62107289 Advances in Feline Neurology (1)

8/3/2019 62107289 Advances in Feline Neurology (1)

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88

Advances in Feline Neurology

Philip A. March, DVM, MSDiplomate ACVIM (Neurology)

Assistant Professor

Department of Veterinary Clinical Sciences

College of Veterinary MedicineThe Ohio State University

Columbus, Ohio 43210

KEY WORDS neurologic examination

meningoencephalomyelitis

myasthenia gravis

epilepsy

meningioma

Neurologic disorders in the cat are a diagnostic and

therapeutic challenge. The inherent difficulties in per-

forming a thorough neurologic examination in cats

and the atypical signs sometimes exhibited by cats

make neurolocalization of lesions difficult. Cats also

are not susceptible to the same types of diseases as

dogs. Specifically, idiopathic inflammatory disorders,

such as granulomatous meningoencephalomyelitis

(GME), idiopathic meningitis disorders, polyradicu-

loneuritis, and polymyositis, are rare in the cat. Infec-

tious, neoplastic, and vascular diseases are common in

cats and can affect the nervous system focally or multi-

focally. Because underlying diseases are common, itis advisable to approach both the diagnosis and treat-

ment of feline neurologic disorders aggressively. This

paper addresses some important differences in the di-

agnosis and treatment of neurologic problems in the

cat compared to the dog. Selected disorders that pref-

erentially affect different areas of the nervous system

are discussed from the standpoint of their usual pre-

sentation, tests now being used for definitive diagno-

sis, and therapeutic modalities currently available for

each condition.

DIAGNOSTIC AIDSThe Neurologic Examination

Stress and the sympathetic overdrive that many cats

experience during the neurologic examination mask

certain deficits, create new ones, and generally

complicate the practitioners ability to neurolocalize

the lesion. It is rare to be able to perform a thorough

examination on cats unless the patient is extremely

cooperative or is dull or obtunded because of the un-

derlying disease. Certain reflex and response tests in

cats are more reliable and not as subject to environ-

mental stress. Even these tests may be difficult to per-

form in an excited, apprehensive cat unless the exam-

iner maintains some patience and minimizes restraint

during the examination.

Certain neurologic examination tests in alert,

nonobtunded cats are frequently unreliable. These in-clude the knuckling tests for conscious proprioception

and myotactic limb reflexes. Hopping, hemihopping,

and tactile placing are more reliable tests of postural

control in cats. The flexor withdrawal reflex is the

most reliable limb reflex in cats, and close attention to

the strength of the withdrawal and the participation of

all muscle groups in this reflex can be very helpful in

determining whether a peripheral or a lower motor

neuron (LMN) disorder is present. Observing for a

crossed extensor (abnormal extension of the opposite

limb) during the flexor reflex is important as well.

Presence of a crossed extensor is indicative of an up-per motor neuron (UMN) lesion (brain or spinal cord).

Gait analysis is also difficult in cats that refuse to

move because of either fright or imbalance. Placing

the cat in an empty, quiet room or observing ambula-

tion in a cage may be helpful techniques. Wheelbarrow-

ing, hopping, placing tests, and gently coaxing the pa-

tient to jump from an elevated surface to the floor are

used to assess strength and coordination. Because

some cats do not menace because of fear and in-

creased sympathetic tone, dropping cotton balls or us-

ing the visual placing test may be a better test of vi-

sion. The dolls eye reflex in cats is best accomplished

by holding the cat in the examiners hands and rotat-

ing the cat around the examiner.

In the final analysis, there is no substitute for a de-

tailed description of neurologic signs that were evi-

dent to the owner in the home environment. Questions

concerning abnormal behavior, seizurelike activity,

sleep-wake cycles, circling tendencies, stumbling,

falling, incoordination, reluctance to jump, bumping

into objects, etc., should be asked. The speed of onset

and progression of clinical signs are likewise critical

pieces of information. A videotape of episodic eventscan provide extremely valuable information.

