key: cord-022283-8ny6j1ny authors: Cuddon, Paul A title: The weak and ataxic or paralyzed cat date: 2009-05-15 journal: Problem-Based Feline Medicine DOI: 10.1016/b978-0-7020-2488-7.50047-8 sha: doc_id: 22283 cord_uid: 8ny6j1ny nan Ataxia and paresis occur when there is physical or functional disruption to both the motor and sensory pathways of the nervous system. Paresis is a deficit of voluntary movement, leading to weakness in one limb (monoparesis), both pelvic limbs (paraparesis), the limbs on one side of the body (hemiparesis), or all four limbs (tetraparesis). It is caused by disruption of the voluntary motor pathways anywhere from the cerebral cortex through the brainstem and spinal cord to the spinal cord segments and the peripheral nerves supplying muscles. Neurological testing to determine whether a cat is paretic includes gait analysis and postural reaction testing, which includes hopping, wheel-barrowing, hemi-standing/hemi-walking, and the extensor postural thrust. The term paralysis is reserved for the patient who has a complete loss of any voluntary movements. Ataxia is a lack of coordination of the limbs or trunk produced by disruption of the sensory proprioceptive pathways of the spinal cord and brainstem. Lesions of the cerebellum and the vestibular system also can produce ataxia. Sensory ataxia, the disruption of sensory proprioceptive pathways, can be assessed via such tests as proprioception and tactile placing. Most cats with spinal cord disease have a combination of both ataxia and paresis, since most myelopathies cause disruption of both the motor and sensory systems. In many circumstances, therefore, separation of ataxia and paresis becomes almost impossible on routine neurological examination. Cats presenting solely with ataxia and paresis/paralysis most commonly have spinal cord disease. Weakness and ataxia can also occur with cerebral and brainstem disease. • However, cats with cerebral disease will usually show seizures, behavior change, aimless wandering, and pacing along with the ataxia and contralateral hemiparesis or tetraparesis. • Cats with brainstem disease will demonstrate cranial nerve abnormalities as well as an ipsilateral hemiparesis or tetraparesis. Most polyneuropathies manifest as generalized weakness without ataxia. In many cases of peripheral nerve disease, sensory tests such as proprioception and tactile placing will be normal despite obvious muscle weakness. Localization of myelopathies is dependent on determining whether the thoracic and pelvic limbs have upper (UMN) or lower motor neuron (LMN) signs. Cats with UMN paresis will demonstrate normal to increased segmental spinal reflexes (myotatic or tendon reflexes, muscle tone and withdrawal reflexes) whereas cats with LMN paresis will show decreased to absent segmental spinal reflexes. An UMN bladder, likewise, will have increased tone and be difficult to express due to external (+/− internal) urethral sphincter hypertonia, whereas a LMN bladder will be flaccid (or atonic) and easily expressed due to external urethral sphincter hypo-to atonia. The classic spinal cord divisions when localizing a myelopathy are as follows: • Cervical spinal cord (C1-C5) -UMN tetraparesis to tetraplegia. • Cervical intumescence (C6-T2) -LMN signs to thoracic limbs and UMN signs to pelvic limbs. The most common causes of spinal cord ataxia and paresis in cats are infectious (including feline infectious peritonitis virus (coronavirus)), neoplasia (lymphosarcoma) and trauma. Primary spinal neoplasia (meningioma), inflammation (feline polioencephalomyelitis), and ischemia (aortic thromboembolism and fibrocartilaginous embolism) are less common. Intervertebral disc disease is very rare. SPINAL LYMPHOSARCOMA*** • Chronic progressive ataxia. • Asymmetric paraparesis. • Focal areas of spinal pain. Lymphosarcoma is the most common feline neoplasia. 5-15% of cats with lymphoreticular malignancies develop neurologic involvement. 88% of cats with CNS involvement show thoracic and lumbar myelopathy, although the brain may also be affected. Epidural lymph channels and extramedullary hematopoietic tissue are possible sites for development of primary spinal lymphosarcoma. Tumor growth commonly occurs longitudinally along the spinal canal (the epidural space is a low-resistance channel). 79% of cats with spinal lymphosarcoma have solitary epidural lesions. Multifocal lesions are also possible, as is tumor involvement of multiple nerve roots. Spinal lymphosarcoma is most commonly seen in young cats (≤ 3 years). Males are more commonly affected. Most cats present with an initial insidious course of neurologic dysfunction followed by acute deterioration. Tumors occur predominantly between T3-L4. Involvement of the brachial intumescence and plexus also can occur. Cervical spinal cord involvement is rare. The most common clinical signs include progressive ataxia, asymmetric paraparesis and focal spinal pain. If there is involvement of the brachial or lumbosacral intumescences, LMN signs will occur. Nerve root involvement may result in lameness and limb pain. Acute exacerbation of signs is commonly associated with hemorrhage. Weight loss is the most common extraneural