summarised as follows: • No dogs showed any worsening of their neurological status in the immediate post-operative period. • Hospitalization was short (mean = 3 days). • All the dogs improved after TLLC. • The only post-operative complication was one case of seroma formation, which was treated by suction drainage. • There was no recurrence of disc herniation in the operated intervertebral space • Postoparative instability was suspected in one case, one year after surgery

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CONCLUSION We recommend TLLC as an alternative technique for the treatment of chronic (lateralized) thoraco-lumbar disc disease in the dog. It avoids manipulation of the spinal cord during the removal of the disc material and avoids (temporary) postoperative worsening of the neurological status of the dog.

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THORACOLUMBAR (TYPE II) DISC PROTRUSION: THE ROLE OF VERTEBRAL STABILISATION Malcolm McKee DSAO Willows Referral Service, 78 Tanworth Lane, Solihull, West Midlands

For a number of reasons the management of thoracolumbar annular protrusions (Hansen type II disc lesions) is challenging. In contrast to the majority of nuclear extrusions (Hansen type I disc lesions), annular protrusions tend to occur slowly and cause chronic spinal cord injury before neurological signs become apparent (especially when back pain is not a feature). Chronic spinal cord compression results in cord atrophy with the irreversible loss of axons and supporting tissues. Thoracolumbar protrusions are often multiple and protruded annular material may be adhered to the dura mater or internal vertebral venous plexuses. Decompression of the spinal cord is technically difficult with thoracolumbar annular protrusions since, in contrast to nuclear extrusions, the compressive disc material in the vertebral canal remains an integral part of the disc. Annulectomy involves risk of iatrogenic spinal cord injury and haemorrhage from the internal vertebral venous plexuses. Following decompression reperfusion injury and altered arterial and venous haemodynamics may occur and cause further cord injury. The annulus fibrosus is the most important stabilising connection between two adjacent vertebrae. In vitro, even an incision into the annulus fibrosus in the canine lumbar spine significantly reduces vertebral stability, and concomitant hemilaminectomy further increases instability (Hill and others 2000). In contrast, multiple hemilaminectomies on the canine lumbar spine without disc fenestration does not significantly alter vertebral stability during flexion and extension (Corse and others 2003). Recurrence of spinal cord compression by further protrusion of the annulus or hypertrophy of soft tissues such as the interarcuate ligament is also possible. This in part may be due to annulectomy-induced vertebral instability.

Management factors As in people the optimal management of thoracolumbar annular protrusions with regard to conservative treatment or surgery is unclear. In one study, nine of 20 dogs managed non-surgically were euthanatised due to progressive paraparesis (Macias and others 2002). There is also controversy regarding the advantages and disadvantages of the surgical options of spinal cord decompression and vertebral stabilisation. Spinal cord decompression may be achieved by either hemilaminectomy and partial annulectomy or lateral corpectomy and partial annulectomy (Moissonnier and others 2004). Vertebral stabilisation in conjunction with spinal cord decompression has also been described (McKee 2000, Macias and others 2002). Management factors to consider include: (1) the location of the protrusion(s), (2) the number of protrusions, (3) the direction of the protrusion(s), (4) the severity of spinal cord compression and (5) the severity of neurological dysfunction.

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The vast majority of thoracolumbar annular protrusions involve T12-T13, T13-L1, L1L2 and L2-L3 (Macias and others 2002, Moissonnier and others 2004, Downes and others 2007). Macias and others (2002) reported the radiographic features of thoracolumbar disc protrusions in 36 dogs weighing over 20 kg. Fifteen dogs (42%) had two or more protrusions. There was myelographic evidence of lateralised spinal cord compression in 20 dogs (55%); oblique (30 degree right laterodorsal-left lateroventral and 30 degree left laterodorsal-right lateroventral) views assisted lateralisation in eight of the latter dogs. The value of oblique versus ventrodorsal view thoracolumbar myelography has recently been reported (Gibbons and others 2006). It is likely that MRI would be more accurate in predicting the site, severity and nature of spinal cord compression compared to myelography, as is the case with cervical spondylopathy (Da Costa and others 2006). In view of the pathological changes associated with chronic spinal cord compression it could be hypothesised that the prognosis would be dependent on the severity of spinal cord compression and this may influence management. Interestingly, with thoracolumbar nuclear extrusions (Hansen type I lesions) where in contrast, cord pathology is often acute, there is a poor correlation between the degree of cord compression documented with MRI and postoperative outcome (Penning and others 2006). The severity of neurological dysfunction may also influence management, in regards to whether or not surgery is indicated, the type of surgery performed (direct decompression vs. vertebral stabilisation vs. both) and the nature of nursing care required.

Is direct spinal cord decompression necessary? The necessity to directly decompress the spinal cord when stabilising affected vertebrae depends on the degree of cord compression and the severity of neurological dysfunction. It may not be necessary when both are mild. Conversely, it is likely to be beneficial in dogs with significant cord compression and severe neurological signs. Achieving complete decompression can be challenging with annular protrusions especially when the disc material is located in the ventral median aspect of the vertebral canal. There is a risk of iatrogenic cord trauma when attempting to remove compressive material. The necessity to achieve complete spinal cord decompression is unknown. Performing a laminectomy or hemilaminectomy and failing to remove compressive disc material is controversial. In one study epidural masses larger than 4mm could not be adequately decompressed via laminectomy alone. Only minor displacement of the spinal cord was possible. The spinal artery and vein remained obstructed and severe neurological deficits persisted (Doppman and Girton 1976). Care should be taken if extrapolating these results to dogs with chronic spinal cord injury since this experimental study involved acute spinal cord injury using balloon catheters in small 4 to 7 kg monkeys.

The role of vertebral stabilisation Complete decompression of the spinal cord via hemilaminectomy and annulectomy is difficulty with thoracolumbar protrusions. Residual persistent cord compression is likely in many cases. This may account for the poor results reported by Macias and others (2002). It is possible that stabilising affected vertebrae may be beneficial. Stability may: (1) prevent further protrusion of the annulus, (2) prevent any dynamic (bending and rotation) component of spinal cord compression and (3) promote long-

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term atrophy of protruded annulus fibrosus. Atrophy of protruded annular disc material has been reported in the cervical spine of dogs following vertebral distractionstabilisation for cervical spondylopathy (McKee and others 1990).

Methods of vertebral stabilisation Techniques which utilise the vertebral bodies (ventral compartment of the spine) are preferred since the dorsal compartment structures are inherently weak. Experimentally, when subjected to bending, stabilisation of vertebral bodies with bone plates in the lumbar spine is stronger than pin-bone cement techniques (Walter and others 1986). When subjected to rotational deformation vertebral body pins and bone cement provide greater stability and strength compared to other techniques (Waldron and others 1991). 1. Vertebral body plates In the study by Downes and others (2007) conventional non-locking plates were used. Stabilising double adjacent protrusions (three vertebrae) was technically difficult due to the natural curvature (kyphosis) of the thoracolumbar region of the canine spine. This is because conventional bone plates can only be contoured with four degrees of freedom. The novel SOPTM (Orthomed, UK) locking plate has the advantage that it can be contoured with six degrees of freedom due to its cylindrical internode. Mediolateral bending, craniocaudal (dorsoventral) bending and torsion are all possible. SOPTM plates can therefore be contoured for application to the dorsolateral aspect of the curved thoracolumbar spine. Accurate contouring is essential since the locking screw design governs the direction of screw placement. It is important that screws do not penetrate the vertebral canal or intervertebral discs, in order to avoid spinal cord injury and to maximise screw purchase, respectively. Locking plates have been reported to be safe in the management of thoracolumbar conditions in people, including degenerative disease between T10 and L5 (Thalgott and others 1997). The locking screw design of SOPTM and other locking plates confers two key advantages compared to non-locking plates. Firstly, the likelihood of damaging spinal nerves exiting the intervertebral foramina is reduced since the plate tends to stand-off the vertebrae rather than being compressed against them. Secondly, when axially loaded locking screws are subject to cantilever bending and are thus less dependent on being bicortical. Despite the latter an attempt should be made to place all screws bicortically to increase bone purchase. The potential biomechanical advantage of bilateral versus unilateral vertebral stabilisation is unknown. The size of the patient is a key consideration.

Application of bilateral SOPTM plates to lumbar vertebrae

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2. Vertebral body pins / screws and bone cement When using bone cement techniques the surgeon has a choice of vertebral body pins or screws. The advantages of screws compared to non-threaded pins are that there have greater pullout resistance, are less likely to migrate, are interchangeable if length inappropriate, and do not need to be bent or cut. Positive profile threaded pins combine the advantages of screws and non-threaded pins. Although accurate insertion is aided by their self-tapping nature it is beneficial to pre-drill a pilot hole whose diameter approximates but does not exceed the inner diameter of the pin. This improves pin stability and reduces microstructural damage that may lead to excessive bone resorption and premature pin loosening (Clary and Roe 1996). Pre-drilling also enables the depth of the vertebral body to be accurately measured prior to pin insertion.

Management of a T12-T13 lateralised thoracolumbar annular protrusion in a 6.1 kg Jack Russell terrier by hemilaminectomy / partial annulectomy and vertebral body stabilisation using screws and bone cement

Clinical results of vertebral stabilisation The management of single and double thoracolumbar disc protrusions by unilateral stabilisation of two or three vertebrae respectively, in conjunction with hemilaminectomy (with or without partial annulectomy) has been reported in 21 dogs (Downes and others 2007). Age ranged from 4 to 11 years (mean 7.4) and weight ranged from 6.1 to 44.5 kg (mean 26.6). The mean duration of clinical signs was 9.4 weeks (range 2 days to 2 years). Two dogs had spinal pain without neurological deficits, 13 were ambulatory paraparetic, five were non-ambulatory paraparetic and one was paraplegic with loss of deep pain perception. Twenty dogs had single, and one dog had double (adjacent) thoracolumbar protrusions that caused significant spinal cord compression. Conventional 3.5 mm and 2.7 mm bone plates and screws were used in 20 dogs, including the dog with the double disc protrusions. The plate was applied to three vertebrae in the latter case. Screws and bone cement was employed in the smallest dog. Hemilaminectomy was unilateral in 20 dogs and bilateral in one dog. A partial annulectomy was performed on 16 of the 22 protruded discs. Immediately following surgery nine dogs were neurologically unchanged and 12 had deteriorated (one of which was euthanatised three days following surgery). At four weeks postoperatively 10 dogs had improved, six were unchanged and one had deteriorated. Eighteen dogs were available for long-term follow-up nine to 52 months following surgery (mean 28.7 months, median 25.5 months). Neurological function had improved in 16 dogs of which 11 were considered to be normal. In one dog spinal pain had resolved, however, pelvic limb function had remained unchanged. In the remaining dog spinal pain had resolved and neurological function had deteriorated. Plate loosening was observed in two cases.