Approach to Diagnostic TestingAs discussed in the previous section, an aggressive

diagnostic approach to a cat with neurologic signs is

often warranted. Infectious, neoplastic, and vascular

disorders can affect multiple body systems, so a com-

plete blood count, chemistry profile, urinalysis, feline

immunodeficiency virus (FIV) and feline leukemia

virus (FeLV) testing, and thoracic radiographs are rec-

ommended if neurologic signs are present. Hepatic


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alanine aminotransferase (ALT) elevations may be

found in cats with feline infectious peritonitis (FIP

dry form), toxoplasmosis, and hyperthyroidism, all

diseases with potential nervous system involvement.

Central nervous system (CNS) lymphosarcoma is

strongly associated with nonregenerative anemia and

positive FeLV status.1 In older cats, a T4 level andblood pressure measurements are indicated, especially

if forebrain signs are present.

A complete ophthalmic examination is recommend-

ed in feline patients with nervous system disease.

Cryptococcosis, toxoplasmosis, and FIP are common

causes of anterior and posterior uveitis. Systemic

hypertension may lead to spontaneous hemorrhage in

both the retina and the CNS. Papilledema may be ob-

served in cats with brain tumors and elevated intra-

cranial pressure. Horners syndrome is relatively more

common in cats than in dogs and pharmacologic test-

ing may be indicated to determine whether the lesionis postganglionic (common cause is a middle/inner ear

disease) or preganglionic (common cause is a cranial

mediastinal mass).

Serology is a critical component of the diagnostic

workup. This is especially important in cats with any

outdoor history or exposure to multiple cats in a

household (catteries, etc.). There are, however, report-

ed cases of cryptococcosis in strictly indoor cats with

no exposure to other cats. The latex agglutination

antigen test is the current test of choice for diagnosis

of Cryptococcus neoformans.24 Paired serum titers

(23 weeks apart) are strongly recommended for diag-

nosis of toxoplasmosis. Coronavirus titers are recom-

mended by this author if signs of FIP are present.

False-negative and false-positive results are possi-

ble,57 but a very high titer in conjunction with typical

clinical signs (fever, uveitis, central vestibular

signs/seizures) is highly suggestive of infection.

Cerebrospinal fluid (CSF) cytology and titers are in-

dicated in certain circumstances. Multifocal signs or

focal signs present in conjunction with a high suspi-

cion of infectious diseases are indications for CSF

analysis. CSF cytology should be performed within 1hour of collection by a laboratory that has cell count-

ing abilities and a cytocentrifuge. Local human hospi-

tal laboratories may be willing to perform this service

and have been very approachable in this authors ex-

perience. The usual delay in processing that occurs

with most veterinary courier services results in cell ly-

sis and a nondiagnostic sample. Colorado State Uni-

versity Veterinary Diagnostic Laboratory performs a

variety of antigen and antibody tests on CSF (includ-

ing tests for cryptococcosis and toxoplasmosis). If

serum is also submitted in conjunction with CSF, this

laboratory will also determine whether intrathecal

antibody is present (a definitive test for CNS infec-

tion). In some cases, serum titers may not reflect what

is occurring in the CNS. Furthermore, cases of CNS

cryptococcosis with negative serum titers have been

reported.8

Imaging is usually indicated if a focal lesion is sus-pected. Examples include focal lesions of the fore-

brain, brain stem, or spinal cord. Skull radiographs

may be useful in cases of craniocerebral trauma or if a

meningioma is suspected (look for areas of focal hy-

perostosis or lysis/thinning of the calvarium). Bulla

radiographs are indicated in cases of middle/inner ear

disease (otitis, neoplasia). Computed tomography

(CT) is a sensitive imaging modality for middle/inner

ear disease in the cat. Plain spinal radiographs and

myelography are sometimes useful, but high-quality

magnetic resonance imaging (MRI) of the spinal cord

is the most sensitive means of detecting intramedullarylesions in cats. MRI is also the diagnostic test of

choice for imaging of intracranial neoplastic masses

in cats. Because of the expense of MRI, it is usually

performed if owners are interested in surgery and/or

radiation therapy for their pet.

Electrodiagnostic testing is used most frequently in

cases of motor unit (peripheral nervous system) dis-

ease. Electromyography (EMG), nerve conduction

tests, and repetitive nerve stimulation are commonly

used in the cat to help localize a lesion to nerve, mus-

cle, or neuromuscular junction. Muscle and/or nerve

biopsies are indicated if EMG and nerve conduction

tests are abnormal.