sign. The most common extraneural tumor site associated with spinal lymphosarcoma is the kidney. Complete blood count, biochemistry parameters and urinalysis are often normal, although non-regenerative anemia or leukemia may occasionally be seen. Many cats are seropositive for FeLV or positive on indirect fluorescent antibody testing of bone marrow. A monomorphous population of neoplastic lymphocytes will be seen in some cases. Survey spinal radiographs are usually normal. MRI scan or myelography shows single or multiple asymmetric extradural spinal cord compression(s). Infectious diseases, such as feline infectious peritonitis, toxoplasmosis and cryptococcosis also may produce signs of progressive spinal cord dysfunction. However, unlike spinal lymphosarcoma, most infectious conditions usually result in multifocal neurologic dysfunction, with involvement of the cerebrum, brainstem and/or cerebellum. Spinal lymphosarcoma is radiosensitive. • Rapid reduction in tumor volume can occur within hours of delivering a single large palliative dose of radiation (3-4 Gy). Chemotherapy is important for systemic control of lymphosarcoma although most chemotherapeutic agents do not cross the blood-brain barrier. Cytosine arabinoside may also help control spinal lymphosarcoma. • This anti-metabolite drug crosses the blood-brain barrier and reaches appropriate CSF levels. • The recommended dosage is 100 mg/m 2 /day as a constant rate infusion intravenously for 4 days. • An alternative regimen is 300 mg/m 2 subcutaneously twice daily for 2 days. • Potential toxicity includes myelosuppression (at 5-7 days); vomiting; and anorexia. • Tumor cells rapidly become resistant to this drug's action. Surgical decompression of the spinal cord and/or nerve roots, and tumor resection or debulking is a potential treatment option, especially if the tumor is localized. Follow-up radiation and chemotherapy is recommended. Prognosis is poor for long-term survival, especially when most cats are infected with the FeLV virus. The only effective means of prevention is test and removal programs directed at controlling the spread of FeLV. Feline infectious peritonitis (FIP) may produce a nonsuppurative meningoencephalitis in 29% of infected cats. The CNS signs are usually associated with the noneffusive ("dry") form of FIP (cell-mediated immunity is defective but not absent) The neurological form of FIP has no breed or sex predilection, although most cases are < 3-4 years of age. In most cases, the neurological signs are multifocal with a predominance of caudal fossa signs (brainstem, vestibular nuclei and cerebellum). • Signs can include nystagmus (positional, nonconstant, rotatory, horizontal or vertical in nature), head tilt, body lean or rolling, facial paralysis, an ipsilateral hemiparesis or tetraparesis, intention tremor, and hypermetria or dysmetria. The spinal cord and the cerebrum also can be involved. • Signs of cerebral disease can include seizures, behavior change, decreased mentation, decreased menace response, compulsive walking, ipsiversive wide circling and head pressing. • Spinal cord involvement will manifest as UMN and/or LMN tetraparesis or paraparesis with ataxia. Tetraplegia or paraplegia are the most severe consequences of spinal cord involvement. Myelopathy is seen either as the sole abnormality or as part of a multifocal distribution in 25% of cases. The onset of FIP can be acute, although most cats have a chronic progressive course over 1 week to 3 months. Extraneural signs may include fever, cachexia, poor body condition, dehydration, lethargy, muscle atrophy, chorioretinitis, dyspnea and gastrointestinal/hepatic signs. Many cats present with the neurological form of FIP without extraneural signs. The diagnosis is best established via CSF analysismarked elevation in protein (usually greater than 1 The CSF FIP viral titer is usually positive if CNS signs are present. It is probable that CSF anti-FIP viral immunoglobulin G is produced within the CNS. Serum biochemical changes often consist of an elevation in total protein and hypergammaglobulinemia. Serum FIP antibody titers are not reliable, and are elevated in only 58% of cats with the neurological form of FIP and are even negative in some cats. Numerous other infectious and immunological diseases can produce meningitis and encephalomyelitis in cats. FeLV-associated CNS lymphosarcoma can usually be differentiated by CSF analysis, and a positive FeLV serum titer. Cryptococcal organisms are usually visible in CSF with confirmation made by a latex agglutination assay or culture. CNS toxoplasmosis is rare in the cat, usually producing signs of intracranial disease rather than myelopathy. Recent or active infection is diagnosed by demonstrating a positive IgM titer, a four-fold increase or decrease in IgG serum titer, a CSF IgM antibody titer or a CSF IgG titer present at a higher CSF:serum ratio than another antibody present in serum that is not produced in CSF, e.g. calicivirus. Feline polioencephalomyelitis usually produces only a mild to moderate increase in protein (mean of 0.48 g/L [48 mg/dl] with a range of 0.1-0.7 g/L [10-70 mg/dl]) and a mild mononuclear pleocytosis (mean of 19 cells/mm 3 [19 