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Management of L1-L2 annular protrusion by hemilaminectomy / partial annulectomy and vertebral body stabilisation using a 3.5 DCP in a German shepherd dog

SOP plate application for the management of multiple disc protrusions Pre-operative planning Lateral radiographs are obtained of the thoracolumbar spine in a neutral position with a magnification marker placed at the level of the dorsal spinous processes. This enables the percentage magnification to be calculated. If digital templating is not available a line drawing of the vertebral bodies to be stabilised can be produced from the radiograph and reduced to actual size using the magnification facility on a commercial photocopier. The direction of vertebral body screw placement can be determined by examining a cadaver spine. In the thoracolumbar spine it is generally 40 to 55 degrees from the vertical axis. The angle of screw placement in the caudal thoracic spine is less than in the cranial lumbar spine (Watine and others 2006). Since torsion can be applied to SOPTM plates variation in screw angle insertion in different areas of the plate is possible. Pre-operative contouring enables a reduction in operative time. Using specific bending irons (Orthomed, UK) the SOPTM plate(s) are contoured from the line drawing. Left and right plates are individually positioned in the bending irons so that the orientation of the screw holes is similar to that measured on the cadaver spine. “Golf tees” are placed in screw holes where bending irons are being applied at the internodes to prevent deformation. Bending the SOPTM plates in the correct plane is aided by placing a screw in an empty screw hole and aligning the screw and the bending irons at the predetermined angle with the aid of a protractor.

Photograph showing pre-operative contouring of a SOPTM plate for spinal fixation

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Hemilaminectomy and partial annulectomy A hemilaminectomy is performed using a high speed spinal bur to expose the protruded intervertebral disc and compressed spinal cord. The internal vertebral venous plexus is identified and a #11 scalpel blade is carefully positioned between this and the dura mater to excise the protruded annulus fibrosus. Cuts are made in cranioventral and caudoventral directions to free segments of disc material that are retrieved with a dental tartar scraper or small rongeurs. Vertebral body stabilisation The pre-contoured left and/or right SOPTM plates are positioned on the corresponding sides of the exposed vertebrae, at the level of the tubercle of the ribs in the thoracic spine and the junction of the pedicles and transverse processes in the lumbar spine. Where necessary, the dorsolateral aspect of the tubercle of the rib is removed with a bur to enable optimal positioning of the plates. Hypodermic needles are used to identify the intervertebral discs. An attempt is made to offset the craniocaudal position when using two plates to reduce the possibility of screw interference. Additional plate contouring is performed as necessary. Self-tapping locking screws are placed in each SOPTM plate using the specific instrumentation (Orthomed, UK).

Management of T13-L1-L2-L3 disc protrusions in a German shepherd dog by selective hemilaminectomy, partial annulectomy (L1-L2) and bilateral SOPTM plate vertebral body stabilisation

The future management of thoracolumbar protrusions It is unknown if vertebral stabilisation offers advantages compared to direct decompression, for example by lateral corpectomy. A prospective randomised controlled study is necessary. The potential role of long-term disc atrophy secondary to vertebral stabilisation has not been determined. Due to metallic artefacts, the use of follow-up MRI to evaluate spinal cord compression would be problematic. Computed tomography or myelography would avoid this problem, however, they would be less favourable imaging techniques,

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especially the latter since the radiopaque vertebral body plates would hamper evaluation of the subarachnoid space. It is unknown whether vertebral fusion would be advantageous compared to vertebral stabilisation. Partial corpectomy and bone grafting may promote vertebral body fusion. Alternatively articular facet debridement, bone grafting and screw fixation may increase vertebral stability. The long-term effect of stabilisation or fusion of multiple vertebrae on adjacent intervertebral discs and articular facet joints in dogs with degenerative disc disease is unknown. The effect of fusion of three vertebrae on adjacent lumbar intervertebral discs has been studied in immature chondrodystrophoid beagles and mature nonchondrodystrophoid greyhounds (Taylor and others 1976, Bushell and others 1978). Interestingly, significant collagen and proteoglycan compositional changes occurred in adjacent discs in the chondrodystrophoid dogs but not in the nonchondrodystrophoid dogs. The fate of adjacent segments after lumbar fusion in people is also a subject of considerable interest. Increased stress has been reported to cause vertebral canal stenosis due to disc herniation and articular facet hypertrophy. Associated symptoms are not uncommon (Lee 1988, Etebar and Cahill 1999). As a result there is a search for more reconstructive surgical techniques including total disc replacement (Mayer 2005). References BUSHELL, G. R., GHOSH, P., TAYLOR, T. K. F., SUTHERLAND, J. M. & BRAUND, K. G. (1978) The effect of spinal fusion on the collagen and proteoglycans of the canine intervertebral disc. Journal of Surgical Research 25, 61-69 CLARY, E. M. & ROE, S. C. (1996). In vitro biomechanical and histological assessment of pilot hole diameter for positive-profile external skeletal fixation pins in canine tibiae. Veterinary Surgery 25, 453462 CORSE, M. R., RENBERG, W. C. & FRIIS, E. A. (2003) In vitro evaluation of biomechanical effects of multiple hemilaminectomies on the canine lumbar vertebral column. American Journal of Veterinary Research 64, 1139-1145 Da COSTA, R. C., PARENT, J., DOBSON, H., HOLMBERG, D. & PARTLOW, G. (2006) Comparison of magnetic resonance imaging and myelography in 18 Doberman pinscher dogs with cervical spondylomyelopathy. Veterinary Radiology & Ultrasound 47, 523-531 DOPPMAN, J. L. & GIRTON, R. T. (1976) Angiographic study of the effect of laminectomy in the presence of acute anterior epidural masses. Journal of Neurosurgery 45, 195-202 DOWNES, C., GIBBONS, S. E., MACIAS, C. & McKEE, W. M. (2007) Vertebral stabilisation and hemilaminectomy (with or without annulectomy) for the treatment of thoracolumbar disc protrusions (Hansen type II disc lesions) in 21 dogs. Veterinary and Comparative Orthopaedics and Traumatology 20, A3 (abstracts of the 13th ESVOT Congress, Munich, 2006) ETEBAR, S. & CAHILL, D. W. (1999) Risk factors for adjacent-segment failure following lumbar fixation with rigid instrumentation for degenerative instability. Journal of Neurosurgery 90, 163-169 GIBBONS, S. E., MACIAS, C., De STEFANI, A., PINCHBECK, G. L. & McKEE, W. M. (2006) The value of oblique versus ventrodorsal myelographic views for lesion lateralisation in canine thoracolumbar disc disease. Journal of Small Animal Practice 47, 658-662

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HILL, T. P., LUBBE, A. M. & GUTHRIE, A. J. (2000) Lumbar spinal stability following hemilaminectomy, pediculectomy, and fenestration. Veterinary and Comparative Orthopaedics and Traumatology 13, 165-171 LEE, C. K. (1988) Accelerated degeneration of the segment adjacent to a lumbar fusion. Spine 13, 375377 MACIAS, C., McKEE, W. M. & MAY, C. (2002) Thoracolumbar disc disease in large dogs: a study of 99 cases. Journal of Small Animal Practice 43, 439-446 MAYER, H. M. (2005) Total lumbar disc replacement. Journal of Bone and Joint Surgery 87B, 10291037 McKEE, W. M., LAVELLE, R. B., RICHARDSON, J. L. & MASON, T. A. (1990) Vertebral distraction-fusion for cervical spondylopathy using a screw and double washer technique. Journal of Small Animal Practice 31, 22-27 McKEE, W. M. (2000) Intervertebral disc disease in the dog 2. Management options. In Practice 22, 458471 MOISSONNIER, P., MEHEUST, P. & CAROZZO, C. (2004) Thoracolumbar lateral corpectomy for treatment of chronic disk herniation: Technique description and use in 15 dogs. Veterinary Surgery 33, 620-628 PENNING, V., PLATT, S. R., DENNIS, R., CAPPELLO, R. & ADAMS, V. (2006) Association of spinal cord compression seen on magnetic resonance imaging with clinical outcome in 67 dogs with thoracolumbar intervertebral disc extrusion. Journal of Small Animal Practice 47, 644-650 TAYLOR, T. K. F., GHOSH, P., BRAUND, K. G., SUTHERLAND, J. M. & SHERWOOD, A. A. (1976) The effect of spinal fusion on intervertebral disc composition: An experimental study. Journal of Surgical Research 21, 91-104 THALGOTT, J. S., KABINS, M. B., TIMLIN, M., FRITTS, K. & GIUFFRE, J. M. (1997) Four year experience with the AO anterior thoracolumbar locking plate. Spinal Cord 35, 286-291 WALDRON, D. R., SHIRES, P. K., McCAIN, W., HEDLUND, C. & BLASS, C. E. (1991). The rotational stabilising effect of spinal fixation techniques in an unstable vertebral model. Progress in Veterinary Neurology 2, 105-110 WALTER, M. C., SMITH, G. K. & NEWTON, C. D. (1986). Canine lumbar spinal internal fixation techniques: A comparative biomechanical study. Veterinary Surgery 15, 191-198 WATINE, S., CABASSU, J. P., CATHELAND, S., BROCHIER, L. & IVANOFF, S. (2006) Computed tomography study of implantation corridors in canine vertebrae. Journal of Small Animal Practice 47, 651-657

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SURGICAL MANAGEMENT OF DEVELOPMENTAL ANOMALIES OF THE SPINE HEMIVERTEBRAE, SPINAL STENOSIS, ARACHNOID CYSTS Jacques Penderis BVSc MVM PhD CertVR DipECVN MRCVS University of Glasgow

Hemivertebrae Congenital anomalies of the vertebral column (including such variants as hemivertebrae, transitional vertebrae and block vertebrae) are frequently identified and have been described in the veterinary literature. In most cases these developmental aberrations are an incidental finding and no clinical signs are observed. However, congenital vertebral anomalies that compromise the stability of the vertebral column or impinge on the neural structures may result in clinical signs consistent with spinal cord compression or vertebral pain. The structures contributing towards the biomechanical stability of the thoracolumbar spine can be subdivided into three compartments: A) the ventral compartment comprising the intervertebral disc and vertebral body, B) the middle compartment comprising the articular facets, dorsal lamina and pedicles and, C) the dorsal compartment comprising the dorsal spine and interligamentous ligaments and surrounding muscles. The intervertebral disc and vertebral bodies are the most important components with regard to biomechanical stability, with the next most important compartment being the middle compartment and in particular the articular facets. Understanding the process of vertebral embryology, which is characterised by membranous, cartilaginous and osseous stages, provides clues as to the causes of congenital vertebral anomalies, although the exact theories as to the underlying causes are largely speculative. It is in particular the onset of the ossification stage that provides a convenient explanation for the development of congenital anomalies. Ossification starts with the appearance of the three primary ossification centres, with one in the vertebral body and one centre on each side of the vertebral arch, and it is aberrations of these primary ossification sites that are responsible for the majority of clinically significant congenital vertebral anomalies. Abnormalities of the large number of independently developing secondary vertebral ossification centres are much less frequently described in the veterinary literature. Of these secondary vertebral ossification centres, it is particularly manifest that anomalies of the articular facets are likely to result in loss of vertebral stability, with the resultant development of neurological deficits. Clinical Presentation One of the most significant congenital vertebral anomalies in small animal clinical practice is the presence of hemivertebrae in the corkscrew-tail breeds, in particular the bulldog and bulldog-related breeds, and in Pugs. These vertebral body anomalies predominantly affect the mid-thoracic region, in particular T7 or T8 and present as either lateral hemivertebrae or dorsal hemivertebrae, with resultant deviation of the

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spinal cord. The clinical and neurological deficits represent the severity and level of the spinal cord involvement, with many of these lesions remaining asymptomatic.

