Simon R. Platt, BVM&S, MRCVS, DACVIM (Neurology), DECVN
Hansen first classified intervertebral disc disease (IVDD) as type I and type II. Hansen type I IVDD is herniation of the nucleus pulposus through the annular fibers and extrusion of nuclear material into the spinal canal. Hansen type I IVDD is commonly associated with chondroid disc degeneration. The disc commonly extrudes through the dorsal annulus, causing dorsal, dorsolateral, or circumferential compression of the spinal cord. Chronic disc extrusion is characterised by extradural fibrous adhesions whilst acute disc extrusion is characterised by extradural haemorrhage and soft disc material. Hansen type I IVDD typically affects small, young, chondrodystrophic dogs and has an acute onset but it can occur in large nonchondrodystrophic dogs, often also having an acute onset. Neurologic dysfunction is a secondary consequence of IVDD. Extrusion of the nucleus causes primary cord injury and associated clinical neurologic signs by concussion and later by compression. Acute and severe disc extrusions cause pannecrosis of the gray and white matter. Sequential haemorrhage, oedema, and neuronal necrosis depend on the severity and type of injury.
The treatment for this disc extrusion is often determined by multiple factors including; neurologic status of the dog, delay in presentation for veterinary attention, concurrent medical treatment, concurrent vertebral instability, previous episodes of spinal pain, method of diagnosis of the extrusion, lesion localisation and economics. This means that criteria for such treatment need to remain 'fluid' and therefore specific treatments may differ in similar patient circumstances.
The method of diagnosis of IVDD is considered to be an important factor in decision-making. Although myelography is well described in the veterinary literature, common problems encountered such as poor distribution of contrast medium, the presence of spinal cord swelling and neurologic deterioration have led to the belief that it is not the technique of choice in the human field. Computed tomography (CT) can be an adjunctive procedure to myelography to further delineate the extent of a compressive lesion or as a sole technique for detecting IVDD. CT myelography may provide a diagnostic image when there is obstruction of contrast medium flow. CT or magnetic resonance imaging (MRI) are extremely useful for diagnosing foraminal or lateral disc extrusions, as well as the extent of associated extradural and subarachnoid haemorrhage. MR imaging is the best available method for early recognition of disc degeneration in dogs. MR imaging is especially useful as a sensitive, accurate, and non-invasive method for evaluating the caudal lumbar spine and lumbosacral space in dogs. Cerebrospinal fluid analysis should always be performed to rule-out concurrent inflammatory disease. This will be more important with protrusions where the clinical signs may be more chronic progressive in nature and difficult to differentiate from other diseases.
Hansen type I most commonly occur within the thoracolumbar region of chondrodystrophoid breeds. The most common site for Hansen type I IVDD in large nonchondrodystrophic breeds is the inter-space between L1 and L2. Functional grading schemes describing hyperesthesia and motor and sensory dysfunction have been used to provide a mechanism for determining treatment for thoracolumbar IVD extrusions. However, the degree of neurologic dysfunction is variable with similar degrees of extrusion and so usually can only be used to assess prognosis rather than treatment options.
Advanced imaging studies are again essential. Myelography may provide up to 75% accuracy in the determination of affected space and lateralization of the disc, especially when combined with neurological examination and history. However, CT has been shown to be at least 90% accurate at site localisation and 96% accurate with prediction of lateralization. Similar studies are lacking at present with respect to the MRI in veterinary patients, but my own experience is that this modality offers similar results in terms of localisation accuracy.
My indications for non-surgical treatment of this condition are limited to a first-time episode of spinal pain only or financial constraints of the owner. Conservative therapy consists of strict cage rest for 4-6 weeks, pain relief and/or muscle relaxant use (diazepam). My indications for surgical management of thoracolumbar IVD extrusion are therefore cases with spinal pain only that are non-responsive to conservative therapy, recurrent disease, cases with neurologic deficits with deep pain, and cases with loss of deep pain perception for less than 72 hours; although I have infrequently had positive experiences with cases that have lost deep pain perception for up-to 7 days duration. The method of choice for surgical decompression is often determined by the imaging study and lesion localisation. With T10-L4 extrusions, I will most often perform a hemilaminectomy at the site of extrusion and extend the defect in the bone cranially and caudally up to a maximum of five intervertebral spaces if necessary until normal epidural fat is identified. For extrusions caudal to L4, I will often perform a dorsal laminectomy and try to combine this with a hemilaminectomy after nerve root visualisation is possible. If there is no deep pain perception present I will perform a durotomy to visualise the spinal cord parenchyma and asses prognosis. I will routinely fenestrate disc spaces T11-L3 after decompressive surgery in chondrodystrophoid dogs.
Methylprednisolone sodium succinate (MPSS) remains the standard of care in humans. MPSS has been shown to be effective because of its free radical scavenging properties rather than its anti-inflammatory effect. In order to obtain this effect, it must be used at high doses and treatment should be initiated within 8 hours of injury. Suggested protocols include initiation of treatment with MPSS within three hours of injury at a dose rate of 30mg/kg given intravenously and followed with either a constant rate infusion of 5.4mg/kg/hr for 24 hours, or second and third boluses of 15mg/kg at two and six hours after the first dose and then a constant rate infusion of 2.5mg/kg/hour for 24 hours. If treatment is initiated between 3 and 8 hours after injury, the recommendation is to continue treatment for 48 hours rather than 24 hours. Delaying initiation of treatment for more than 8 hours has a detrimental effect on outcome in people. As MPSS has both glucocorticoid and free radical scavenging effects, it is postulated that delaying treatment until after the majority of free radical induced damage has occurred is more likely to result in glucocorticoid side-effects. Indeed, although there continues to be wide spread use of glucocorticoids, such as dexamethasone, to treat acute spinal cord injuries in veterinary practice, there is no good evidence that such drugs are beneficial and the side effects have been well documented and at this time they cannot be recommended as efficacious treatments.
Recently, substances that fuse membranes ("fusogens") have been proposed as a treatment for acute spinal cord injury. Polyethylene glycol (PEG) is a hydrophilic polymer that targets damaged membranes following intravenous administration and seals membranes preventing intracellular leak of ions and subsequent axonal disruption, restoring axonal conduction. In an experimental model of spinal cord injury in guinea pigs, there was rapid improvement of electrophysiological parameters and of the cutaneous trunci reflex following treatment with PEG. No adverse effects were reported in a phase I trial of PEG completed in dogs with paralysis and loss of pain sensation due to acute disc herniations; 60% of the dogs did recover function but this preliminary study was not blinded and included a historical control group.