cells/μl] with a range of 0-46 cells/mm 3 [0-46 cells/μl]) on CSF. This is not typical of FIP. No effective therapy is known against FIP. Immunosuppressive corticosteroid therapy may slow the disease course (1-2 mg/kg prednisone or prednisolone orally twice daily). All cats with the neurological form of FIP will eventually die from their disease. • Acute variably located spinal cord dysfunction (UMN or LMN signs). • Focal spinal hyperesthesia. • Spinal crepitus. • External abrasions and bruising. External spinal trauma can result from automobile accidents, gunshot injuries, falls from heights and blunt trauma. Sacrocaudal fractures most often occur when the cat's tail is forcefully pulled away from the body. • This most commonly occurs when the cat's tail is trapped under the tire of an automobile. The rotating tire luxates the tail at the sacrococcygeal junction or between two coccygeal vertebrae, resulting in damage to the coccygeal, sacral and lumbar nerve roots (cauda equina). Most spinal fractures occur at the junction of mobile and immobile segments of the spine, such as the thoracolumbar, lumbosacral and sacrocaudal junctions. Traction on the cauda equina in sacrocaudal luxations can also damage the nerve cell bodies in the caudal lumbar and sacral spinal cord due to cranial transmission of the forces through the dura mater and filum terminale of the cord. The degree of spinal cord compression; the length of time of compression; and the velocity of the initial impact injury are important contributors to the resultant spinal cord injury. There are two forms of spinal cord injury -mechanical (primary) injury, consisting of physical disruption of vessels and axons and ischemic (secondary) injury. The latter leads to energy compromise within the spinal cord, cellular accumulation of calcium and resultant intracellular stimulation of enzymes. This leads to protein and lipid breakdown (phospholipid hydrolysis), release of arachidonic acid, free radical and eicosanoid formation, and cell death. Gray matter hemorrhages and white matter edema occur within minutes following acute spinal cord injury, progressing rapidly over the 4-6-hour posttraumatic period. Signs depend on the injury level and the degree of physical or functional disruption of the cord. Signs in cats with sacrocaudal injuries range from hyperesthesia over the tail base to flaccid analgesic tails with varying degrees of urinary reflex dyssynergia or LMN urinary/fecal incontinence. • Reflex dyssynergia involves a failure of urethral relaxation when the cat attempts to urinate and the bladder undergoes contraction. This leads to the production of only very small quantities of urine. The bladder will still be large and the cat will often dribble urine in between attempts to urinate. Many cats with sacrococcygeal trauma also show signs of LMN paraparesis (sciatic nerve injury), consisting of dragging of the hind paws on their dorsum and a failure to flex the pelvic limb(s) when walking or when the withdrawal reflex is performed. There will also be a hypo-to areflexia of the cranial tibial and gastrocnemius reflexes. Palpation of the sacrocaudal area of the spine will result in crepitus and pain. The tail will often be malaligned with the sacrum and the rest of the vertebral column. Cats with spinal trauma commonly have concurrent thoracic, abdominal or pelvic trauma. Neurological and physical examination determine the localization and severity of the cord injury. Non-contrast spinal radiographs (lateral and across the table ventrodorsal views of the entire spine) establish the type of vertebral disruption (fracture vs. subluxation) and the location(s) of the vertebral trauma. Myelography, MRI or CT scans will determine the degree of spinal cord compression. Any other cause of acute myelopathy must be considered as a differential diagnosis in cats with spinal trauma. Most other causes can be eliminated based on history and physical examination -external abrasions, bruising, splintering of claws and spinal pain are seen with trauma. Sacrocaudal fractures must be differentiated from aortic thromboembolism, which also can produce an acute onset of LMN paraparesis to paraplegia, with pain. • However, cats with this disease do not have dysfunction associated with the perineum, bladder, rectum and tail. • The lack of femoral pulses and the presence of cold, cyanotic pelvic limbs would strongly support aortic thromboembolism. Pathologic vertebral fracture secondary to neoplasia will present as an acute, painful myelopathy, and may appear superficially similar to a traumatic fracture on non-contrast spinal radiographs. However, closer examination should reveal areas of lysis within the involved vertebral body. Ischemic myelopathy secondary to fibrocartilaginous embolism most commonly involves the lumbosacral intumescence as is the case with sacrococcygeal trauma. • A differentiating feature of ischemic myelopathy is the absence of spinal pain. Initial medical emergency treatment should include intravenous methylprednisolone sodium succinate (30 mg/kg), administered within 8 hours (and preferably within 3 hours) of the spinal trauma. Continued treatment consists of a constant