Broad classification of the main clinically significant types of hemivertebrae that require surgical stabilisation in small animal practice. Red in the left hand image demonstrates the area of failure of bony ossification in the vertebra. The right hand images represent the consequence of this failure.

Diagnosis Diagnosis of congenital vertebral anomalies relies on radiography to identify the bone development abnormality. However, because many of these breeds will have congenital vertebral anomalies present in the absence of clinical signs, the definitive diagnosis that a vertebral anomaly is causing the lesion relies on an accurate neurological examination, combined with demonstration of spinal cord compression due to the hemivertebrae by myelography or advanced imaging. CSF analysis is not helpful.

Figure 2. Lateral thoracic radiograph and sagittal MR image of a 10 month old Bulldog with hemivertebra affecting the 7th and 8th thoracic vertebrae.

Treatment and Prognosis Treatment is aimed at addressing the underlying spinal column instability and resolution of the spinal cord compression by distraction of the spinal column. Although there are description in the literature, surgical techniques aimed primarily at relieving the spinal cord compression without addressing the spinal column instability (e.g.

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dorsal or hemilaminectomy) invariably further diminish the spinal column stability and result in catastrophic collapse of the spinal column. We have successfully treated two pugs and one bulldog (and unsuccessfully treated two pugs, which died due to respiratory complications) by spinal distraction and fusion, either with a combination of PMMA cement and implants, or the SOP plate and screws. Error!

Image from the case in figure 2 demonstrating successful distraction and fusion of the vertebral bodies, while maintaining the integrity of the vertebral arch and facet joints.

Spinal stenosis Stenosis of the vertebral canal may occur due to a variety of causes, including as a congenital anomaly, secondary to other congenital anomalies of the spine, secondary to degenerative joint disease of the articular facets and secondary to intervertebral disc disease. One of the examples where spinal stenosis occurs secondary to other vertebral anomalies is in the case of aplasia or severe hypoplasia of the caudal vertebral articular processes. In these cases there is thoracolumbar spinal cord compression and ataxia, the severity of which depends on the degree of hypoplasia and therefore the degree of vertebral column instability. Compensatory hyperplasia of the adjacent cranial articular facets and ligamentum flavum occurs, which protrude into the vertebral canal, resulting in a compressive myelopathy as demonstrated by myelography and magnetic resonance imaging. Figure 4. Lateral lumbar radiograph and myelogram demonstrating spinal canal stenosis occurring due to new bone formation resulting secondary to a congenital vertebral anomaly, aplasia of the caudal articular facets (arrow).

However, this discussion will focus only on congenital stenosis of the spinal canal occurring as a primary bony stenosis, and not where this stenosis occurs secondary to instability, other vertebral anomalies or intervertebral disc disease. There are also certain specific examples of congenital spinal cord stenosis, including “Wobbler

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syndrome” in the juvenile great Dane and congenital lumbosacral stenosis that are better covered in those section. Clinical Presentation The clinical and neurological deficits represent the severity and level of the spinal cord compression and the expectation is that most of these cases will present as juveniles or young adults. However, clinically this does not always seem to be the case, and in older cases presenting with an apparent spinal canal stenosis, the case should be evaluated for other underlying spinal cord and spinal column diseases that may be contributing to the neurological deficits. Diagnosis Spinal canal stenosis may occur focally, segmental or be generalised throughout the vertebral column. Spinal canal stenosis has been reported in the cranial thoracic region in the Dobermann pincher, and this appears to be consistent with the region in which we see the majority of our clinical cases, particularly in German shepherd dogs. The cervical region is also frequently affected, although in many cases this can be ascribed to cervical spondylomyelopathy (“Wobblers syndrome”), particularly in juvenile Bassett dogs and great Danes. The confirmation of spinal stenosis relies on myelography or advanced imaging and CT myelography is particularly useful in these cases to accurately describe the bony stenosis. MRI is superior to myelography and CT in determination of associated soft tissue anomalies, although the cranial thoracic region in large breed is a difficult region from which to obtain good diagnostic images.

Figure 5. Serial CT-myelography images demonstrating segmental compression of the spinal cord due to two regions of congenital spinal canal stenosis. A similar appearance may occur due to articular facet joint hyperplasia and this may be difficult to distinguish in young dogs.

Treatment and Prognosis The treatment of choice in the management of congenital spinal canal stenosis depends on the severity of the condition, the presence or absence of other contributing neurological spinal cord diseases and the owner’s expectation. The surgery is difficult and prolonged and is associated with a high degree of morbidity. The surgical method of choice is decompression by dorsal laminectomy with undercutting of the sides of the vertebral canal if there is lateral stenosis. Secondary stabilisation may be required if the spinal column stability has been substantially compromised.

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Arachnoid Cysts Arachnoid cysts comprise CSF-filled, intradural-extramedullary cystic lesions that result in spinal cord compression in dogs and to a lesser degree in cats. Similar lesions (intracranial intra-arachnoid cysts) have also been described within the cranial cavity in both cats and dogs resulting in compression of brain structures (primarily in the cerebello-pontine region, the quadrigeminal cistern and in the region of the pineal). A variety of terms have been used to describe arachnoid cysts, including intra-arachnoid cysts, arachnoid diverticulae, meningeal cysts and leptomeningeal cysts. The cysts are usually located within the dorsal aspect of the meninges surrounding the spinal cord, but may occur laterally or ventrally in some cases. Physically the cysts are CSF filled, ill-defined and associated with course arachnoid trabeculation. The aetiology underlying the development of arachnoid cysts is not fully understood and they may resemble type-III spinal meningeal cysts in human patients (in which it is thought to represent a developmental abnormality). However, other potential explanations include: secondary to trauma (in one published case disc herniation was though to contribute to the development of the cyst), infection, inflammation, subarachnoid haemorrhage and genetic causes (particularly as there is an apparent breed predilection in Rottweilers and arachnoid cysts have been described in related Schipperke dogs and in Shih Tzu littermates. Figure 6: MRI appearance of a spinal arachnoid cyst, with the cyst predominantly dorsal to the spinal cord and a smaller ventral component. Caudal to the spinal arachnoid cyst is a region of spinal cord enlargement representing early syringohydromyelia.

Clinical Presentation Arachnoid cysts are uncommon, but have been reported in a wide spectrum of breeds, from relatively small dogs such as the Pug, to large breeds such as the Rottweiler. An apparent breed predilection is evident in the Rottweiler, with 8 out of 14 dogs in one study being Rottweilers. The location of the arachnoid cyst along the spinal cord determines the neurological deficits, but invariably the condition is characterised by slow progression of neurological deficits over a matter of months. The main sites at which arachnoid cysts are reported are in the mid to cranial cervical spine and within the caudal thoracic and cranial lumbar spine. There is no evidence of spinal pain. Most dogs are young at the time of presentation, usually less than two years of age, but dogs as old as 12 years have been described. Diagnosis Diagnosis of arachnoid cysts depends on myelography or advanced imaging to demonstrate the cyst and associated spinal cord compression. CSF analysis is not helpful, although allows exclusion of inflammatory disease. The cyst is not visible on survey radiograph, but can be demonstrated by myelography: often the cyst may not 63

fully fill with contrast medium but the spinal cord compression can still be demonstrated. In these cases repeating the myelogram, but injection the contrast medium from the opposite side (i.e. performing a cisterna magna puncture instead of a lumbar puncture) will result in filling of the cyst. CT myelography allows good visualisation of the cyst position and degree of spinal cord compression, but MRI is preferred in the evaluation of arachnoid cysts because it allows the secondary spinal cord changes (including spinal cord oedema and syringohydromyelia) to be demonstrated. The arachnoid cysts typically appear as tear-drop shaped or oval lesions situated dorsal to the spinal cord, but within the dura mater. The cysts are usually relatively short, often less than once vertebral length, but in some cases may extend some way down the spinal cord or may even be multiple.

Figure 7. Comparison of the myelographic and MRI appearance of a spinal arachnoid cyst within C5 vertebra, with early syringohydromyelia within C6 vertebra.

Treatment and Prognosis The treatment of choice in the management of arachnoid cysts is surgical excision. A variety of methods have been described, including: durotomy and drainage of the cyst; durotomy and partial excision of the cyst (fenestration); dural marsupialisation and; durectomy with dissection of the cyst. The best long term results appear to be by durectomy with dissection of the cyst and full clinical resolution is possible. There is the potential for recurrence of the arachnoid cyst and due to the chronic compression of the spinal cord, residual neurological deficits are a possibility. The spine is usually approached via a dorsal laminectomy as the arachnoid cysts are usually dorsally located. Successful medical management using a tapering anti-inflammatory course of prednisolone has been reported in one dog.

Figure 8. Wide excision of the dura mater over a spinal arachnoid cyst (left) and removal of the thickened, jelly-like abnormal arachnoid mater (right).

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LUMBOSACRAL DISEASES: PATHOLOGY Laurent Garosi DVM, Dip ECVN, MRCVS Davies Veterinary Specialists, Hitchin, Bedfordshire

Cauda equina syndrome, lumbosacral disease & degenerative lumbosacral stenosis The cauda equina lies within the lumbosacral canal and is defined anatomically as the seventh lumbar, sacral, and caudal spinal cord segments and their respective nerve roots. The clinically important peripheral nerves that arise from the spinal nerve roots of the cauda equina are the sciatic, pudendal, parasympathetic pelvic and caudal nerves. Cauda equina syndrome (CES) is a definitive term describing sensory and/or motor neural dysfunction that results in compression, inflammation, destruction, displacement, or vascular disruption to the nerve roots of the cauda equina. Any disease affecting the caudal lumbar vertebrae, sacral vertebrae or the first five caudal vertebrae can potentially lead to CES and deficits of function. Terminology regarding cauda equina dysfunction is confusing, as lumbosacral disease has been used synonymously with cauda equina syndrome. Lumbosacral disease is a collective term encompassing many diseases that can lead to pathologic changes of the cauda equina. Lumbosacral disease is often caused by stenosis of the lumbosacral vertebral canal. The term lumbosacral vertebral canal stenosis encompasses a spectrum of disorders that cause a narrowing of the vertebral canal or intervertebral foramina with compression of the cauda equina nerve roots or their blood supply. Degenerative lumbosacral stenosis (DLSS) is a common cause of cauda equina syndrome in dogs. However, CES may result from numerous causes other than lumbosacral vertebral canal stenosis. DLSS is characterized by intervertebral disc degeneration, Hansen type-2 disc herniation, osteophyte formation at the vertebral endplates and facet joints, and hypertrophy of the interarcuate ligament and joint capsules leading to a narrow vertebral canal or intervertebral foramina. The term lumbosacral instability is a misleading term, as instability is not demonstrated consistently in association with lumbosacral vertebral canal stenosis.

