Spinal diseases: non-surgical options

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1 Vet Times The website for the veterinary profession Spinal diseases: non-surgical options Author : MARIANNE STABAEK MARTIN Categories : Vets Date : June 2, 2008 MARIANNE STABAEK MARTIN believes the road to successful spinal disease management can be long, but is worth trying THIS article highlights some of the non-surgical methods of treatment for canine spinal diseases, which include: discospondylitis; degenerative myelopathy; granulomatous meningoencephalitis; and spinal cord ischaemia. Discospondylitis Definition This is an infection that affects the intervertebral disc with concurrent osteomyelitis of adjacent vertebral endplates and vertebral bodies. Signalment The disease mainly affects largebreed dogs and, out of those, mostly males due to their higher 1 / 10

2 level of activity. Most dogs are middle-aged around five to nine years old. German shepherd dogs (GSDs) seem to be predisposed to this disease. History and physical findings The disease is insidious and progressive. The hallmark of the condition is that patients suffer from spinal hyperpathia (such as neck or back pain on deep palpation) associated with systemic disease. The patients may have been depressed and anorexic for weeks or months previously, with difficulty jumping and subtle lameness. The physical findings depend largely on the site of infection and when it is presented. Normally, patients that are presented later on in the disease cycle have more profound neurological signs than the patients presented earlier in the disease process. The latter often have more systemic signs. Clinically relevant pathophysiology Discospondylitis is most frequently the result of haematogenous spread, often from secondary septic foci in the cardio vascular, urogenital and skeletal tissues. Occasionally, it is caused by a migratory foreign body, or as a sequel to a disc fenestration operation. Immunosuppressed animals may be predisposed to develop discospondylitis. Anatomically, predisposing factors in the spinal cord may promote the infection. A subchondral vascular loop may slow circulation in the vertebral epiphysis, promoting blood sludging and colonisation by the organisms. The infection then spreads by local extension to the disc, resulting in lysis of endplates, disc necrosis and collapse of the intervertebral space. The organisms commonly cultured from animals with discospondylitis are Staphylococcus aureus, S intermedius and Brucella canis. Streptococcus species and Escherichia coli have also been reported. Uncommonly the infection is caused by a fungal agent, Aspergillus terrus. The areas of the spine typically affected are those where, with the exception of the midthoracic spine, there is a statickinetic junction of the spine, such as an area of spinal stability adjacent to an area of relative spinal mobility. The most affected areas are the lumbosacral junction, cervicothoracic junction, thoracolumbar junction and midthoracic discs. Diagnosis This is confirmed by radiography. About 10 to 14 days after the initial infection, the radiographic signs become evident the first of which is lysis of one or both vertebral endplates, followed by collapse of the intervertebral disc space. The lysis of the invertebral disc is the hallmark of discospondylitis. Laboratory findings may show a urinary tract infection in up to 40 per cent of the cases. Occasionally, the same organism is found in blood and bone cultures. Cerebrospinal fluid (CSF) is generally normal: so is the general serum biochemical profile, unless a systemic disease is present. It is worth noting that, due to the public health risk, a Brucella titre should be performed in suspected cases of discospondylitis. 2 / 10

3 Discospondylitis should be differentiated from spondylosis deformans and spinal neoplasia. Spondylosis deformans does not have intradiscal lysis. Vertebral endplate lysis is only seen with infection and not in spinal neoplasia. Treatment This usually depends on presenting neurological examination, laboratory data and serial neurological examination. The latter is done to detect neurological deterioration (such as paraparesis and tetraparesis) and, if so, may then become a surgical patient. If the animal presents with an acute onset of spinal hyperpathia, paraparesis or tetraparesis, the treatment is surgical. However, if none of the above occurs, the preferred treatment of discospondylitis is medical. For patients presenting with pain, or pain and mild paresis, treatment consists of analgesia and antibiosis, with four to six weeks of strict confinement. Antibiotics should be chosen on the basis of urine or blood and/or bone culture, susceptibility tests and a Brucella titre. The antibiotics need to be bactericidal, achieve minimal inhibitory concentration in bone and be effective against the causative agent. If the bacterial cultures are negative, empirical selection of antibiotics is necessary. The choice of antibiotics is then based on the most likely causative agent. A?-lactamase-resistant antibiotic is then chosen, such as clindamycin, cloxacillin or cephradine. If the Brucella titre is positive, a combination of a tetracycline plus an aminoglycoside is then chosen. Treat the patient with this method until the Brucella titre is negative. Approximately 80 to 90 per cent of patients respond to medical treatment. If the animal is unresponsive to treatment in the first seven to 10 days, the antibiotic should be changed. A third antibiotic may be added if pain persists, or a surgical curettage may be performed to obtain a bone sample for culture and sensitivity analysis. Granulomatous meningoencephalitis The incidence of granulomatous meningoencephalitis (GME) ranges from five to 25 per cent of all central nervous system (CNS) diseases that affect dogs. Definition This is an acute, progressive inflammatory disease of the CNS. It has many synonyms like granulomatous meningoencephalomyelitis, focal GME, ocular GME, reticulosis, histiocytic encephalitis, neoplastic reticulosis, GME and inflammatory GME. 3 / 10