rate intravenous infusion of methylprednisolone at 5.4 mg/kg/hour or, if not possible, a second bolus intravenous injection (15 mg/kg) at 2 hours after the initial treatment, followed by 15 mg/kg at 6 hours and then 4 times daily for 24-48 hours. Most cases of spinal trauma will require emergency surgical intervention (spinal cord decompression [laminectomy and/or hemilaminectomy] and spinal fixation). The type of decompression and stabilization technique is determined by non-contrast and contrast spinal radiographs or CT/MRI scans. Surgical spinal stabilization is rarely necessary in sacrocaudal fractures/luxations and, due to the oftenmarked separation of the involved vertebrae, is difficult to achieve. Surgical decompression of the cauda equina in sacrocaudal trauma is also unnecessary since it is a traction, not compressive, injury. If the cat is incontinent, attention should be paid to cleanliness, bladder and bowel management, and prevention of decubital ulcers, urine scalding, and cystitis. If there is UMN or LMN urinary incontinence, manual expression or indwelling catheterization of the bladder is required. Pharmacological management of UMN urinary incontinence or reflex dyssynergia, related to sacrocaudal trauma, consists of phenoxybenzamine, an alpha-adrenergic receptor antagonist, to relax the internal sphincter (5 mg orally three times daily) together with diazepam (1.25-2 mg/cat orally two to three times daily) to relax the external sphincter. Bladder detrusor dysfunction can then be treated with bethanechol, a parasympathomimetic agent (5-10 mg orally two to three times daily). Bethanechol may help LMN urinary incontinence (encourages detrusor muscle contraction). Fecal retention can be treated by increasing the bulk of the feces with bran, psyllium or canned mashed pumpkin. In cats with sacrocaudal injury with only tail paresis, conservative medical management will often result in return of tail function. • If this does not occur after 4-6 months, amputation of the tail is recommended. Prognosis is based on the severity of the spinal cord injury. The milder the neurological deficits, the better the prognosis for recovery. Cats with severe myelopathy or cauda equina injury with analgesia have a very poor to hopeless prognosis since they commonly have physical or functional spinal cord or cauda equina transection. • Only 25% or less of cats with flaccid tail, perineal analgesia and LMN urinary and fecal incontinence from a sacrocaudal injury will regain neurologic function. • 75% of cats with only tail flaccidity can regain tail function. Prognosis should NEVER be determined based on the degree of radiographic displacement of the involved vertebra(e). The only preventative measure is for cats to avoid situations where trauma is a distinct possibility. • Chronic, progressive UMN or LMN tetraparesis or paraparesis dependent on tumor location. • Focal areas of spinal pain. Although most meningiomas are found intracranially, they may also develop along the spinal cord with an intradural, extramedullary predilection site. Meningiomas arise from any cell of the meningesblood vessels, fibroblasts or arachnoid cells. Meningiomas produce signs by compressing the adjacent spinal cord causing vasogenic edema Occasionally, other tumors such as an astrocytoma occur. Most cats are > 9 years of age. The nature of the ataxia and paresis (UMN versus LMN signs) depends on the tumor's location. A focal area of spinal pain or more diffuse spinal discomfort may occur weeks prior to the development of neurological dysfunction. Signs are slowly progressive. Non-contrast spinal radiographs may reveal thinning or deformation of the vertebral lamina secondary to pressure necrosis from the expanding tumor. Lumbar CSF most commonly reveals increased protein (> 0.25 g/L [25 mg/dl]) without an accompanying pleocytosis. Tumor cells are rarely seen. Any cause of chronic, progressive myelopathy should be considered. The focal nature of the myelopathy with meningioma eliminates most infectious and inflammatory myelopathies, with the exception of FeLV-associated spinal lymphosarcoma. Ischemia and trauma produce an acute myelopathy and can usually be eliminated. Age of disease onset for meningiomas would eliminate congenital and inherited myelopathies. Differentiation from nerve root tumors often requires histopathology following surgical removal. Surgical removal of the tumor is the only definitive treatment. Post-operative radiation therapy is recommended. Corticosteroids only transiently improve neurological function. The long-term prognosis is guarded to fair if surgical removal of the tumor appears complete. Follow-up radiation probably further improves this prognosis. Without surgery, the long-term prognosis is poor. There is no known prevention of spinal meningiomas in cats. • Acute LMN paraplegia. • Severe pain associated with the pelvic limb musculature. • Vocalization and anxiety. • Weak or absent femoral pulses. • Cyanotic and cold nail beds and foot pads. Aortic thromboembolism results from a thrombus that is dislodged from within the left heart or aorta, leading to obstruction of the aortic trifurcation and severe ischemia to pelvic limb