Causes of cauda equina syndrome Disorders of the cauda equina that result in CES can be either congenital or acquired, or may be a combination of both these categories. Disorders that result in clinical signs of cauda equina dysfunction in dogs include: 1.Congenital disorders • Congenital idiopathic stenosis of the vertebral canal • Spinal dysraphism • Transitional vertebrae • Dysgenesis of lumbosacral vertebrae • Spina bifida 2. Acquired disorders • Discopondylitis and spinal epidural empyem

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• • • • • • •

Primary or metastatic vertebral tumour and malignant nerve sheath tumour Intervertebral disc disease Spinal fracture and/or luxation Ischaemic myelopathy Granulomatous meningomyelitis Infectious meningomeylitis Cauda equina neuritis

3. Combined disorders Combination of congenital and acquired disorders (e.g., disc degeneration and lumbosacral vertebral canal stenosis)

Pathogenesis of degenerative lumbosacral stenosis Many similarities have been noted between vertebral and soft tissue alterations seen in dogs with DLSS and cervical stenotic myelopathy. As it stands, we have a limited understanding of what we are treating. Many questions remain unanswered about the pathogenesis of DLSS, the natural progression of the disease, and the role of medical treatment as opposed to the various types of surgical options considered for this condition. A number of degenerative changes may combine to cause compression of the cauda equina: Hansen type II disc herniation at L7/S1, osteophytosis of the articular processes, articular facet synovial hypertrophy or cyst formation, soft tissue proliferation of the ligamentous structures. Large breed dogs, especially GSD, are most commonly affected. Breed-specific differences in the anatomic conformation of the lumbosacral region and type of motion at the discovertebral junction have been suspected to play an important role in the development of this condition. Chronic degenerative disc disease Most cases of acquired lumbosacral stenosis appear to be related to intervertebral disk degeneration at L7 - S1, especially Hansen type 2 protrusion with dorsal bulging of the dorsal annulus into the vertebral canal, intervertebral foramina or both. The presumed sequence of pathophysiological events in DLSS is that mechanical stress or other factors result in early degeneration of the intervertebral disc. The loss of shockabsorbing and stabilizing function of the intervertebral disc is presumed to elicit development of osteophytes at L7 - S1 endplates and articular facets, narrowing of the disk space at L7 - S1, subluxation of articular facets, thickening and in-folding of the normally taut interarcuate ligament. The end result is DLSS with compression of the cauda equina. The role of lumbosacral motion Range of motion is influenced by the condition of the discovertebral junction and the dorsal elements, which include the facet joint capsules, ligamentum flavum, laminae, and pedicles of the vertebrae. These structures are stretched during flexion. As degeneration develops, these elements become rigid and flexion is reduced. Results of studies with vertebral columns of human indicate that lumbar disc degeneration in an early stage caused segmental instability that mainly affected translational motion. However, in severely degenerated discs, motion is reduced. Many studies have examined lumbosacral conformation and mobility in normal and affected dogs with

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many questions remaining unanswered regarding the role of lumbosacral motion in the pathogenesis of DLSS. The lumbosacral joint has the highest mobility of the lumbar spine with considerable transfer of forces between the 7th lumbar vertebrae and the sacrum. This high mobility may predispose to high wear and tear and may be a risk factor for disc degeneration. Flexion and extension are the main movement of the LS joint, but lateral and rotational movements also occur. Lumbosacral angle and range of motion during flexion – extension and vertebral alignment have been assessed as possible cause for disc degeneration in dogs with clinical signs of cauda equina compression. However, in these studies survey radiographs were used and the degree of disc degeneration was not known. Recent ex-vivo 3-dimensional motion pattern studies in dogs suggest that while GSD are predisposed to DLSS, mobility in the lumbosacral junction is significantly smaller in that breed compared to other breeds (Benninger et al. AJVR 2004). These findings indicate that the amount of motion alone does not explain the high prevalence of DLSS in GSDs. The significance of the ventrodorsal translation of the sacrum in the pathogenesis of DLSS in dogs remains unknown. In humans, the term spondylolisthesis refers specifically to a forward (anterior) movement of a lower lumbar vertebra relative to a lumbar vertebra or sacrum directly below it. The term “retrolisthesis” has been proposed to describe this “reverse spondylolisthesis” of dogs. Some authors consider this as a clinical instability which could lead to disc degeneration, however, ventrodorsal translation of the sacrum is not always associated with clinical signs of cauda equina compression or intervertebral disc degeneration. Whether increased ventrodorsal translation is a primary problem leading to abnormal shearing forces and lumbosacral disc degeneration, or whether disc degeneration precedes increased translation, is not yet known. The role of anatomic conformation of the lumbosacral junction Although GSDs are most commonly affected by degeneration of the lumbosacral disc, vertebral columns in that breed appear to have less mobility at L7 – S1 than in dogs of other breeds. Therefore, in addition to mechanical load, other factors have to be considered as causes of disc degeneration. The orientation and shape of canine articular process joints and their association with disc degeneration have also been investigated. Articular process joint tropism, defined as an asymmetry of left and right articular process joints, was analysed as a possible cause of abnormal axial rotation and increased torsional stress on the intervertebral disc (Benninger et al. 2004 Am J Vet Res). However, the higher degree of tropism in GSD was not associated with the severity of disc degeneration. Different shapes of the facet joint have also been described, and differences have been found between levels within an individual, within the same breed, and also between breeds (Rossi et al 2004 Vet Rad & Ultrasound). In GSD, straighter facet joint were found, whereas those dogs of other breeds were more commonly round. The study by Rossi et al. supported the hypothesis that a different anatomical conformation of the articular process plays an important role in the pathogenesis of degenerative lumbosacral stenosis. A positive association between articular process orientation (articular process joint angle difference) and MR-imaging stage of disc degeneration in the caudal lumbar spine was found in GSD. In this group, vertically oriented articular process joints at L6 – L7 with a sudden change to more horizontally oriented articular process joints at the lumbosacral junction were associated with a higher degree of disc degeneration.

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Seiler et al. (2002) found that large facet joint angles were also more commonly associated with disc degeneration. It was proposed that disc degeneration could be a consequence of increased axial rotation as a result of large facet joint angles. However, more recent cadaver studies by Benninger et al. (2006) revealed that larger, less sagittally oriented facet joint angles at L7-S1, were associated with mainly increasing flexion and extension and only a low influence on axial rotation. This was in accordance with other studies on human vertebral column specimens where it was concluded that the facet joint angle was not correlated with axial rotation and was not a critical factor for disc degeneration. Although the facet joints act as a positive stop to axial rotation, different facet joint shape does not seem to influence the motion pattern and has to be regarded as polymorphism of the facets with no effect on the 3-D motion pattern (Benninger et al. 2006). In vivo kinetic and biomechanic studies of normal and abnormal dogs are needed to investigate if this different anatomic conformation leads to an altered and potentially harmful force distribution on the vertebral column and in particular the intervertebral disc. The role of congenital and developmental vertebral anomalies Predisposition to DLSS may be caused by congenital or developmental vertebral anomalies. If a dog is born with a relatively narrow vertebral canal, minimal degenerative changes may be sufficient to cause clinical signs. Vertebral malformations such as transitional vertebrae may initiate DLSS by altering spinal biomechanics. An association has been described between transitional vertebrae (vertebrae having anatomic features of two adjacent vertebral regions), cauda equina syndrome, and degenerative disc disease. Because transitional vertebrae may result in asymmetry of the lumbosacral junction including the disc space, altered mechanical stress on the disc could result in disc degeneration. Developmental vertebral anomalies such as sacral osteochondrosis, in which the attachment of the disc to the endplate is damaged, is always associated with disc degeneration. The GSD is over-represented in the population of dogs with sacral osteochondrosis and transitional vertebrae. Lateralised disc herniation on the side of the abnormal sacroiliac attachment is a common finding in dogs with asymmetrical, transitional, lumbosacral vertebral segments with the disc protrusion tending to occur on the opposite side from the broadest fusion of the vertebra with the ilium.

Diagnosis of DLSS 1. Clinical presentation DLSS affects middle-aged medium to large breeds, particularly GSD, with a male to female ratio close to 2:1 in most reports. The most common historical findings is pain in the caudal lumbar region and pelvic limb weakness manifested as a reluctance or difficulty in jumping, climbing, rising, or sitting. Affected animal often stands with the pelvic limb tucked under the caudal abdomen to flex the spine which lessen canal stenosis and nerve root compression. Lumbosacral hyperaesthesia can be differentiated from pain associated with hip dysplasia by transrectal palpation of the lumbosacral joint and by applying digital pressure on the spinous processes of L7 and S1 with the dog standing and laying on its side. Neurologic deficits are lower motor neuron in nature and relate either to the sciatic nerve (conscious proprioceptive deficits, decreased hock

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flexion, or patellar pseudo-hyperreflexia) or to the pudendal, pelvic, or caudal nerves (urinary or fecal incontinence, motor or sensory deficits to the perineum or tail). Reflex dysfunction of the limbs commonly involves those muscles innervated by sciatic nerve (L6 – S1 nerve roots but L7 and S1 provide the major contribution) particularly the flexor and extensor muscles of the hock. The patellar reflex may be hyperreflexic due to loss of antagonism form the flexor muscles (pseudohyperreflexia). In some animals with L/S disc herniation, one pelvic limb may be held in partial flexion or a repetitive “stamping” motion may be observed. These animals frequently show considerable amount of pain on manipulation of the limb and lumbosacral spine. This combination of signs is termed “root signature” and is believed to be associated with nerve root compression or entrapment by lateralised disc herniation or stenotic intervertebral foramen. The term “neurogenic intermittent claudication” is used to describe the occurrence of exercise-induced pain in some affected dogs. This condition is believed to be related to dilation of radicular vessels and subsequent compression of adjacent nerve roots in a stenotic intervertebral foramen or lateral recess of the caudal L7 vertebral foramen narrowed by a degenerative process. Definitive diagnosis of DLSS is difficult because no one test has a 100% specificity and sensitivity, causing false positives and negatives. 2. Conventional radiography Interpretation of survey radiographs is difficult due to the highly complex anatomic region and the non-specific nature of commonly observed findings, leading to false positive conclusions. Survey radiographs help to identify conditions such as discospondylitis, vertebral tumour, traumatic spinal fracture/luxation, and to detect predisposing factors for DLSS such as sacral osteochondrosis or transitional vertebrae. Indirect evidence of DLSS such as end plate sclerosis, spondylosis deformans at L/S and narrowing of the L/S disc space may be seen. However, these findings are not specific and may be observed in clinically normal dogs. Ventral displacement of the sacrum with respect to L7 and diminished dorsoventral dimensions of the lumbosacral spinal canal may be seen; however, such findings must be interpreted with caution, as they may be seen in normal dogs in association with slight rotation of the vertebral column on lateral radiographs. Furthermore, the inability to assess soft tissue structures and therefore neural tissue compression limits the use of conventional radiography alone to assess patients with suspected CES. 3. Positional radiography The exact role of positional radiography in detecting CES is unclear. Several attempts to separate normal dogs from dogs with L/S vertebral canal stenosis by means of objective measurements made from positional radiographs have not been successful. 4. Myelography Myelography has limited value in the evaluation of the cauda equina because the dural sac is elevated from the vertebral canal floor and often ends before the L/S junction. Myelography provides however a means to “screen” the entire spinal cord for abnormalities, particularly the lumbar enlargement, where a lesion may result in signs of CES. Cisterna magna injection is preferred to prevent epidural leakage which may hinder assessment of the lumbosacral vertebral canal. Myelography is not helpful in the diagnosis of DLSS when the dural sac ends cranial to the L/S junction (common in large breed dogs) or when compressive lesions are located in the intervertebral foramen

