Evaluation of the feline neurologic patient can be challenging and mystifying. The feline species is difficult to evaluate in the clinic environment and the neurologic diseases they acquire are much different on presentation than those seen in the canine.
Causes of feline neurologic diseases can be degenerative, anomalous, metabolic, nutritional, neoplastic, inflammatory, infectious, immune-mediated, toxic or traumatic.
The feline neurologic examination includes an evaluation of mentation (assessment of content and level of consciousness), cranial nerve function, gait, proprioception, motor and sensory modalities. The first thing that must be established in the feline is whether or not the patient has disease of the nervous system and if so, where in the nervous system it is: brain, spinal cord, or neuromuscular? This lecture will concentrate on some neurologic diseases specific to the feline species. The first will be diseases that affect the neuromuscular system.
Components of the neuromuscular system include: the nerve root, the peripheral nerve, the neuromuscular junction and the muscle. Disease that affected the neuromuscular system in the feline include: myasthenia gravis, diabetic neuropathy, hyperthyroidism and ischemic myoneuropathy. Myasthenia gravis (MG) is a junctionopathy in which the normal neurotransmitter, acetylcholine (ACh), is blocked from being received at the post-synaptic membrane by an accumulation of antibodies at the post-synaptic ACh receptor on the muscle. In the feline, the acquired form of MG is seen most commonly and has a breed predilection for the abyssinian. There is also an association with acquired MG and thymoma in the feline. The cardinal feature of MG in the feline is profound weakness with normal proprioception. This weakness is usually exacerbated with activity. Pelvic limbs may be affected greater than forelimbs. Animals may exhibit generalized tremor, diminished palpebral and menace deficits, but have normal reflexes and muscle tone. Other clinical signs of feline MG include: a voice change, megaesophagus, regurgitation, ventral neck flexion, and in severe cases, respiratory distress.
Diagnosis of acquired MG includes a thorough assessment of the clinical presentation, signs, physical and neurologic exams and response to anticholinerase drugs such as edrophorium chloride (Tensilon®) at a dose of 0.2-1 mg IV. Improvement should occur within 1 minute of drug administration and last 10-15 minutes. A more accurate diagnostic tool is a positive result on a serum ACh antibody titer. Normal is < 0.3 nmol/L, some affected casts have titers >8.0. Treatment of feline MG entails use of long-acting ACh esterase inhibitors such as pyridostigmine bromide (Mestinon®) which is best used in liquid form at a dose of 0.25-1 ml PO BID and may need to be titrated according to response. Other treatment s include upright feedings, immunosuppressive drugs such as prednisone or Azothiaprine (Imuran®) and surgical removal of thymoma.
The most common neuropathy noted in the feline is diabetic neuropathy (secondary to diabetes mellitus). Clinical signs occur most commonly in the middle to older aged feline and present as lower motor neuron signs (plantigrade stance) in the hind limbs. Patellar reflexes may be diminished, although flexor reflexes and pain sensation are usually intact. The etiology and pathogenesis of diabetic neuropathy involves primary and secondary axonal degeneration due to slowing of axon transport secondary to hyperglycemia, alteration of macromolecular transport, interference with axon maintenance and repair by the neuronal cell body, and neural hypoxia. Progression to this state may occur over several months. Diagnosis and treatment is through the establishment of underlying disease (diabetes mellitus) and characteristic neurologic exam findings, and in most cases will resolve in 6 to 12 months if the DM is treated appropriately.
Ischemic myoneuropathy occurs a secondary to effects from aberrations in blood flow due to hypertrophic cardiomyopathy in the feline. Thrombus formation occurs most commonly in the caudal aorta or external iliac vessels and vasoactive substances such as serotonin and thromboxane A2 are released that further exacerbate signs. Within 30 minutes, the resultant ischemia can lead to muscle and nerve hypoxia and significant neural dysfunction, caused by demyelination, necrosis and finally, Wallerian degeneration. The sciatic nerves, cranial tibial, and gastrocnemius muscles are most commonly affected. Clinical signs include acute paraparesis, firm, painful gastrocnemius and/or cranial tibial muscles, weak or absent femoral pulses, and cyanotic nail beds. Treatment involves correcting the underlying cause, although recurrence is common.
Hyperthyroidism can cause neuromuscular signs in the cat, particularly involving the muscle, which can result in generalized weakness muscle atrophy, ventral neck flexion, fatigue, muscle tremors, and gait disturbances. CNS signs (forebrain) can include restlessness, irritability, aimless wandering, circling, abnormal sleep/wake patterns and seizures as a result of some instances of hypertensive encephalopathy. The pathophysiologic basis of the neuromuscular signs involves the effect of high circulating T4 levels on muscle oxidative metabolism. The forebrain CNS signs can be attributed to increased cerebral blood flow, cerebral O2 and glucose consumption since T4 and T3 levels are closely regulated in the brain. Diagnosis and treatment of hyperthyroidism has been described; neurological signs may be aided with treatment. Other polymyopathies of the feline include hypokalemic polymyopathy and immune-mediated polymyositis. Clinical signs of each can include ventral neck flexion, generalized weakness, a short choppy gait and, at times, muscle pain (polymyositis). Diagnosis of each involves establishing the underlying cause (whole body depletion of potassium vs an immune-mediated cause); serum CPK can aid in diagnosis. Treatment involves potassium supplementation (either IV or oral) in cases of hypokalemic polymyopathy, and corticosteroids in cases of confirmed immuno-mediated polymyositis. Each has a fair to guarded prognosis.
Feline vestibular disease can be divided into peripheral and central categories. Peripheral decrease involves CNN VIII and its receptor. Clinical signs can include normal mentation, a head tilt towards the side of the lesion, CNN VIII +/- VII neuropathy, vestibular ataxia and horizontal or rotary nystagmus that does not change with a position change. These cats should have normal proprioception and strength. Causes of feline peripheral vestibular disease can include idiopathic vestibular syndrome, otitis media/interna, nasopharyngeal polyp, trauma or ototoxicity. Central vestibular disease affects those structures found within the brain stem (vestibular nuclei, CNN III, IV, and VI nuclei, medial longitudinal fasiculus) or cerebellulum (flocculonodular lobe). Signs are similar to peripheral vestibular disease except that ipsilateral weakness, proprioceptive loss and/or complete CNN deficits may be observed, as well as a changing nystagmus along with an altered level of consciousness. Causes include inflammatory/infectious diseases such as FIP, toxoplasmosis or cryptococcosis, neoplasia (lymphoma), thromboembolism, or trauma. Diagnosis of vestibular disease includes a thorough owner history physical and neurologic exams, blood work, radiographs (bulla films), otic examination under anesthesia, CSF analysis and if warranted, CT scan or MRI. Treatment is dependent upon the cause and it is important to remember that patience is a virtue. Not all felines with neurologic signs have a poor prognosis and owners must be given all options.