4 Signalment It usually occurs in young to middle-aged dogs, such as two to six year olds. Females are more predisposed than males. Toy breeds, especially poodles and terriers, seem to be especially at risk. Clinically relevant pathophysiology This neurological disorder may affect any part of the CNS (such as the meninges, brain and spinal cord) and then mainly the white matter. Many dogs also have meningeal involvement and, occasionally, grey matter may be affected. Three forms of the disease have been described: disseminated; focal; and ocular. Consequently, the history, neurological examination, laboratory findings and course of the disease may vary considerably. The cause of the disease is unknown, although many theories have been proposed. Suggested hypotheses include a cell-mediated immune response to an infectious agent; this is an inflammatory process that transforms into a neoplastic one, possibly involving a cell-associated virus. Another theory involves a genetic predisposition to the disease. History and physical findings Patients present with an acute history of episodic or continuous progression of a multifocal neurological disease. Physical examination depends very much on lesion localisation and the form of the disease. Patients with the disseminated form may present with fever and cervical pain, evidenced by nuchal rigidity. Lesions are usually located in the lower brainstem, cervical spinal cord or the meninges. The onset is acute and prognosis is grave; patients may only live for another 12 to 16 weeks. Clinical signs referable to the brain stem, cerebral cortex, cerebellum and cervical spinal cord are most common with focal involvement. The signs are consistent with a spaceoccupying lesion and are more insidious in the onset, with a duration of three to six months. The prognosis is unfavourable, with a lifespan of up to one year. The ocular form often presents with sudden blindness or papillary abnormalities. It affects the ocular nerve, and the duration of signs spans 4 / 10

5 three to six months. This form carries a somewhat longer lifespan 12 to 18 months but the prognosis is still unfavourable. Diagnosis A presumptive diagnosis of GME is based on signalment, history, progression of clinical signs, CSF analysis and the results of a contrast-enhanced CT scan. The latter may reveal one or more masses in the spinal cord or brain. CSF may reveal an increase in protein concentration and a mildmarked pleocytosis, consisting primarily of lymphocytes, monocytes and occasionally plasma cells. Neutrophils are seen in two-thirds of the samples. Definitive diagnosis requires biopsy or necropsy for histological examination. Treatment Corticosteroids can occasionally halt or reverse the progression of clinical signs. The presenting signs determine, however, the type of steroids used, route of administration, dosage schedule and duration of therapy. Treatment regime for moderate to severe clinical signs Dexamethasone is started on a dose of 2mg/kg IV. The dose is reduced to 0.2mg/kg daily over three to four days, or until neurological improvement has been noted. The patient is then discharged on prednisone postoperatively. The dose used depends very much on the response to therapy. The dog must be kept on prednisone as a maintenance dose indefinitely, as the clinical signs will return if it is taken off the medication. A second remission is unlikely to occur. Treatment regime for mild clinical signs Treat with prednisone at 1mg/kg to 2mg/kg postoperatively (bid) for two to three weeks and taper over a three to four-week period with a 2.5mg to 5mg total dose every other day. Degenerative myelopathy (DM) Definition This is a neurological disease, of an unknown aetiology, that causes progressive white matter demyelination of the long tract fibres that starts in the thoracolumbar spinal cord. This disease is also known as GSD myelopathy. 5 / 10

6 Signalment GSDs are particularly exposed, although other large-breed dogs also become affected. Usually, it affects middle-aged to older dogs (five to seven year olds). Patients present with a history of progressive hindlimb weakness without back pain. These signs may have been present for months and the owners complaints are often that the animal cannot rise on its hindlimbs. Clinically relevant pathophysiology The cause is unknown, although several theories have been proposed, such as a deficiency in the nutrients and vitamins that are responsible for the demyelination taking place. An inherited cause has also been suggested in GSDs. The disease is compared to multiple sclerosis in humans. Diagnosis Including the signalment and history, the general physical examination is unremarkable, aside form the presenting signs. There is no spinal hyperpathia but neurological examination reveals upper motor neuron (UMN) signs and either ambulatory or weakly ambulatory paraparesis. There may be loss of symmetric or unsymmetrical conscious proprioception, exaggerated patellar reflexes and crossed extensor reflexes. Thoracic limbs are not involved in the disease. Survey radiography and myelography are normal, as are laboratory findings, including CSF analysis. Myelography is performed to eliminate diseases that mimic this disease, including chronic disc protrusion (Hansen type two), hip dysplasia and spinal neoplasia. GSDs can have disc protrusion and degenerative myelopathy at the same time, but surgical disc compression, while facing an additional diagnosis of DM, is not warranted. Definitive diagnosis is based on characteristics such as histopathological changes in the spinal cord parenchyma. Treatment There are no current treatments for this disease. Multiple regimes have been suggested, such as corticosteroids, NSAIDs, vitamins and immune modifiers, but none have proved beneficial. The use of corticosteroids may actually cause further muscle waste and muscle weakness. Exercise may be helpful in slowing the progression of the disease, and walking, swimming and running for 30 minutes every other day is recommended. The use of aminocaproic acid (500mg postoperatively bid) has been reported to be beneficial. The drug blocks the final common pathway of tissue inflammation and may slow or halt the progression of DM in a few cases. The drawbacks are gastrointestinal upsets, high cost and no visible effect for 6 / 10