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or lateral recess through which spinal nerves travel. The use of “stressed” radiographs (flexion and extension projections) may be combined with myelography. 5. Discography Discography consists of radiography completed following the injection of contrast material into the nucleus pulposus of an intervertebral disc. This technique has special application to the lumboscral disc space. While it should not be possible to inject more than 0.3 mL of contrast medium in a normal disc, intradiscal accumulation and focal extravasation of contrast medium into the vertebral canal strongly suggest disc herniation. 6. Epidurography Alone, epidurography has been reported to be diagnostic in 78%-93% of dogs confirmed surgically. It is easier to perform than myelography and has less morbidity. The disadvantage is that filling of the epidural space may be incomplete because this space is poorly defined, contains fat and has multiple lateral openings. 7. Electrophysiology Electromyographic (EMG) studies can help to confirm neurological disease affecting the cauda equina as well as mapping out denervation. Unfortunately, a large number of dogs with L/S disease (particularly those presented with only pain) have normal findings on EMG. Although an abnormal EMG can aid in confirming a clinical suspicion of DLSS, it does not provide information on the etiology. 8. Computed tomography Computed tomography (CT) is useful in the investigation of DLSS as it shows clearly the vertebral canal, intervertebral foramina, lateral recess and articular processes in cross-sectional images. Individual nerve roots can be visualized directly because of the inherent contrast provided by the epidural fat. CT images of dogs with suspected DLSS are best obtained prior to injection of any contrast medium into the vertebral canal or subarachnoid space. Abnormalities observed on CT in dogs with DLSS include loss of epidural fat, bulging of the intervertebral disc, spondylosis, increased soft tissue opacity in the intervertebral foramen, thecal sac discplacement, degenerative changes affecting the articular processes and facets. 9. Magnetic resonance imaging MRI is now considered as the best imaging modality to evaluate the lumbosacral vertebral canal by providing important information regarding soft tissue stenosis of this canal. MRI can clearly reveal soft tissue such as the cauda equina, epidural fat, and intervertebral disc, at the lumbosacral region. However, no correlation was found between severity of the clinical signs and the severity of cauda equina compression as assessed by MRI in one study (Mayhew et al. 2002 JAAHA). In humans, it has been proposed that MR imaging can lead to overdiagnosis of disc disease because many people without back pain have disc bulges or protrusions on MR imaging. In one series of people with clinical signs of disease in the lower back, >25% had various radiologic evidence of intervertebral disc herniation (Gorman et al. 1997 J Okla State Med Assoc). In another MRI study of 98 asymptomatic people, it was found that 52% had a bulge in at least one level of the vertebral column and 27% had a protrusion (Jensen et al. 1994 N Engl J Med).

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TREATMENT FOR LUMBOSACRAL DISEASE: THE ROLE OF CONSERVATIVE MANAGEMENT FROM A SURGEON’S VIEWPOINT Steven J Butterworth MA VetMB CertVR DSAO MRCVS Weighbridge Referral Centre, Swansea, Wales

In the past, the management of lumbosacral disease has revolved around the choice between conservative or surgical treatment. The former has essentially involved resting the patient and administering NSAIDs to control pain. In a series of 16 cases suffering only pain and/or mild proprioceptive deficits, this management strategy was considered effective in 8 (Ness, 1994). Surgical treatment has generally involved dorsal compression +/- disc fenestration +/- facetectomy with success rates of between about 65-70% (DeRisio and others, 1999; Janssens and others, 2000) through 79% (Linn and others, 2003) to 92% (Danielsson and Sjostrom, 1999). Concern has arisen over the limited success being achieved in many series and by the frequency of recurrence of clinical signs in about 17% of dogs that return to normal (Danielsson and Sjostrom, 1999; Linn and others, 2003) and 55% of dogs that significantly improved (Linn and others, 2003). The procedures involved with decompressive surgery have been shown to destabilise the site (Hill and others, 2000; Smith and others, 2004) and this has been considered a potential contributor to recurrence. Distraction fusion of the lumbosacral junction might be advantageous in both treating the problem and reducing the incidence of recurrence but no long-term clinical studies are available to show this. Furthermore, the source of perceived pain in any given patient is uncertain and thus the response to specific surgical intervention unpredictable. Possible contenders for causing pain are one or more of: • • • •

Articular facet osteoarthritis (possibly involving more than just the L-S junction) Degenerative intervertebral disc Degenerative sacroiliac joint(s) Nerve root entrapment : 1. osseous stenosis 2. disc protrusion 3. reactive fibrous tissue encroaching on an intervertebral foramen



Secondary pain: 1. muscle spasm 2. osteoarthritic joint pain accentuated by inco-ordination

In general, therefore, it is probably safe to say that because of the unpredictability for outcome in both the short and long terms following surgery that such procedures have been reserved for situations where conservative measures are deemed to have failed. What has changed in recent years is what we should consider as conservative management. This is no longer just lead exercise and a tablet bottle full of the latest NSAID. Various strategies can be aimed at the two main clinical aspects of the condition, pain and paresis.

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Pain:

• • • • • • • • •

Paresis: •

Nutraceuticals NSAIDs Acetominophen (paracetamol) Opiate analogues (tramadol hydrochloride) Anticonvulsants & Ca channel blockers (gabapentin) –neuropathic pain Skeletal muscle spasmolytics (methocarbamol) Acupuncture TENS Physical therapy (physiotherapy, aquatherapy, rehabilitation)

Physical therapy (physiotherapy, aquatherapy, rehabilitation)

Conservative versus surgical management The “gold standard” for investigating the cause of clinical signs that might be related to lumbosacral disease is currently taken as MRI. However, there are limitations in interpreting these images since they will not necessarily indicate the source of pain and there is poor correlation between neurological deficits seen and evidence of nerve root compression visible on MRI (Mayhew and others, 2001). Despite this it remains the optimal way to differentiate degenerative lumbosacral compression syndrome from other causes of lumbosacral disease or cauda equine syndrome. After such an investigation, and if a diagnosis of degenerative LS compression syndrome was made, what would lead to deciding whether to pursue conservative or surgical management? First and foremost, the “rules of engagement” are still being drawn and nobody knows the correct answer. Perhaps it would still be best to point all cases in the direction of “proper” conservative management, but possibly with particular exceptions such as cases showing: • • •

marked or deteriorating neurological deficits with MRI evidence of neural compression significant lameness with MRI evidence of neural compression extreme pain where a definitive cause is suspected that could respond rapidly to surgery

Following these guidelines depends on having access to good pain management / physical therapy but does appear to lead to very few cases actually requiring surgery.

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References Danielsson, F and Sjostrom, L (1999) Surgical Treatment of Degenerative Lumbosacral Stenosis in Dogs. Veterinary Surgery 28, 91-98 DeRisio, L., Sharp, N., Thomas, W. and Munana, K (1999) Long term follow up of 37 dogs who underwent dorsal laminectomy for lumbosacral compressive disease. ECVS Scientific Absracts in Veterinary Surgery 28, 202 Hill, T.P., Lubbe, A.M. and Guthrie, A.J. (2000) Lumbar spine stability following hemilaminectomy, pediculectomy, and fenestration. Veterinary and Comparative Orthopaedics and Traumatology 13, 165171 Janssens, L.A.A., Moens, Y., Coppens. P. Peremans, K and Vinck, H. (2000) Lumbosacral Degenerative Stenosis in the Dog. Veterinary and Comparative Orthopaedics and Traumatology 13, 97-103 Linn, L.L., Bartels, K.E., Rochat, M.C., Payton, M.E. and Moore, G.E. (2003) Lumbosacral Stenosis in 29 Military Working Dogs: Epidemiologic Findings and Outcome After Surgical Intervention (19901999). Veterinary Surgery 32, 21-29 Mayhew, P.D., Kapatkin, A.S., Wortman, J. and Vite, C.H. (2001) Association of lumbosacral neural structure compression on magnetic resonance images and clinical signs in dogs with degenerative lumbosacral stenosis. BSAVA Scientific Abstracts in Journal of Small Animal Practice 42, 528 Smith, M.E.H., Bebchuk, T.N., Shmon, C.L., Watson, L.G. and Steinmetz, H. (2004) An in vitro biomechanical study of the effects of surgical modification upon the canine lumbosacral spine. Veterinary and Comparative Orthopaedics and Traumatology 17, 17-24

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TREATMENT FOR LUMBOSACRAL DISEASE: THE ROLE OF CONSERVATIVE MANAGEMENT FROM A PHYSIOTHERAPIST’S VIEWPOINT Lowri Davies BVSc MRCVS Cert Vet Acup(IVAS) CCRP The SMART Veterinary Clinic, Weighbridge Referral Centre, Kemys Way, Swansea

Rehabilitation or conservative management of any neurological or musculoskeletal condition requires a thorough understanding of the underlying pathological process coupled with an appreciation of all compensatory changes that have potentially developed as secondary complicating factors. Once this has been established then the aim of any rehabilitation programme should be to restore function and manage pain. Both must be addressed simultaneously and a failure to do so is unlikely to lead to a successful outcome. In the case of lumbosacral disease, a similar clinical presentation is possible from a spectrum of underlying pathological processes including: idiopathic stenosis, discospondylitis, trauma, neoplasia, inflammatory disease, vascular compromise and congenital abnormalities (1,2). Potential considerations for rehabilitation include deficits of sciatic, pudendal, pelvic, perineal and caudal rectal nerve function (3). The clinical picture may therefore include paresis, lameness, lumbosacral pain, urinary and faecal incontinence and abnormal skin sensation. Theoretically, suitable candidates for conservative management or rehabilitation are those dogs showing mild to moderate pain and minimal neurological dysfunction. Unfortunately despite good experimental correlation between neurological deterioration and mechanically induced cauda equina compression (4), in practice there seems to be poor correlation between diagnostic imaging and the severity of clinical signs. Therefore cases with minimal compression can exhibit severe pain and those with significant compression may show little in the way of neurological degeneration. There does seem to be better correlation around the L7 nerve root where minimal compression can lead to severe pain and neurological dysfunction (5,6). During locomotion, the canine back will undergo both transverse and vertical movement resulting in periods of flexion and extension and some rotation. At present, imaging is a static process and may not be able to offer accurate information regarding lumbosacral anatomy during dynamic, weight bearing movement. It is therefore extremely difficult to predict which cases are suitable candidates for conservative management. Ideally, it should be applied in individuals where instability rather than significant compression is responsible for the clinical signs. Furthermore, all cases showing L7 nerve root compression should possibly be avoided. Studies have also shown that further pathology at the level of L4/L5 can adversely affect restoration of function. A recent Kinematic study on a small group of clinically sound dogs did show small but significant differences in spinal movement between those with no radiographic changes and those with evidence of lumbosacral pathology (7). Possibly further work combining kinematic and MRI imaging of the area may provide a more complete picture of the disease process and aid in case selection. In the case of lumbosacral disease, restoration of function must address both locomotor function and trunk muscle function.