SELECTED DISORDERSDiseases of the Forebrain

Lesions of the forebrain in cats typically cause signs

of behavior change, seizures, circling or body turn to-

ward the side of the lesion, contralateral visual

deficits, and contralateral postural deficits (slow hop-

ping reactions). Any or all these signs may be present.

Head trauma, infectious agents (FIP, toxoplasmosis,

cryptococcosis), feline ischemic encephalopathy (FIE)and other vascular disorders, and neoplastic diseases

may cause forebrain signs in cats.

FIE refers to a condition of unilateral cerebro-

cortical infarction due to vasospasm and/or occlusion

of the middle cerebral artery. Typical signs of FIE in-

clude a peracute onset of circling, behavior change,

visual deficits, and seizures. In some cases, seizures

may be the only sign observed.9,10 Recently, FIE has

been associated with aberrant migration ofCuterebra

spp. larvae in the cat brain.10 This finding may relate

to the high incidence of FIE in the late summer and

ADVANCES IN FELINE NEUROLOGY 89


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90 PROCEEDINGS OF THE 23rd WALTHAM/OSU SYMPOSIUM

early fall, times of the year when Cuterebra spp. are

most prevalent in the environment.

The most common cause of forebrain signs in older

cats is neoplasia. Among primary brain tumors, feline

meningiomas are by far the most common tumors

found and are also a frequent cause of seizures in this

age group. The signs, diagnosis, and treatment of fe-line meningiomas are discussed next.

MeningiomasFeline meningiomas may arise from meninges (the

arachnoid layer) covering the cerebral cortex, brain

stem, falx and tentorium, or tela choroidea of the third

ventricle. The most common site of involvement is

the external surface of the cerebral cortex.11,12 As the

tumor grows and expands, adjacent brain tissue is

slowly compressed but rarely invaded directly by neo-

plastic cells. The brain has an enormous capacity to

compensate for slowly compressive lesions, which iswhy signs may be so insidious in onset. In many cases,

the signs reported by owners are subtle and include

mild lethargy, decreased appetite, decreased respon-

siveness, and pacing. Seizures (partial or generalized)

may be the only sign observed. A thorough neurologic

examination may uncover contralateral postural and

visual field deficits. It is not uncommon for large,

space-occupying meningiomas to cause positional

nystagmus. This is probably due to elevated intra-

cranial pressure and early forebrain herniation with

brain stem compression.11,12 MRI is the diagnostic test

of choice to image the tumor and also can be used to

plan an eventual surgical approach.

Signs are initially prednisone responsive for many

weeks, until the tumor reaches a critical volume. If

signs of early herniation are present, mannitol therapy

(1 g/kg IV over 20 minutes) may be required to stabi-

lize the patient. The treatment of choice is surgical re-

section. The tumor often shells out because it is so

well encapsulated. Recurrence may or may not occur

in months to years. In one study, 6 out of 10 cats that

underwent surgical meningioma resection lived for

longer than 2 years postsurgery.13

Antiepileptic drug(AED) therapy is often required postoperatively to

control seizures.

Idiopathic EpilepsyPrimary or inherited epilepsy, as found in many ca-

nine breeds, is not commonly recognized in cats.

Some feline patients with epilepsy are classified as

idiopathic when no obvious lesions are found

through antemortem diagnostic tests (including CSF

analysis, MRI, etc.). It is important to realize that pre-

vious insults (traumatic, inflammatory, vascular) to

the brain often leave little evidence of a lesion, even

on MRI. The insult, however, may leave an area of

hyperexcitable brain tissue (a seizure focus) that

leads to a condition of epilepsy (recurrent seizure ac-

tivity of neural origin).