muscles and nerves. In cats it is most commonly associated with hypertrophic, dilated and restrictive cardiomyopathy, with thrombus formation in the left atrium. It also occurs with thyrotoxic cardiac disease. Thrombus formation requires either damage to the endocardium as occurs in cardiomyopathy, especially the dilated left atrium; blood stasis which also occurs in the dilated left atrium; or altered blood coagulability. Disseminated intravascular coagulation (DIC) was found in 75% of cats with cardiomyopathy and was associated with consumptive or liver-mediated coagulopathy or thromboembolism. Embolism occurs when the thrombus lodges in a blood vessel. The thrombus most often lodges in the distal aorta at the trifurcation, leading to a saddle thrombus and occlusion of blood supply to the hindlimbs. Ischemic neuromyopathy occurs and is most severe distal to the stifle. Signs are usually asymmetrical. Occasionally the right brachial artery is occluded, resulting in lameness or paresis of the right forelimb. Occasionally cats with thromboembolic disease do not have underlying heart disease. Thrombosis may also occur with infectious or neoplastic disease. There is no breed or age predilection (average 9 years, range 2-16 years) although males are twice as likely to be affected. Aortic thromboembolism usually produces an acute onset of LMN paraplegia and severe pain. The hindlimbs drag behind the cat, as the hocks cannot be flexed. Hip extension and flexion is present. Less severe ischemia leads to mild to moderate paraparesis or pelvic limb lameness. The gastrocnemius muscles usually are firm, but soften 1-3 days after embolization. Femoral pulses are weak or absent and the nail beds and footpads are cyanotic and cold. The distal limbs are often swollen. Extraneural signs include vocalization, tachypnea/ dyspnea, a cardiac murmur and arrhythmias. Heart failure is present in about 50% of cats with aortic thromboembolism. Dehydration and hypothermia are often present. Tail movement, perineal reflexes and urinary function remain intact. Increases in serum creatine kinase (often 1000-10 000 IU/L [normal: 60-300 IU/L]) occur secondary to severe muscle damage. Creatinine and BUN are increased in more than 50% of cats and may be prerenal or renal. In some cats, concurrent embolization of the renal artery occurs. Thoracic radiography reveals cardiomegaly (85-90% of cats) and pulmonary edema and/or pleural effusion (66%). Electrocardiography most commonly reveals sinus tachycardia. Atrial fibrillation, and supra-/ventricular arrhythmias can also be seen. Doppler (color flow) will often demonstrate the decrease in blood flow through the site of thromboembolism. MRI angiography will reveal a complete or partial blood flow obstruction at the aortic trifurcation. A major feature that differentiates aortic thromboembolism from traumatic, infectious, neoplastic and ischemic myelopathies is the presence of paraparesis to paraplegia without involvement of the perineum, tail and bladder. Cold, cyanotic pelvic limbs without femoral pulses and firm gastrocnemius muscles also are unique. With current treatment modalities, the results of pallative therapy are as good as aggressive thrombolytic therapies or physical removal of the thrombus, and considerably less expensive. • Physical removal is via surgery or balloon embolectomy. • Thrombolytic agents include tissue plasminogen activator, urokinase and streptokinase. -Current information should be consulted on administration and monitoring of thrombolytic and intensive anti-thrombotic therapies if they are to be used. • Reperfusion effects are a major problem with aggressive thrombolytic therapies and physical removal. Rapid onset of severe hyperkalemia associated with reperfusion is common and often fatal. Renal hemorrhage may also occur during thrombolysis, adversely affecting survival. Clinical hemorrhage may require a blood transfusion to control. Pallative therapy consists of relieving pain, heparin to help prevent another clot forming in the left atrium, fluid, electrolyte and nutritional support, warmth, physiotherapy (passive massage and flexing/extending legs) and treatment of underlying heart disease. Potassium concentrations should be monitored carefully. Injectable analgesics and a fentenyl patch should be used to provide adequate levels of pain relief. Excessive licking or chewing of the affected limb may occur resulting in self-mutilation. Loose bandaging of the limb or an Elizabethan collar are usually effective. Dehydration and electrolyte imbalances, especially hyper-and hypokalaemia, need correcting. Nutritional needs should be met in anorexic cats by the placement of a nasoesophageal tube for feeding. Acutely, heparin (400 U/kg subcutaneously followed by 200 U/kg subcutaneously three times daily) can be given to prevent further activation of the coagulation cascade, although it will not have any effect on the formed thrombus. Continue palliative therapy for 5-6 days and look for rewarming of the toes and returning pulses as an initial sign of improvement. Doppler is useful for detecting blood flow. If there is no sign of reperfusion after 6 days, the prognosis is hopeless and the cat