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The locomotor pattern in healthy individuals is complicated and dependent on the sequential bilateral activation of muscles acting on different joints. Within the spinal cord, a network of interneurones form a central pattern generator which activate motor neurones in an appropriate sequence. This CPG also sets the excitability of other interneurones involved in transmitting sensory information. This CPG is activated by various descending pathways and can be modulated through neurotransmitter agonists and antagonists. Though peripheral afferent inputs are not essential for generation of movement they are crucial in the development of appropriate and adaptive movement (8). Normal locomotion involves dynamic interaction between various components of the nervous system, however, depending on the site of the lesion, the spinal cord can adapt in the damaged state and can re-establish motion from the functioning units within the CNS. This ability to modify is exploited during rehabilitation. Though the basic locomotor pattern is innate, training can alter the expression of this pattern (9,10). Various studies have shown that training is very specific and is mediated centrally, thus animals trained to walk will walk better than stand and those trained to stand will stand better than walk (11,12,13). Therefore for optimal restoration of function it is essential that techniques to improve both posture and movement are employed. Thus no single modality or exercise in isolation will provide adequate restoration of function. Furthermore, rehabilitation must be progressive as the gain achieved from repeating an exercise becomes diminished over time unless the exercise is varied. One important feature of this training is the loading of the limbs and force feedback from extensor muscle afferents which stimulate leg muscle activation. Repeated loading facilitates this process (14). The design of a rehabilitation programme is individual in nature and should reflect each case’s specific set of problems. At the first assessment, a thorough musculoskeletal and neurological examination should be carried out. A detailed gait analysis should also be performed. Details such as age, concurrent disease status and background level of fitness should also be determined as they will affect the intensity and duration of the rehabilitation programme. Furthermore it is essential to establish what the owner’s expectations are at the onset as rehabilitation is time consuming and potentially costly. If the owner’s expectations are too high and progress appears slow then their commitment to the programme may wane and the outcome will inevitably be poor. Though it is impossible to be prescriptive when designing a rehabilitation programme, the majority are made up of appropriate pain management (inflammatory, chronic, neuropathic), and a therapeutic exercise programme. When deciding on the most appropriate therapeutic exercise regime to implement an understanding of how tissues respond to injury and their adaptation to disuse and remobilization is essential. Without this understanding it is impossible to achieve the correct balance between allowing tissues to heal and stressing them correctly in order to improve function. For example, a simple exercise such as a sit to stand may well be appropriate in the early stages of hip dysplasia to promote hind limb muscle development and to improve function. Such an exercise applied even at a low level in spinal rehabilitation where neurogenic inhibition of locomotor function exists is likely to be damaging. In this case hind limb paresis will result in utilisation of the forelimb and paraspinal musculature to bring about elevation with subsequent muscle damage and potentiation of local inflammation.

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Appropriate exercises in the early stage include: aquatic treadmill activity, slow lead walking, slight forelimb elevation and lateral work to maintain paraspinal muscle function. Postural control can be improved by utilisation of airbeds, balance cushions and proprioceptive roads. Later more strenuous treadmill activity can be introduced coupled with low cavaletti work, hill walking, gym ball activity and trampolines. It is important to remember that inappropriate rehabilitation is worse than no rehabilitation as it will further damage inflamed tissues. Carried out correctly and appropriately however it can successfully restore function and alleviate pain.

References 1. 2. 3. 4. 5.

6. 7.

8. 9. 10. 11. 12. 13. 14.

DeRisio L, Thomas WB, Sharp NJH, Degenerative Lumbosacral Stenosis:Vet Clin North AmSm Anim Prac 2000;30:111-132 Travin G, Prata RG. Lumbosacral stenosis in dogs. J Am Vet Med Assoc 1980:177:154-159 Fletcher TF, Spinal cord and meninges. In:Evans H, Christiansen G,eds. Miller’s anatomy of the dog. 3rd ed. Philadelphia:WB Saunders, 1993:800-802 Bodner DR, Delamarter RB, Bohlman HH et al. Lumbar spinal stenosis. Clinical and radiologic features. Spine 1995;20:1178-1186 Mayhew PD, Kapatkin AS, Wortman JA, Vite CH, Association of Cauda Equina Compression on Magnetic Resonance Images and Clinical Signs in Dogs With Degenerative Lumbosacral Stenosis: J Am Anim Hosp Assoc 2002;38:555-562 Suwankong M et al J Am Vet Med Assoc 2006;229:1924-1929 Gradner G, Bockstahler B, Peham C, Henninger W et al, Kinematic Study of Back Movement in Clinically Sound Malinois Dogs with Consideration of the Effect of Radiographic Changes in the Lumbosacral Junction: Veterinary Surgery 2007; 36:472-481 Rossignol S et al. Recovery of locomotion in the cat following spinal cord lesion: Brain Research Reviews 2002;40:257-266 Forssberg.H, Grillner S, The locomotion of the low spinal cat.1 Coordination within a hindlimb: Acta Physiol. Scand, 1980;108:269-281 Forssberg.H, Grillner S, The locomotion of the low spinal cat 11 Interlimb coordination: Acta Physiol. Scand, 1980;108:283-295 R.D.de Leon et al, Full weight bearing hind limb standing following stand training in the adult spinal cat: J.Neurophysiol. 1998;80:83-91 R.D.de Leon et al, Locomotor capacity attributable to step training versus spontaneous recovery after spinalization in the adult cat: J.Neurophysiol. 1998;79:1329-1340 R.D.de Leon et al, Retention of hindlimb stepping ability in adult spinal cats after the cessation of step training: J.Neurophysiol. 1998;81:85-94 Fouad K, Metz G, Merkler D et al, Treadmill training in incomplete spinal cord injured rats: Behavioural Brain Research 2000;115:107-113

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TREATMENT FOR LUMBOSACRAL DISEASE: THE ROLE OF SURGERY Luisa De Risio, DVM, MRCVS, PhD, DipECVN Neurology/Neurosurgery Unit, Centre for Small Animal Studies, Animal Health Trust, Lanwades Park, Kentford, Newmarket, Suffolk

Lumbosacral disease (also termed lumbosacral stenosis, degenerative lumbosacral stenosis, lumbosacral spondylopathy, spondylolisthesis, lumbosacral malformationmalarticulation) is characterised by narrowing of the vertebral canal and/or the intervertebral foramina in the lumbosacral area with compression of the nerve roots that form the cauda equina (L6-7 + S1-3 + Cd1-5) and/or their related vasculature. Cauda equina compression may result from a number of abnormalities including: • • • • • •

degeneration and protrusion of the intervertebral disk between the last lumbar vertebra and the sacrum, osteophytes, thickening, joint capsule proliferation, and subluxation of the articular processes, thickening and in-folding of the normally taut interarcuate ligament, epidural fibrosis, thickened lamina and pedicles instability and misalignment between the last lumbar vertebra and the sacrum

Lumbosacral osteochondrosis, a developmental disturbance of the end plate of either the sacrum or L7 vertebra, with subsequent separation of an osteochondral flap, has been reported as a cause of lumbosacral stenosis in mature dogs. This condition is often associated with disk disease, consequently, compressive lesions result from the flaps alone or in combination with disk material. Acquired degenerative lumbosacral stenosis occurs most commonly in large breed dogs, and particularly in working dogs. German Shepherds are especially at risk for this degenerative disorder, possibly because of the presence of destabilizing transitional lumbosacral vertebral anomalies that predispose to premature disk degeneration. Clinical signs are noted usually when dogs are mature to middle-aged (e.g., 5 to 8 years), possibly associated with age-related soft tissue and bony changes, along with altered spinal mechanics, resulting in cauda equina compression. Males appear to be at higher risk than females. In dogs with lumbosacral osteochondrosis, the mean age has been reported to be 6.3 years, German Shepherds (56%), Boxers (11%) and Rottweilers (9%) were overrepresented, and the male: female ratio was 4:1. Dogs with lumbosacral stenosis usually show varying signs of a lumbosacral syndrome depending on the level and extent of the lesion. Owners often note that affected dogs have difficulty rising or climbing stairs, and are reluctant to perform extensive physical activity. Clinical signs include hyperalgesia (the most commonly reported sign) during direct palpation (especially downward pressure) of the lumbosacral area or during lumbosacral hyperextension, unilateral or bilateral pelvic limb lameness (commonly), ataxia, paresis, proprioceptive deficits, patellar pseudo-hyper-reflexia, decreased withdrawal reflex (especially at the hock), tail paresis, hypotonia of anal sphincter with fecal incontinence, and urinary incontinence. In some cases paraesthesia manifested as self-mutilation of pelvic limbs, tail, perineum, and genitalia may be noted. Exerciseinduced lameness, termed neurogenic intermittent claudication, may occur when 78

exercise-induced dilatation of radicular vessels causes compression of adjacent nerve roots in a stenotic region, e.g., intervertebral foramen or lateral recess of the caudal L7 vertebral foramen narrowed by a degenerative process. The clinical suspicion of degenerative lumbosacral stenosis can be confirmed with diagnostic imaging however even the most advanced diagnostic imaging techniques may not always provide a definitive answer. Survey radiographs need to be performed with the animal deeply sedated or under general anaesthesia, properly positioned and preferably with an empty colon. Survey radiographs may show indirect evidence of degenerative lumbosacral stenosis including spondylosis deformans, disk space narrowing, and end-plate sclerosis. However, none of these abnormalities are specific, and they may occur in clinically normal dogs. Survey radiographs may rule out lumbosacral fracture/luxation, osseous neoplasia, osteomyelitis associated with discospondylitis, or identify predisposing factors to degenerative lumbosacral stenosis such as osteochondrosis and transitional vertebrae. In one study, over 30% of German Sheperds with clinical signs of cauda equina compression had radiographic abnormalities compatible with osteochondrosis of the sacral end-plate. In another study, transitional vertebrae were found in nearly 40% of German Sheperds with degenerative lumbosacral stenosis and in 11% without. The greatest limitation of survey radiography is the inability to assess compression of neural tissue. Stress radiography, such as dynamic flexion/extension studies, may accentuate the lumbosacral instability. One study evaluated the LS angle and degree of subluxation of the sacrum in relation to L7 as seen on survey radiographs in 52 normal dogs and 32 normal dogs with LS spondylosis (of which 24 had neurological deficits). The conclusion was that such measurements were not helpful in the diagnosis of this disease. Contrast-enhanced radiography Epidurography and discography may provide useful information mostly regarding LS disc degeneration and protrusion. In one study, combined survey radiography and discography-epidurography were correctly positive in 16 of 18 dogs (89%). Alone, epidurography has been reported to be diagnostic in 78%-93% of dogs confirmed surgically. Epidurography is easier to perform than myelography and has less morbidity. The disadvantage is that filling of the epidural space may be incomplete because this space is poorly defined, contains fat and has multiple lateral openings. Extended views of the LS joint during epidurography may accentuate a compressive lesion. Concomitant filling of the vertebral venous sinuses or the paravertebral venous system may occur in normal dogs but is more common in those with LS disease. Myelography allows evaluation of the spinal cord cranial to the LS region and thus may help to rule out other diseases, however it may be of limited value in the evaluation of the cauda equina in those dogs in which the dural sac is physiologically elevated from the vertebral canal floor and ends before the lumbosacral junction. It has been reported that 85% of normal dogs and 80% of dogs with degenerative lumbosacral stenosis had a dural sac that ended at the level of the sacrum and that myelography with the LS joint in neutral, flexed and extended positions was successful in the diagnosis of LS disease. In another study, 77% of 30 dogs had a dural sac that ended within the sacrum. A normal myelographic study does not rule out lumbosacral disease.