Treatment of epilepsy in the cat is similar to treat-

ment of epilepsy in the dog, but there are some impor-tant differences. Phenobarbital is considered the first

drug of choice for feline epilepsy. Phenobarbital is

metabolized at a slower rate in the cat than in the dog,

and cats are generally more susceptible to the sedative

effects of the drug. The recommended starting dose is

2.5 mg/kg daily.14 This dose may need to be increased,

depending on serum concentrations actually achieved

and response to therapy. The therapeutic blood con-

centration in cats is 10 to 30 g/ml, which differs

from the 15 to 40 g/ml therapeutic range in dogs.

Steady-state phenobarbital concentrations are attained

in about 9 days.14 Concurrent administration of drugsthat are highly protein bound, such as sulfonamides

and aspirin, should be avoided. Potential side effects

of phenobarbital in the cat are excessive sedation, be-

havior change, dermatitis, and blood dyscrasias.15

Hepatotoxicity has been reported with phenobarbital

therapy in cats, but this author has not observed this

side effect.

The pharmacokinetics of potassium bromide (KBr)

has recently been examined in the cat.16 The dose re-

quired to achieve blood concentrations in the 100 to

150 mg/dl range is similar to that used in dogs (30

mg/kg daily). The half-life of KBr in cats is 10 days,

which is considerably shorter than that in dogs (2128

days). This means that steady-state drug concentra-

tions of bromide in cats are achieved in 7 to 8 weeks.

Efficacy of KBr in feline epilepsy is still not docu-

mented, although early reports claim that successful

seizure control has been achieved in some patients.

The best way to administer KBr in cats (because of

their sensitivity to liquid preparations) is as capsules

containing 50 to 100 mg of active compound per cap-

sule.15

Diazepam is an effective oral AED in cats. The rec-ommended dose is quite variable in the literature. This

author usually starts at 0.5 mg/kg every 8 to 12 hours

and increases the dose in increments if satisfactory

seizure control is not achieved. A recent report of ful-

minant hepatotoxicity in a small number of cats has

caused diazepam to fall out of favor as a first-line

AED.17 Careful monitoring of ALT after 1 week and

again after 1 month of therapy usually detects this id-

iosyncratic drug reaction.

Clorazepate has been used by the Neurology Ser-

vice at The Ohio State University Veterinary Hospital


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as a long-term AED in several epileptic cats. This

AED is especially useful for persistent partial seizures

in cats.14 The recommended dose is 3.75 to 7 mg per

cat daily. Rarely, this may need to be increased to atwice daily dosing interval. Excellent seizure control

in this small population of cats suggests that cloraze-

pate may be a very effective AED in the feline. See

Table 1 for a list of the most commonly used AEDs in

cats.

Diseases of the Brain StemThe cat brain stem is highly susceptible to a variety

of disorders. C. neoformans, FIP virus, and Toxoplas-

ma gondii commonly affect brain stem structures. The

primary sign of brain stem involvement from any

cause is a central vestibular syndrome. Head tilt,

vestibular ataxia, and nystagmus are common features

of this syndrome. Specific diagnostic and therapeutic

recommendations for cryptococcosis, toxoplasmosis,

and FIP are discussed in the next sections.

CryptococcosisC. neoformans can cause signs of nasal, ocular, and

nervous system disease in cats. A chronic mucoid

nasal discharge in conjunction with central vestibular

signs (ataxia, nystagmus) or seizures should immedi-

ately raise ones suspicions for this disease. Clinicalsigns of CNS involvement are due to the inflammato-

ry response to the organism (granulomatous meningo-

encephalomyelitis) or to a coalescence of large aggre-

gates of encapsulated organisms, resulting in a mass

lesion. Signs may be multifocal or focal. Some cats

may also exhibit weight loss, coughing, subcutaneous

granulomas around the face and nose, and lym-

phadenopathy. Serum and/or CSF antigen titers, as

previously discussed, are highly sensitive and specif-

ic.2,9,11 CSF analysis usually shows a mixed pleocytosis

and a mild to moderate elevation in protein. Occasion-

ally, organisms can be seen in CSF, especially if India

ink staining is used. Cytology of nasal exudates often

reveals the organism (512 m in diameter budding

yeasts with a thick capsule).The treatment of choice is currently fluconazole 50

mg/cat every 12 hours for a minimum of 2 to 4

months, although long-term studies of efficacy for

CNS disease have not been performed on a large pop-

ulation of cats.24 Itraconazole therapy 10 to 25 mg/kg

every 24 hours for 4 to 16 months is useful for treat-

ment of extraneural signs, but its efficacy for CNS in-

fection has not been adequately studied.3 Traditional-

ly, cats with CNS cryptococcosis have been given

poor prognoses for recovery. As newer antifungal

pharmaceutical agents become available, this outlook

may change (Table 2).