should be euthanized. Various other treatments have been advocated but there are no studies showing increased survival. These include aspirin, periactin, acepromazine and vasodilator agents. Aspirin may be beneficial during and after an episode of thromboembolism due to its antiplatelet effects and decreased production of the vasoconstrictor thromboxane A 2 , as well as analgesic effects. The dosage is 1/4 × 325 mg adult aspirin (81 mg) every second to third day. Blockade of prostacyclin production by the endothelium with aspirin is of concern, and some advocate lower doses of aspirin more frequently (1-5 mg/cat q 24 h). Prostacyclin inhibits platelet aggregation and vasoconstriction. Acepromazine (0.1-0.5 mg subcutaneously three times daily) can be used for sedation and vasodilation. Vasodilation with alpha-blockers is advocated by some but unproven. Long-term warfarin therapy may decrease the frequency of rethrombosis, but needs careful monitoring using the International Normalization Ratio (INR) for PT to achieve a INR between 2 and 3. Doses of 0.06-0.20 mg/kg PO q 24 h have been advocated. A lower dose of 0.5 mg/cat PO q 48 h has also been used. Only 30-50% of cats survive the initial episodes and go home. Most will re-embolize -long-term prognosis is poor (average survival is 6-11 months with therapy) with less than 50% surviving 1 year. • 50% of cats have rethrombosis even when treated with warfarin. Most cats that survive an initial episode will show varying degrees of neurological recovery to their pelvic limbs, although this often takes weeks to months. Rarely does the neuromuscular function fully recover. Hypothermia and azotemia prior to therapy and hyperkalemia during thrombolysis are negatively associated with survival. Echocardiographic evidence of another thrombus in the left atrium also decreases the long-term prognosis. Little can be done to prevent aortic thromboembolism if the underlying cardiac disease has not been previously recognized. If cardiac disease is diagnosed, the risk of thromboembolism may be reduced by appropriate treatment of the cardiomyopathy (see Chapter 6). Efficacy of longterm aspirin (low dose 1-5 mg/cat q 24 h or a regular dose 81 mg/cat, q 48-72 h PO) or warfarin therapy in preventing thromboembolism has not been demonstrated, and most cats rethrombose. • Stiff staggering gait. • Inability to jump. • Chronic pelvic limb ataxia and paraparesis. • Inability to retract their claws. • Thoracolumbar hyperesthesia. • Thoracic limb paresis and ataxia. • Decreased mentation and seizures. • Fever (in 50% of cases). Feline polioencephalomyelitis is a chronic, progressive disease affecting the spinal cord and brain of cats. The cause is unknown, although neuropathology is suggestive of a neurotrophic virus. Recently, specific antibodies to the Borna disease virus have been found in 44% of cats with feline polioencephalomyelitis in Sweden. Feline polioencephalomyelitis is a sporadic worldwide disease. Affected cats range from 4 months to 12 years of age. Both male and female cats are affected. All domestic cat breeds as well as large non-domesticated cat species can contract the disease. Neurologic signs usually develop over 2-3 months with a subacute to chronic progressive course. The most striking neurologic signs include a stiff staggering gait, inability to jump, pelvic limb ataxia and paraparesis. • Some cats have decreased spinal reflexes and some are unable to retract their claws. Other signs may include thoracic limb ataxia and paresis, hyperesthesia over the thoracolumbar and lumbosacral regions, decreased mentation, behavior change, decreased pupillary light reflexes, hypersensitivity to external stimuli, impaired vision, seizures, increased salivation, intention tremors and pruritis. With disease progression, paraplegia eventually occurs. A fever is present in approximately 50% of cats. Serologic testing for FIV and FeLV antibodies is negative. Definitive diagnosis can only be made on necropsy. Histopathology reveals a disseminated meningoencephalomyelitis with lymphocytic perivascular cuffs that is most severe in the spinal cord (gray matter) and brainstem. Infectious diseases (FIP and toxoplasmosis) also may produce signs of progressive spinal cord dysfunction, making differentiation based on neurological signs difficult. Uveitis, chorioretinitis and optic neuritis are often present with CNS infections, but not with polioencephalomyelitis. Cats with spinal CNS lymphosarcoma commonly are FeLV positive and may have other systemic signs of tumor involvement. CSF analysis may help differentiate between the infectious diseases, lymphosarcoma and feline polioencephalomyelitis (see sections on lymphosarcoma and FIP), although the range of values overlap between the diseases. Immunosuppressive steroid therapy (prednisone 1-2 mg/kg BID) is the recommended treatment against this disease, although data are lacking. This may be combined with other immunosuppressive agents such as cytosine arabinoside. Aggressive and persistent therapy may result in remission and possible cure after several months. Prognosis is guarded. The disease tends to be progressive if untreated. Since this disease is of unknown