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Computed Tomography (CT) and Magnetic Resonance Imaging (MRI) Computed tomography and MRI are the diagnostic procedures of choice. Their main advantage is the possibility to evaluate structures that cannot be visualised completely with conventional radiography such as the lateral recesses, intervertebral foramen and articular processes. It is important to scan from L4 vertebra to the sacrum not to miss any lesions affecting the spinal cord segments L6-7-S1-3, and to place the patient in the scanner a standard position. A neutral or flexed position of the LS joint reduces compression compared to an extended position. CT provides bone detail superior to that seen with MRI and soft tissue contrast superior to that of conventional radiography. It allows visualisation of individual nerve roots because of the contrast provided by the epidural fat. However loss of epidural fat may not be of clinical significance in older animals as it has been described in the lumbosacral joint older dogs without clinical disease. Reformatting can be used to create dorsal and sagittal images and facet subluxation may be visible using bone window images or 3D reconstructions. In a study evaluating canine lumbosacral stenosis using intravenous contrast- enhanced CT, the positive predictive values for compressive soft tissues involving the dorsal canal, ventral canal and lateral recesses were 83%, 100%, and 81% respectively. MRI can clearly reveal soft tissue, such as cauda equina, epidural fat, and intervertebral disk, at the lumbosacral region. MRI also provides better information about the condition of the intervertebral disc (e.g., the hydration status of the nucleus pulposus) in dogs with degenerative lumbar spine diseases, than radiography or CT. However, no correlation was found between severity of the clinical signs and the severity of cauda equina compression as assessed by MRI in one study. In humans, it has been proposed that MR imaging can lead to over-diagnosis of disc disease because many people without back pain have disc bulges or protrusions on MR imaging. As MR imaging is used more frequently now in veterinary medicine, inconsistency between disc abnormalities and clinical signs must be considered, and the diagnosis should always be based upon clinical acumen in addition to the imaging. Electrophysiology Electrophysiology useful to confirm a lower motor neuron disease and provide functional evidence of cauda equina involvement. Electromyography (EMG) may reveal spontaneous activity in lumbosacral paraspinal muscles, pelvic limbs, coccygeal muscles, and anal sphincter. However, these findings do not specify the etiology and may be absent in patients with LS disease. One study found that EMG was accurate in predicting the presence or absence of cauda equina compression in all cases. Another study found that some dogs with LS disease (particularly those presented with only pain) had normal findings on EMG. The main advantage of EMG is to reduce the number of false positive diagnosis of LS disease associated with MRI or CT evidence of nerve root compression. CSF analysis CSF analysis may be useful to rule out infectious/ inflammatory disorders of the central and peripheral nervous system (e.g. cauda equina neuritis, polyradiculoneuritis) TREATMENT The conservative treatment of LS disease is indicated in case of intermittent lumbosacral pain and mild sensory and/or motor deficits. It consists of the use of nonsteroidal anti-inflammatory drugs (e.g. carprofen, meloxicam) or steroids

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(prednisolone), restricted exercise for 6-12 weeks, gradual reintroduction to normal exercise level, and weight reduction in case of obesity. Gabapentin can be used to control neuropathic pain. Physiotherapy helps to maintain and improve muscle trophism and tone during and after exercise restriction. Three to four months of exercise restriction produced an improvement in 8 of 16 dogs treated conservatively (24) Another study has reported recurrence of signs in working dogs when normal activities were resumed. (19). SURGICAL TREATMENT is indicated when conservative treatment has failed and in dogs with persistent lumbosacral hyperalgesia or moderate to severe sensory and motor deficits. In dogs with urinary and/or faecal incontinence surgery should be performed as soon as possible as incontinence for longer than 6 weeks preoperatively has been associated with a poor prognosis (2). Surgical procedures for the treatment of lumbosacral disease can be classified as: 1. decompressive: dorsal laminectomy, partial discectomy, foraminotomy 2. distraction-stabilization-fusion These techniques can be combined, however the indications for decompression versus fusion versus both have not been defined yet. The main limitation in selecting the most appropriate surgical treatment is the lack of a general consensus on how to assess for the presence of lumbosacral instability and its significance. The role of dynamic radiography, CT or MRI is still debated in veterinary medicine and even in humans there is no gold standard to assess for the presence and significance of lumbosacral instability. In addition, it is still unknown what the “normal range of motion” of a lumbosacral joint with and without degenerative changes is in middle-aged or old dogs of different breeds. Dorsal laminectomy has been used to access the vertebral canal and decompress the nerve roots of the cauda equina. This technique allows good visualization of the S1-Cd5 nerve roots and generally limited visualization of L7 nerve roots, unless the osseous base of the L7 caudal articular processes is weakened. To improve visualization of L7 nerve roots, the lateral recesses and the intervertebral foramina the laminectomy needs to be extended cranially within L7 vertebral lamina. However, this should be removed cautiously as excessive thinning of the base of L7 caudal articular processes may result in their fracture. Once the dorsal laminectomy has been completed the cauda equina can be thoroughly inspected and sources of compression can be removed. In case of epidural fibrosis, which is probably the response to chronic compression, adhesions around nerve roots should be broken cautiously using magnification and adequate light source. Dorsal laminectomy can be combined with partial discectomy (partial dorsal anulectomy and nuclear pulpectomy) to remove compression associated with a protruding intervertebral disc. Partial discectomy should be performed to achieve complete decompression of the cauda equina, mimimise the risk of recurrence of disc protrusion, but without compromising lumbosacral stability. In a recent study with follow-up information on 105 dogs, 55 dogs that underwent dorsal laminectomy and partial discectomy showed significantly less improvement than the remaining 50 dogs that underwent dorsal laminectomy alone (52) The authors of this study hypothesize that this may be related to the initial severe degree of disc degeneration and protrusion

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or due to further accelerated degeneration of the lumbosacral junction with increasing spinal instability (52). The removed disc material should be submitted for culturesensitivity any time there is the suspicion of occult discospondylitis. In a recent study, bacterial culture was positive in 12/52 (23%) of cases in which it was cultured following partial discectomy for degenerative lumbosacral disease (52). Dorsal laminectomy can be combined with foraminotomy and/or distraction-stabilizationfusion if necessary. Dorsal laminectomy combined with partial discectomy and/or foraminotomy has been associated with a good outcome (substantial clinical improvement and resolution of incontinence) in 54/69 (2), 122/131 (19), and 83/105 (52) dogs in 3 different studies with a mean follow-up of 38, 26, and 22 months respectively (2, 19, 52). Foraminotomy is the surgical procedure to enlarge a stenotic intervertebral foramen preserving the articular processes. In dogs undergoing surgery for degenerative lumbosacral stenosis foraminotomy may be necessary in order to decompress the L7 nerve root which is one of the major contributors to the sciatic nerve. One or both intervertebral foramina between the last lumbar and the first sacral vertebrae may be stenotic due to osseous and soft tissue changes such as: 1. osteophytes, thickening, and subluxation of the articular processes, 2. proliferation of the articular processes joint capsule 3. lateralised protrusion of the intervertebral disk. Advanced diagnostic imaging such as CT and MRI allow accurate assessment of the intervertebral foramina. To further classify the site of stenosis within the intervertebral foramen this has been subdivided in 3 zones: entrance, middle and exit zones (3, 48). Accurate assessment of the intervertebral foramen is very important as unrecognized or recurrent foraminal stenosis is thought to be an important cause of “failed back surgery syndrome” in human neurosurgery (11-13). The stenotic intervertebral foramen may be approached medially after performing a dorsal laminectomy and the soft tissue and bony proliferations can be removed by means of small rongeours, bone curette and eventually a high speed burr. Extreme care must be taken to protect the nerve roots, especially while drilling. The articular processes, particularly the L7 ones, should not be weakened excessively as they may fracture following surgery. In addition, if transarticular screw fixation is also to be performed, this may no longer be possible due to excessive bone removal. In case of osseous stenosis of the intervertebral foramen undercutting the entire length of the foramen may be particularly difficult especially in large breed dogs. A medial approach to the intervertebral foramen may not allow adequate decompression of the middle and exit zones, especially in large breed dogs. Partial or total facetectomy as described by Tarvin and Prata (4) is no longer recommended, unless associated with adequate stabilization with implants, as it can induce/exacerbate mechanical instability of the lumbosacral joint (29). Endoscopicassisted lumbosacral foraminotomy has been proposed to improve intraoperative visualization in dogs with foraminal stenosis as a component of degenerative lumbosacral stenosis (48). Lateral foraminotomy (performed externally to the vertebral canal) has been proposed in order to improve degree and extent of foraminal decompression within the middle and exit zones (49-50). Lateral foraminotomy can be combined with partial dorsal decompression (S1 laminectomy + removal of the ligamentum flavum) when there is concurrent foraminal and vertebral canal stenosis. Lateral foraminotomy can be performed uni or bilaterally. This procedure has been