In studies of cats infected with Cryptococcus but

not showing CNS signs, serum antigen titers have

been followed over time during and after treatment. In

one study, titers generally decreased during therapy

and this tended to coincide with clinical improve-

ment.3 However, positive titers were seen in some re-

covered cats in another study.4 Although the results

of the two studies on this subject differ somewhat, it

appears that some cats retain a positive titer after

treatment and do not show clinical signs of infection.

Current recommendations for therapy are to treat 2 to3 months beyond resolution of clinical signs. If titers

become negative, two negative antigen titers 1 month

apart are recommended before therapy is discontin-

ued.3,4

ToxoplasmosisToxoplasmosis is a very interesting and still not ful-

ly understood infection of the CNS of cats. Many cats

previously infected with T. gondii have bradyzoite or-

ganisms encysted in various tissues, including brain

and muscle. In most cats, these encysted organisms


Table 1

Commonly Used Antiepileptic Drugs in Cats

Antiepileptic Drug Dose and Dose Interval Approximate Half-Life Time to Steady State Therapeutic Range

Phenobarbital 2.5 mg/kg PO every 1224 hours IV: 3643 hours 9 days 1030 g/ml

PO: 58 hours

Diazepam 0.52 mg/kg PO every 812 hours PO: 1520 hours 45 days (calculated) 0.50.7 g/ml (?)

(diazepam and metabolites)

Potassium bromide 30 mg/kg PO every 24 hours or 10 days 78 weeks Not established

divided every 12 hours

Clorazepate 3.757 mg PO per cat every 3.6 hours (?) Unknown Unknown

1224 hours (N-desmethyl-diazepam)

IV = intravenously; PO = per os.


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remain in this latent phase, may produce some chronic

antigenic stimulation, but are usually incidental.

Immunocompromising factors (steroid therapy, viral

infection [FIV or FeLV], stress, neoplasia) appear to

initiate the recrudescence of these organisms. Dur-

ing recrudescence, organisms enter a proliferative

phase and incite an inflammatory response. The in-

flammatory response can be exuberant, with forma-

tion of microscopic and macroscopic granulomas.

Typical signs of multifocal or focal CNS injury in-

clude seizures (often partial seizures), central vestibu-

lar signs, cerebellar signs, and, occasionally, cord

signs.6,9,18 As discussed previously, paired serum titers

or combination serum/CSF titers are very useful in di-

agnosing CNS toxoplasmosis. This author prefers touse CSF titers and the IgG index to estimate intrathe-

cal antibody production. This information combined

with compatible clinical signs is usually adequate to

make a tentative diagnosis of toxoplasmosis. CSF cy-

tology may show a mixed pleocytosis (usually non-

suppurative, although neutrophils may be present

also). Protein in CSF may be normal to moderately el-

evated.

The treatment of choice for toxoplasmosis is either

clindamycin or trimethoprim-sulfadiazine with

pyrimethamine (Table 2). Although clindamycin is

usually better tolerated by cats, its penetration of the

intact blood-brain and blood-CSF barriers is

marginal at best. In human studies, clindamycin did

not cross the blood-brain barrier even if meningitis

was present. Despite this finding, clindamycin is ad-

vocated for use in feline CNS toxoplasmosis at 25

mg/kg every 12 hours for 4 to 6 weeks.18 The author

has recently used clindamycin in an infected cat

(positive CSF titers) with CNS signs. Clinical signs

disappeared while the cat was treated with the drug.