etiology and very sporadic, there are no recommendations for prevention. • UMN or LMN paraparesis or tetraparesis dependent on the anomaly and its location. • Scoliosis (lateral curvature of the spine), lordosis (downward arching spine), or kyphosis (upward arching spine) resulting from a hemivertebra. • Cervical pain and UMN tetraparesis to paralysis (atlantoaxial subluxation). • LMN paraparesis to paraplegia (spina bifida and sacrococcygeal dysgenesis). • LMN urinary and fecal incontinence (spina bifida and sacrococcygeal dysgenesis). Spinal cord and vertebral anomalies are classified into abnormalities originating in the tissues of mesodermal origin (vertebral body and intervertebral disc) and those arising from tissues of ectodermal origin (spinal cord and meninges). • Block vertebrae. -Caused by improper segmentation of somites, resulting in stable vertebral fusion. • Butterfly vertebrae. -Abnormal persistence of the notochord (the embryological precursor of intervertebral discs), producing a midline cranial to caudal cleft in the vertebral body (when viewing the vertebra from the dorsoventral direction). • Hemivertebrae. -Produced by fusion of one lateral somite to one on the contralateral side that is not directly opposed or by a lack of vascularization, leading to a failure of ossification in part of the vertebral body. This produces a wedge-shaped vertebra, and scoliosis, lordosis or kyphosis. • Transitional vertebrae. -Sacralization of the last lumbar vertebra is the most common in cats. In this condition, the last lumbar vertebra has characteristics of both lumbar vertebrae and the sacrum. Clinical signs are dependent on the type of congenital malformation and its location. Block vertebrae are usually stable. • Occasionally they can be stenotic or angulated, causing extradural spinal cord compression. • Disc extrusion can occur at disc spaces immediately cranial and caudal to the block vertebrae. Butterfly vertebrae are generally incidental findings. Hemivertebrae commonly lead to scoliosis, lordosis or kyphosis. • Signs are due to spinal cord compression or repeated trauma associated with vertebral instability. Instability produces osseous changes that secondarily compress the spinal cord. • Signs may be acute, chronic, progressive or intermittent, but are usually first noted within the first 1-2 years of life. • Conformation may be visibly or palpably abnormal. Breed association (Manx cat). Signs are most commonly observed in immature animals (< 6 months of age). The cat's conformation may be visibly or palpably abnormal (scoliosis, skin dimple, etc.). • Block vertebra -joining of two adjacent vertebral bodies. • Butterfly vertebra -sagittal vertebral body cleft. • Hemivertebra -abnormal vertebral wedging and shortening. • Atlantoaxial subluxation -abnormally shaped or absent dens. • Spina bifida -vertebral arch defect. MRI scan or CT myelography reveals soft tissue abnormalities associated with a spinal cord that is tethered (fixed) by either meningocutaneous attachments (spina bifida) or by a failure of the terminal cord-like attachment from the spinal cord to the dura to stretch with growth. They will also reveal cord compression. Major differentials for hemivertebra include traumatic or pathologic fracture with secondary collapse of the vertebral body. • Hemivertebrae, however, have smooth end plates and well-formed adjacent disc spaces. • Difficulty in differentiation arises when vertebral osteophytes are present. Differential diagnoses for block vertebrae include vertebral fusion secondary to discospondylitis, vertebral fracture/luxation, collapsed disc space secondary to disc extrusion, or previous disc surgery. However, all have associated reactive bone, which is not present with block vertebrae. Atlanto-axial subluxation and spina bifida have few rule-outs, except trauma. Spinal cord compression from a hemivertebra can be treated via surgical decompression and stabilization (if necessary). Treatment for atlantoaxial subluxation involves stabilization of the atlantoaxial joint via ventral crosspinning or screws (preferred) or dorsal wiring. Specific treatment for spina bifida and sacrococcygeal dysgenesis is rarely attempted. • If signs are associated with spinal cord tethering or there is a meningocutaneous fistula without primary spinal cord anomalies, reconstructive surgery may be possible. Prognosis depends on the type of congenital anomaly and the degree of dysfunction. Cats with mild signs due to a surgically treatable hemivertebra or block vertebra, have a guarded to good prognosis for improvement. Morbidity and mortality is high with surgical stabilization of atlantoaxial subluxation. • With successful stabilization, however, cats with initially mild to moderate neurological dysfunction have a fair to good prognosis. Prognosis for cats with spina bifida or sacrococcygeal dysgenesis with anomalies associated with the spinal cord or cauda equina, is grave. These cats should be euthanized if the neurological dysfunction is incompatible with a good quality of life. Cats with spinal cord tethering (spina bifida) have a potentially fair to good prognosis with surgery. Prevention of further congenital