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reported to be successful in the treatment of 19 of 20 dogs with LS foraminal stenosis in a recent study with a median follow-up of 10.9 months (50). The main limitations of lateral foraminotomy include: restricted visual exposure due to interference with ilial wings, difficult orientation because of multiple arthritic changes, bleeding, and risk of iatrogenic damage to the nerve root (49). Positioning the patient in ventral recumbency with the spine tilted to an angle of about 20° away from the surgeon improves visualization of the foraminal exit zone (50). Distraction-stabilization-fusion has been advocated by some authors as an alternative or in association with decompressive surgery. The principles of distraction-stabilizationfusion techniques are to distract and stabilize a misaligned/unstable/collapsed LS joint, increase the diameter of the intervertebral canal and foramina and, indirectly, decompress the cauda equina. Few authors have suggested achieving LS distractionstabilization-fusion by performing an arthrodesis of the LS articular processes (26-28, 54). This can be done by removing the articular cartilage from the facets, placing cortical bone screws or treated pins through the articular processes of L7-S1 and into the body of the sacrum (without entering into the ilium), and using autologous cancellous bone graft. The only published clinical study on this technique has reported a successful outcome in 14 dogs with LS pain and mild to moderate neurologic deficits (26). In 2 of the 14 dogs included in this study breakage of the treated pin was documented with radiographs, however this complication did not seem to result in functional deficits. (26) LS distraction-stabilization-fusion can be achieved also using treated pins or screws trough the body of the sacrum and the pedicles and/or body of L7 and PMM or rods as connectors (52, 55, 56). These latter 2 techniques are more likely to provide solid stabilization compared to the transarticular screws. The only clinical report on the use of pedicle screws and rod fixation in 5 dogs has described favourable results (56). At present there are still a lot of questions that need to be answered on LS disease and in particular on how best to treat it. There is no study that compares the long term outcome of conservative treatment (using rest, anti-inflammatory drugs and medications for neuropathic pain such as gabapentin), and decompressive surgery alone, distractionstabilization-fusion alone or the two surgical procedures combined. In addition, the ideal study on treatment of such a complex syndrome should require appropriate assessment and categorization of the varied clinical presentations. There is no consensus on the definition and significance of lumbosacral instability and how this should be objectively assessed preoperatively. There is no information on whether following L7-S1 distraction-stabilization-fusion in dogs with lumbosacral disease the altered biomechanics at the adjacent lumbar intervertebral discs/joints predisposes to additional lesions. References and suggested reading 1. De Risio L, Thomas WB, Sharp NJ: Degenerative lumbosacral stenosis. Vet Clin North Am: Small Anim Pract 30:111–132, 2000 2. De Risio L, Sharp NJ, Olby NJ, Munana KR, Thomas WB. (2001) Predictors of outcome after dorsal decompressive laminectomy for degenerative lumbosacral stenosis in dogs: 69 cases (1987-1997) J Am Vet Med Assoc. Sep 1;219(5):624-8. 3. Lee C, Rauschning W, Glenn W: Lateral lumbar spinal canal stenosis: classification, pathologic anatomy and surgical decompression. Spine 13:313–320, 1988

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4. Tarvin G, Prata R: Lumbosacral stenosis in dogs. J Am Vet Med Assoc 177:154–159, 1980 5. Jones JC, Wilson ME, Bartels JE: A review of high resolution computed tomography and a proposed technique for regional examination of the canine lumbosacral spine. Vet Rad Ultrasound 35:339–346, 1994 6. Jones JC, Sorjonen DC, Simpson ST, et al: Comparison between computed tomographic and surgical findings in nine large-breed dogs with lumbosacral stenosis. Vet Radiol Ultrasound 37:247–256, 1996 7. Jones JC, Shires PK, Inzana KD, et al: Evaluation of canine lumbosacral stenosis using intravenous contrastenhanced computed tomography. Vet Radiol Ultrasound 40:108– 114, 1999 8. Adams WHDG, Pardo AD, et al: Magnetic resonance imaging of the caudal lumbar and lumbosacral spine in 13 dogs (1990–1993). Vet Radiol Ultrasound 36:3–13, 1995 9. de Haan J, Shelton S, Ackerman N: Magnetic resonance imaging in the diagnosis of degenerative lumbosacral stenosis in four dogs. Vet Surg 22:1–4, 1993 10. Ramirez O, Thrall DE: A review of imaging techniques for canine cauda equina syndrome. Vet Radiol Ultrasound 39:283–296, 1998 11. Fritsch E, Heisel J, Rupp S: The failed back surgery syndrome: reasons, intraoperative findings and long term results (a report of 182 operative treatments). Spine 21:626–633, 1996 12. Jenis L, An H: Spine update: lumbar foraminal stenosis. Spine 25:389–394, 2000 13. Stambough J: Failed back: etiologies. Semin Spine Surg 11:162–175, 1999 14. Weisel S: The multiply operated back, in Chapman M (ed): Operative Orthopedics (ed 2). Philadelphia, PA, JB Lippincott, 1993, pp 2809–2814 15. Inufusa A, An H, Lim T: Anatomic changes of the spinal canal and intervertebral foramen associated with flexion extension movement. Spine 21:2412–2420, 1996 16. Fujiwara A, An H, Lim T: Morphologic changes in the lumbar intervertebral foramen due to flexion– extension, lateral bending, and axial rotation. Spine 26:876–882, 2001 17. Cook J: Decompressive procedures: indications and techniques. Vet Clin North Am: Small Anim Pract 22:917–921, 1992 18. Bitetto WV, Brown NO: Selection of the appropriate surgical approach for intervertebral disc disease. Probl Vet Med 1:415–433, 1989 19. Danielsson F, Sjostrom L: Surgical treatment of degenerative lumbosacral stenosis in dogs. Vet Surg 28:91– 98, 1999 20. Palmer R, Chambers J: Canine lumbosacral disease part II: Definitive diagnosis, treatment and prognosis. Comp Cont Educ Vet 13:213–222, 1991 21. Janssens L, Moens Y, Copper P, et al: Lumbosacral degenerative stenosis in the dog. Vet Comp Orthop Traumatol 13:97–103, 2000 22. Chambers JN, Barbara A, Scicer BA, et al: Results of treatment of degenerative lumbosacral stenosis in dogs by exploration and excision. Vet Comp Orthop Traumatol 3:130–133, 1988 23. Watt R: Degenerative lumbosacral stenosis in 18 dogs. J Small Anim Pract 32:125–134, 1991 24. Ness M: Degenerative lumbosacral stenosis in the dog: a review of 30 cases. J Small Anim Pract 35:185– 190, 1994 25. Schulman A, Lippincot C: Canine cauda equina syndrome. Compend Cont Educ Pract Vet 10:835 844, 1988 26. Slocum B, Devine T: L7-S1 Fixation–fusion for treatment of cauda equina compression in the dog. J Am VetMed Assoc 188:31–35, 1986 27. Slocum B, Devine T: L7-S1 fixation–fusion for cauda equina compression: an alternative view, in Slatter D (ed): Textbook of Small Animal Surgery (ed 2). Philadelphia, PA, WB Saunders, 1993, pp 1105–1110 28. Slocum B, Devine T: L7-S1 fixation–fusion technique for cauda equina syndrome, in Bojorab M (ed): Current Techniques in Small Animal Surgery (ed 5). Philadelphia, PA, Lea & Febiger, 1998, pp 861–864 29. Smith M, Bebchuk T: An in vitro biomechanical study of the effects of surgical modification upon the canine lumbosacral spine. Vet Surg 31:505–506, 2002 30. Efstathiou P, Moskovich R, Casar R, et al: A biomechanical evaluation of internal lumbar laminoplasty: the preservation of spinal stability during laminectomy for degenerative spinal stenosis. Bull Hosp Jt Dis 55:7–11, 1996 31. Osman S, Nibu K, Panjabi M, et al: Transforaminal and posterior decompressions of the lumbar spine: a comparative study of stability and intervertebral foramen area. Spine 22:1690–1695, 1997 32. Weiner BK, Walker M, Brower RS: Microdecompression for lumbar spinal canal stenosis. Spine 24:2268–2272, 1999 33. Dirksmeier P, Parsons I, Kang J: Microendoscopic and open laminotomy and discectomy in lumbar disc disease. Semin Spine Surg 11:138–146, 1999 34. Burke T, Caputy A: Microendoscopic posterior cervical foraminotomy: a cadaveric model and clinical applications for cervical radiculopathy. J Neurosurg 93:126–129, 2000

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35. Adamson T: Microendoscopic posterior cervical laminoforaminotomy for unilateral radiculopathy: results of a new technique in 100 cases. J Neurosurg 95:51–57, 2001 36. Roh S, Kim D, Cardoso A, et al: Endoscopic foraminotomy using MED system in cadaveric specimens. Spine 25:260– 264, 2000 37. McCulloch J:Microsurgical spinal laminotomies, in Frymoyer J (ed): The Adult Spine. New York, Raven Press, 1991 38. YoungS, VeerapenR,O’Laoire S: Reliefof lumbarcanal stenosis using multilevel subarticular fenestrations as an alternative to wide laminectomy. Neurosurgery 23:628–633, 1988 39. Weiner B, Brower R, McCulloch J: Minimally invasive alternatives in the treatment of lumbar stenosis. Semin Spine Surg 11:253–261, 1999 40. Baba H, Uchida K, Maezawa Y, et al: Microsurgical nerve root canal widening without fusion for lumbosacral intervertebral stenosis: technical notes and early results. Spinal Cord 34:644–650, 1996 41. Guiot B, Khoo L, Fessler R: A minimally invasive technique for decompression of the lumbar spine. Spine 27:432–438, 2002 42. Trotter E, Crissman J, Robson D, et al: Influence of nonbiologic implants on laminectomy membrane formation in dogs. Am J Vet Res 49:634–643, 1988 43. Mattoon J, Koblik P: Quantitative survey radiographic evaluation of the lumbosacral spine of normal dogs and dogs with degenerative lumbosacral stenosis. Vet Radiol Ultrasound 34:194–206, 1993 44. Chen Q, Baba H, Kamitani K, et al: Postoperative bone regrowth in lumbar spinal stenosis: a multivariate analysis of 48 patients. Spine 19:2144–2149, 1994 45. Postacchini F, Cinotti G: Bone regrowth after surgical decompression for lumbar spinal stenosis. J Bone Jt Surg 74-B:862–869, 1992 46. Jones JC, Banfield CM, Ward DL: Association between postoperative outcome and results of magnetic resonance imaging and computed tomography in working dogs with degenerative lumbosacral stenosis. J Am Vet Med Assoc 216:1769–1774, 2000 47. Herno A, AiraksinenO, SaariT: Computed tomography after laminectomy for lumbar spinal stenosis. Spine 19:1975–1978, 1994 48. Wood BC, Lanz OI, Jones JC, Shires PK. Endoscopic-assisted lumbosacral foraminotomy in the dog. Vet Surg. 2004 May-Jun;33(3):221-31 49. Goedde T. Anterior foraminotomy as a new treatment modality in degenerative lumbosacral disease. 2003 ECVN Annual Meeting Proceedings 50. Goedde T, Steffen F. Surgical treatment of lumbosacral foraminal stenosis using a lateral approach in twenty dogs with degenerative lumbosacral stenosis. Vet Surg 36:705-713, 2007 51. Van Klaveren NJ, Suwankong N, De Boer S, et al: Force plate analysis before and after dorsal decompression for treatment of degenerative lumbosacral stenosis in dogs. Vet Surg 34:450–456, 2005 52. Suwankong N. Degenerative lumbosacral stenosis in dogs. PhD Thesis. University of Utrecht. 2007 53. Suwankong N, Meij BP, Van Klaveren NJ, et al. Assessment of decompressive surgery in dogs with degenerative lumbosacral stenosis using force plate analysis and questionnaires. Vet Surg. 2007 Jul;36(5):423-31. 54. Bagley R. Surgical stabilization of the lumbosacral joint. In Slatter D (ed): Textbook of Small Animal Surgery (ed 2). Philadelphia, PA, WB Saunders, 2003, pp 1238-1243. 55. Sharp NJ, Wheeler SJ (2005) Lumbosacral disease. In; Small Animal Spinal Disorders. Mosby 56. Meheust P, Mallet C, Marouze C. A new surgical technique for lumbosacral stabilization: arthrodesis using the pedicle screw fixation. A clinical study of 5 cases. Pratique medicale et chirurgicale de l’animal de compagnie. 2000; 35:201-207.

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