When the drug was discontinued, the cats clinical

signs returned in 4 to 8 weeks. Trimethoprim-

sulfadiazine at 15 to 30 mg/kg every 12 hours for 3

to 4 weeks with or without pyrimethamine (0.51.0

mg/kg/day orally for 710 days) may also be effec-tive. This drug combination may cause signs of nau-

sea and salivation in cats and also has the potential

of producing bone marrow suppression. Folic acid

supplementation (1 mg/kg orally every 24 hours) is

recommended for cats on long-term sulfadiazine/

pyrimethamine therapy.18,19

Feline Infectious PeritonitisThe FIP virus (dry form) can cause a granulomatous

to pyogranulomatous inflammation of the meninges,

ependyma (ventricular linings) and subependymal tis-

Table 2

Antimicrobial Drugs for Central Nervous System Infections in Cats

BBB Bactericidal vs Frequency

Drug Target Pathogen(s) Penetration Bacteriostatic Dose (mg/kg) Route (hours)

Amphotericin B Cryptococcus spp./other fungi Poor Static 0.150.5 (in 5% IV 48dextrose in water)

Ampicillin Bacteria Intermediate Cidal 1020 IV 6Cefotaxime Bacteria Good Cidal 2550 IV or IM 8

Ceftriaxone Bacteria Good Cidal 20 IV 12

Cephalexin Bacteria Poor Cidal 1030 PO 8

Chloramphenicol Bacteria/ Rickettsia spp. Good Static 1525 PO 12

Clavamox Bacteria Poor Cidal 1020 PO 812

Clindamycin Toxoplasma spp. Poor Static 12.525 PO 12

Doxycycline Bacteria/ Rickettsia spp. Intermediate Static 2.55.0 PO 12

Enrofloxacin Bacteria/ Rickettsia spp. Intermediate Cidal 2.55.0 PO 12

Fluconazole Cryptococcus spp./other fungi Good Static 510 PO 12

Flucytosine Cryptococcus spp./other fungi Good Static 2550 PO 68

Gentamicin Bacteria Poor Cidal 2.04.0 IV or IM 8

Itraconazole Cryptococcus spp./other fungi Poor Static 5 PO 1224

Ketoconazole Cryptococcus spp./other fungi Poor Static 510 PO 812Metronidazole Bacteria (anaerobic) Good Cidal 25 PO 1224

Penicillin G Bacteria Intermediate Cidal 20,00040,000 IV 6units/kg

Pyrimethamine Toxoplasma spp. Good Cidal 0.51.0 PO 24

Tetracycline Bacteria/ Rickettsia spp. Poor Static 1520 PO 8

Trimethoprim- Toxoplasma spp./bacteria Good Cidal 1530 PO 12sulfadiazine

BBB = blood-brain barrier; IM = intramuscularly; IV = intravenously; PO = per os.


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sues, and choroid plexus. Central vestibular signs are

the most common neurologic signs seen with FIP

virus infection of the CNS. Feline infectious peritoni-

tis virus is also a common cause of seizures in cats

less than 1 year of age. Hyperesthesia and caudal

paresis may be seen with spinal cord involvement. A

secondary hydrocephalus (with dullness, blindness,etc.) can occur because of obstruction of the fourth

ventricle by fibrinous exudate and pyogranulomatous

tissue. A cavernous sinus syndrome with a unilater-

al fixed pupil, ophthalmoplegia, and absent ocular

sensation has recently been seen with FIP infection of

the forebrain in cats.9 FIP is primarily found in very

young cats, and clinical signs are more likely to occur

after repeated exposure to the virus. Ocular signs,

fever, weight loss, and anorexia often accompany

CNS signs. A definitive diagnosis of FIP can be made

only by finding pyogranulomatous inflammation in

multiple tissues at necropsy.57 A tentative diagnosis issupported by high coronavirus titers and a CSF tap

that shows a neutrophilic pleocytosis (some mono-

nuclear inflammation also may be seen) and a very el-

evated protein content (often greater than 200 mg/dl).

Coronavirus titers may be negative in some affected

cats.57 Recently, molecular techniques (probes gener-

ated against FIV RNA in leukocytes and probes gen-

erated by polymerase chain reaction against smaller

viral nucleotides) are showing some promise for

definitive diagnosis of virulent FIP strains. There is

no effective treatment for CNS FIP. Prednisone and

other immunosuppressive/immunomodulatory therapy

may help in the short term, but the disease is invari-

ably progressive and ultimately fatal. Some vaccines

have shown some efficacy in protection against exper-

imental FIP challenge in cats, but efficacy against nat-

ural exposure requires further study.