7 the first two to three months of therapy. The combination of this drug with the antioxidant acetylcysteine should be considered in the lack of any other treatment regimes. The prognosis is unfavourable. Although the rate of progression to total non-ambulatory paraparesis varies considerably, it may take months or years. Spinal cord ischaemia Definition Fibrocartilaginous embolisation (FCE) is the ischaemic necrosis of a segment of the spinal cord caused by the herniation of interverterbral disc material into the spinal cord microvasculature. There are many synonyms, including necrotising myelopathy, embolic myelopathy, ischaemic myelopathy, vascular episode and fibrocartilaginous infarct. Signalment and history FCE most commonly affects large-breed dogs, such as great Danes, St Bernards, Labrador retrievers and GSDs. Any age is at risk, although the disease is most common in young adults (three to seven year olds). The patients have a history of pain, which has resolved over time when presented with acute, nonprogressive, ambulatory or non-ambulatory, tetra, para, hemi or mono-paresis without spinal hyperpathia. About 50 per cent of cases occur after trauma or exercise. Clinically relevant pathophysiology The pathogenesis of canine FCE is poorly understood, but it is believed to follow the pattern described here. Emboli, histochemically identical to the nucleus pulposus of the intervertebral disc, travel to the spinal cord via either the veins or the arteries. To elicit clinical disease, the clot must simultaneously compromise many closely associated small blood vessels. It is thought that a sudden elevation in central venous pressure, caused by coughing or vomiting, may propel the emboli into the spinal cord s venous drainage system. Diagnosis Physical examination is generally normal, although the neurological signs seen depend on where in the spinal cord the disease strikes. The most common sites for FCE to occur are C6-T2 or L4-S3. Survey radiography is generally normal. 7 / 10

8 One can perhaps notice a mild collapse of an intervertebral space. Myelography, done early enough (within 12 to 24 hours), might detect a spinal cord swelling that, if the myelography is performed later, will have disappeared and give a normal appearance. Laboratory findings are unremarkable. Differential diagnoses include spinal cord fracture and/or luxation, intervertebral disc extrusion and spinal neoplasia. Any disease causing acute, focal or lateralising signs and non-progressive paresis without spinal pain must be included. A definitive diagnosis is achieved by the elimination of other diseases of the spinal cord and histopathological identification of a characteristic fibrocartilaginous emboli and resultant spinal cord infarction. Treatment This depends on the time of presentation. If it is within 72 hours of the onset of clinical signs, the problem is treated with corticosteroids, physiotherapy and two to three weeks padded cage confinement. Dexamethasone is the corticosteroid of choice. Frequent bladder expressions are necessary. After 72 hours of the onset of clinical signs, the problem is treated with supportive care only. Prognosis This is dependent on the site of emboli in effect, whether it is causing UMN or lower motor neuron (LMN) signs, the degree of improvement within 14 days and the extent of spinal cord damage. Prognosis is better for patients with UMN than LMN disease and those showing improvement within 14 days. The extent of spinal cord damage is assessed on neurological examination. Summary The diagnosis of spinal diseases can offer a great challenge for the veterinary surgeon and, often, the definitive diagnosis is only concluded at postmortem. Corticosteroids seem to be the therapy with the greatest effect in the majority of these diseases, apart from DM. The therapy should be used in conjunction with constant neurological assessment of the dog, to see whether the dose can be lowered. Often, these cases require a great amount of nursing and hospitalisation and can, therefore, pose the problem of negative owner compliance from the start. Even if one starts therapy, the road to success can be a long and expensive one but that is not to say that one should not give it a try. 8 / 10

9 Poodles are predisposed to GME, as are several toy breeds. 9 / 10

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SPINAL CORD DISEASE IN DOGS PART TWO: MOST LIKELY CAUSES

Vet Times The website for the veterinary profession https://www.vettimes.co.uk SPINAL CORD DISEASE IN DOGS PART TWO: MOST LIKELY CAUSES Author : RITA GONÇALVES Categories : Vets Date : April 7, 2014 RITA