malformations is best achieved by a spay/neuter program. • Cervical and thoracic limb hyperesthesia and rigidity. • Thoracic limb lameness. • Chronic progressive ataxia. • Reluctance to move. • Chronic tetraparesis to paralysis. Hypervitaminosis A is a skeletal disease, secondary to excessive intake of vitamin A (liver or vitamin A supplementation (cod liver oil) (> 1000 IU/ml). Affected cats are usually 2-9 years of age. Signs include cervical and thoracic limb hyperesthesia and rigidity due to extensive confluent exostosis in the cervical and thoracic spine, thoracic limb lameness, ataxia, reluctance to move, and tetraparesis to paralysis. Other signs include lethargy, anorexia, constipation, weight loss and an unkempt haircoat due to an inability to groom. Exostoses develop insidiously with the above signs occurring only after the disease is advanced. Non-contrast spinal radiographs show new bone formation involving the cervical vertebrae. • The sternum, costal cartilages, and long bone metaphyses also show new bone formation. • Joints may show arthrodesis. Analgesics may symptomatically treat the clinical signs. • Aspirin -10 mg/kg PO q 48 h. • Narcotic analgesics such as morphine (4 mg/ml) -0.5 mg/kg PO three times to four times daily. • Non-steroidal anti-inflammatory drugs. • Fentanyl patch. • Acute, non-progressive, non-painful, asymmetrical LMN paraparesis to paraplegia. • LMN urinary and fecal incontinence. Spinal cord infarction secondary to fibrocartilaginous embolism is uncommon. The embolus is histochemically identical to the fibrocartilage of the nucleus pulposus. It is unknown how the embolus reaches the spinal vasculature from its origin. Embolization of arteries, veins or a combination of the two may occur. Sudden increases in intra-abdominal pressure (hard exercise) may facilitate retrograde passage of disc material through the venous sinuses and spinal veins. Embolism results in segmental hemorrhagic necrosis and malacia of the spinal cord. Clinical signs reflect the location of the lesion along the spinal cord. In cats, the lumbosacral intumescence is the most common site of myelopathy, resulting in an acute LMN paraparesis to paraplegia, and LMN urinary and fecal incontinence. Other findings include a lack of spinal pain, lack of disease progression and marked asymmetry of neurological dysfunction. Diagnosis is based on exclusion of other etiologies. History and neurological exam are important. Survey radiographs are normal. CSF analysis is variable, ranging from normal, hemorrhagic, or showing a mild mixed pleocytosis (6-25 cells/mm 3 [6-25 cells/μl]). Myelography will either be normal or occasionally show cord edema. MRI diffusion studies may reveal the ischemic area of spinal cord, if the affected area is large enough. Definitive diagnosis can only be made at necropsy. Differential diagnosis includes any cause of acute paraparesis to paraplegia. The unique clinical signs and usual absence of abnormalities on work-up separate fibrocartilaginous embolism from other acute myelopathies. Immediate treatment consists of methylprednisolone sodium succinate (see spinal trauma). Embolic myelopathy is non-surgical. Long-term corticosteroid therapy is not recommended. Prognosis depends on density of neurological dysfunction and degree of irreversible cord damage. Cats with severe LMN paraplegia, absent pain sensation and LMN urinary incontinence associated with involvement of the lumbosacral intumescence have a poor to hopeless prognosis. Cats with less severe signs have a guarded to favorable prognosis for partial to full recovery. There are no preventive measures that can be undertaken. A review of the clinical diagnosis of feline infectious peritonitis viral meningoencephalomyelitis JR (ed) Consultations in Feline Internal Medicine 1 ed) Textbook of Veterinary Internal Medicine Congenital abnormalities of the spinal cord and vertebrae, Chapter 52 JR (ed) Consultations in Feline Internal Medicine 1 Feline non-suppurative meningoencephalomyelitis. A clinical and pathological study Inflammatory disorders of the central nervous system Encephalitis and meningitis. In: Bagley R (ed) Veterinary Clinics of North America Small Animal Practice -Intracranial Disease Feline Thrombotic Disease Veterinary Information Network Vascular disorders, Chapter 52 Based on the clinical and neurological examinations, other differentials include infectious meningitis and myelitis, vertebral neoplasia, mucopolysaccharidosis and discospondylitis (rare).Non-contrast spinal radiographs eliminate all differentials with the possible exception of mucopolysaccharidosis VI, a rare autosomal recessive storage disease produced by deficiency of the lysosomal enzyme, arylsulfatase B. • Mucopolysaccharidosis VI occurs in 4-7-monthold Siamese cats, producing spinal cord compression secondary to fusion of the cervical and thoracolumbar vertebrae with bony proliferation. • These cats also have a flat, broad face, widely spaced eyes, corneal clouding and enlarged feet. Remove excess vitamin A from the diet to prevent further development of exostoses.Use a balanced commercial cat diet.Skeletal improvement is monitored by radiography and neurological examinations.