Peripheral Vestibular DiseaseCauses of peripheral vestibular problems in cats in-

clude idiopathic vestibular syndrome, inflammatory

polyps, otitis (mites/bacteria), and middle and inner

ear neoplasia (ceruminous gland adenocarcinoma andsquamous cell carcinoma are the most common). In-

fections or mass lesions of the middle and inner ear

may produce vestibular signs (head tilt, ataxia with or

without nystagmus), cranial nerve VII signs (facial

paralysis), and Horners syndrome.

Idiopathic feline vestibular syndrome is the most

common cause of peripheral vestibular signs in cats.

Only vestibular signs are present and these signs may

be severe (pronounced head tilt, rolling, falling, rotary

or horizontal nystagmus with fast phase away from

the side of the lesion). This disorder is usually seen in

the late summer or early fall and, like FIE, coincides

with the time of year when Cuterebra larvae are abun-

dant. Peracute signs are usually self-limiting over 3 to

7 days with no treatment. Supportive care (nutritional

support, intravenous or subcutaneous fluids, etc.) may

be necessary if anorexia, vomiting, or both accompa-

ny the vestibular signs.

Spinal Cord DiseasesSpinal cord diseases in cats are relatively uncom-

mon compared to the dog. Intervertebral disk hernia-

tion can occur in cats, but clinical disease is extremely

rare. More common causes of spinal cord injury in-

clude trauma, infectious meningomyelitis (as from

toxoplasmosis, cryptococcosis, FIP), lymphosarcoma,

and other neoplastic processes. Recently, vaccine-

associated fibrosarcomas have been identified that

have invaded the spinal canal and spinal cord follow-

ing surgical excision from subcutaneous and musculartissues. Spinal radiographs, CSF analysis, serum and

CSF titers, and sometimes myelography or MRI are

indicated in a cat with spinal cord signs. This author

recommends myelography if CSF analysis is normal

and an extradural lesion is suspected. MRI is pre-

ferred if an intramedullary lesion is suspected.

Intramedullary lesions in cats include infectious

myelitis (inflammation of the cord parenchyma itself),

intradural lymphosarcoma, and intramedullary glial

tumors (gliomas).

Treatment guidelines depend on the underlying

cause. Spinal cord lymphosarcoma carries a poor

prognosis, but temporary remission of clinical signs

can sometimes be achieved with chemotherapy.20

Cobalt 60 teletherapy may also provide some benefit

if used in conjunction with chemotherapy. Combined

therapy may provide remission of clinical signs in

many cats, but relapses often occur within 6 months

of onset of treatment.20 FeLV status should be checked

because prognosis and response to therapy tend to be

poorer in FeLV-positive cats.

If trauma (vertebral fracture/luxation or a traumatic

disk) is the source of injury, medical therapy is indi-cated and surgical decompression and stabilization

may be necessary. The cat served as one of the major

animal models of spinal cord injury in the mid to late

1980s, and methylprednisolone sodium succinate

(MPSS, or Solu-Medrol [Pharmacia & Upjohn])

therapy trials were attempted in cats during this time.

Solu-Medrol was shown to be effective for spinal

trauma if administered at 30 mg/kg within several

hours of the trauma.21 Subsequent doses of 15 mg/kg

at 2 hours and 6 hours followed by a constant rate in-

fusion at 2.5 mg/kg/hour for 24 to 48 hours also im-



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proved outcome. The primary mechanism of action of

MPSS is its ability to scavenge free radicals and pre-

vent lipid peroxidation of cell membranes.21 The lim-

iting factor is that this drug is effective only if admin-

istered within hours of injury. Its use beyond 6 to 8

hours of injury probably provides little benefit.

Motor Unit DisordersMotor unit diseases in cats are uncommon. My-

opathies and neuropathies may occur but are often sec-

ondary to metabolic or endocrine disorders. Acquired

myasthenia gravis (MG) is found sporadically in cats, es-

pecially in purebred or mixed Abyssinian and Somali

breeds. This is an immune-mediated junctionopathy

characterized by the presence of autoantibodies directed

against the acetylcholine receptor on the muscle mem-

brane. The typical clinical signs are development of a

stiff, choppy gait with exercise, severe weakness and/or

collapse, ventral neck flexion due to cervical muscleweakness, and weak palpebral reflexes.22,23 One cat de-

scribed in the literature had signs of focal MG

(dropped jaw and dysphagia due to focal cranial nerve

involvement).24 Megaesophagus is also a common find-

ing. The definitive test for acquired MG is the serum

acetylcholine receptor antibody test, but because serum

has to be sent to special laboratories that perform this

test, there is often a significant time delay before results

are known. Intravenous injection of edrophonium chlo-

ride, a short-acting anticholinesterase drug, will alleviate

clinical signs for a few minutes and is a provocative di-

agnostic test for MG. According to one author, the re-

sponse of cats to Tensilon (ICN) is not as predictable as

it is in dogs.19 Repetitive nerve stimulation is quite reli-

able, although other neuromuscular junction disorders

(botulism, chronic organophosphate toxicity) can also

cause a decremental response during stimulation. Treat-

ment is directed at treating the immune-mediated disor-

der with prednisone and/or other immunosuppressive

agents. Concurrent treatment with long-acting anti-

cholinesterase agents (pyridostigmine bromide at 0.53.0

mg/kg orally every 8 to 12 hours) is also helpful in alle-

viating the tetraparetic state. Cats have a greater sensitiv-ity to pyridostigmine bromide than do dogs, so starting at

0.5 mg/kg and slowly titrating upward until a clinical re-

sponse is seen is the most rational approach.19,24 My-

asthenia gravis in the cat is often self-limiting, but signs

can persist for months before clinical remission is

achieved. Monitoring the serum acetylcholine receptor

antibody titer is used as a gauge to decide when to start

tapering immunosuppressive therapy.

Feline Hyperesthetic SyndromeFeline hyperesthetic syndrome is a poorly under-

stood disorder characterized by episodes of agitation,

rippling of the thoracolumbar muscles, swishing of

the tail, biting of the pelvic limbs and lumbosacral re-

gion, vocalization, and often running frantically as if

startled. Various explanations for this behavior have

been proposed, including a psychic behavioral distur-

bance, allergic skin disease, partial complex seizure,and true hyperesthesia due to focal spinal cord or

nerve root disease. This author has attempted hypo-

allergenic diets, serotonin reuptake inhibitor therapy

(fluoxetine, tricyclic antidepressants, etc.), anti-

epileptic drug therapy, and corticosteroid drug therapy

with little success. Recently, the Neurology Service at

The Ohio State University Veterinary Teaching Hospi-

tal has identified EMG changes and pathologic alter-

ations in epaxial muscles of affected cats. Abnormali-

ties in muscle include the presence of inclusion bodies

that resemble those found in inclusion body my-

opathies of humans. Although the significance ofthese inclusions is as yet unknown, they may provide

a clue to the etiology of this syndrome.

CONCLUSIONSCats with signs of neurologic disease may be diffi-

cult to diagnose because of problems inherent in per-

forming a thorough neurologic examination and be-

cause of the great number of acquired disorders that

can affect cats. Localization of the lesion(s) to specific

compartments of the nervous system helps to narrow

down the list of differential diagnoses, but, ultimately,

extensive ancillary diagnostic testing is required to de-

termine the etiologic basis of the clinical signs.

Considerable progress has been made recently in

the diagnosis and therapy of CNS cryptococcosis and

toxoplasmosis. Clearly, understanding the long-term

efficacy of many antimicrobial agents in the treatment

of CNS infections is an area of weakness. On the oth-

er hand, therapy for other disorders (epilepsy, spinal

trauma, neoplasia, myasthenia gravis, etc.) has ex-

panded dramatically in the last decade and many

treatment options are available. Greater knowledge of

the dynamic interplay between the CNS and the sys-temic response to injury is critical for the develop-

ment of rational therapeutic strategies for feline ner-

vous system disease in the future.

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62107289 Advances in Feline Neurology (1)

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