Nervous System Disorders PDF

Nervous System Disorders 19 CH A P TE R Patricia A. Schenck...

Nervous System Disorders 19 CH A P TE R Patricia A. Schenck 2. Proprioceptive positioning: Turn paw so ani- DIAGNOSTIC APPROACH mal bears weight on dorsal surface. The animal I. Principles of neurologic examination should quickly flip the paw over to the normal A. Determine whether neurologic disease is present, position and localize the lesion 3. Hemihopping: Hold limbs on one side off the B. Perform examination in a consistent manner ground and hop the animal sideways on the other 1. Start with a general examination and progress two limbs. If conscious proprioception (CP) is to a specific examination intact and there is adequate strength in the limbs, 2. Do painful parts of the examination last a normal hopping response is quickly initiated II. Procedures for the neurologic examination 4. Wheelbarrowing: Hold either front or hind legs A. General observations off the ground and walk the animal forwards 1. Mental status is regulated by the brainstem and backwards. A normal animal can walk easily and cerebrum D. Cranial nerve examination a. Evaluate level of consciousness (alert, de- 1. Menace response: Make a menacing gesture to- pressed, stuporous, comatose) ward the animal; a normal animal should try to b. Evaluate behavior (appropriate, demented). avoid the gesture. Tests both cranial nerves Dementia reflects a cerebral disorder (CN) 2 and CN7. 2. Head posture is reflective of the vestibular sys- 2. Pupillary light reflex: Illuminate the eye with a tem. A head tilt suggests a vestibular injury bright light; both pupils should constrict. Tests 3. Coordination of head movement is regulated both CN2 and CN3. Lesions of CN2 cause loss by the cerebellum of constriction in both pupils when the af- 4. Circling is usually toward the diseased side. fected eye is examined. Lesions of CN3 cause Any brain lesion can cause circling loss of constriction in the affected eye, with B. Gait and stance constriction in the unaffected eye, regardless 1. A normal gait requires integration of the entire of which eye is illuminated nervous system 3. Pupillary symmetry evaluates CN3 and the a. Ataxia is rarely caused by cerebral or pe- sympathetic nerve to the eye. If CN3 is abnor- ripheral nerve lesions mal, the large pupil is denervated, and the pap- b. Cerebellar lesions typically cause ataxia illary light reflex (PLR) is absent. If the sympa- c. Cerebral lesions may produce mild thetic nerve is damaged, the smaller pupil is weakness abnormal, but the PLR is normal in both eyes d. More pronounced weakness is caused by in- 4. Pupillary size reflects the integrity of CN3 and jury to the brainstem, spinal cord, or pe- sympathetic nerve. Large pupils can be due to ripheral spinal nerves CN3 paralysis. Small pupils may be due to loss 2. An abnormal stance may be caused by de- of sympathetic tone creased proprioception, weakness, or pain 5. Ocular position is determined by CN3, CN4, C. Tests of postural reactions CN6, and CN8 1. General findings a. Injury to CN6 causes medial strabismus a. Cerebral lesions: Postural deficit is on the b. Injury to CN3 or CN8 causes ventrolateral opposite side of the body (contralateral) strabismus b. Brainstem lesions: Postural deficits are bi- 6. Ocular motility lateral, but worse on the same side as the a. Voluntary eye movement requires cerebral, lesion (ipsilateral) CN3, CN4, and CN6 activity. With a cerebral c. Cerebellar, spinal cord, peripheral nerve le- lesion, both eyes look toward the diseased sions: Postural deficits are ipsilateral hemisphere. With a CN lesion, only one eye d. Vestibular lesions: Postural reactions are is involved preserved, but the animal leans or falls to- b. Nystagmus involves involuntary eye ward the diseased side movements 277 278 SECTION II SMALL ANIMAL (1) Vertical nystagmus suggests central b. Crossed extensor reflex. With UMN disease, vestibular disease the stimulated limb flexes and the contralat- (2) Horizontal nystagmus suggests eral limb extends peripheral vestibular disease F. Nociceptive evaluation (3) Rotatory nystagmus suggests either pe- 1. Decreased pain perception can be the result of ripheral or central vestibular lesions peripheral nerve, spinal cord, brainstem, or ce- (4) Resting nystagmus suggests peripheral rebral lesion vestibular disease but can occur with 2. Increased sensitivity or exaggerated response central vestibular lesions to pain. A nonpainful stimulus is applied down (5) Positional nystagmus occurs when the the spine, looking for an area of acute response head is in an abnormal position and to the stimulus suggests central vestibular lesions III. Interpretation of the neurologic examination 7. Facial symmetry assesses CN7; abnormalities A. Central nervous system (CNS) vs. peripheral suggest a cerebral lesion if contralateral, and nerve disease brainstem or peripheral nerve lesions if ipsi- 1. If there are proprioceptive deficits, then lesion lateral is most likely within the CNS 8. Palpebral reflex assesses CN5 and CN7. Touch 2. If there are UMN signs, there is usually a CNS the palpebral margins to produce a blink lesion normally 3. If seizures or altered consciousness is present, 9. Corneal reflex tests CN5 and CN7. Touching a CNS lesion is usually the cause the cornea should produce a normal blink 4. If there are CN deficits and limb signs, the le- 10. Retractor oculi reflex tests CN5 and CN6. sion is in the CNS Touching the cornea should produce a retrac- 5. If there are CN deficits with no other signs, the tion of the eye into the orbit normally lesion is most likely in the peripheral nervous 11. Facial sensory examination tests CN5. Stimu- portion of the CN lation of the nasal mucosa should result in an 6. If there is diffuse weakness, diminished re- avoidance response flexes, without postural deficits, the lesion is 12. Gag reflex tests CN9, CN10, and brainstem. usually in the peripheral nervous system Lack of a swallowing reflex indicates either a B. Location of lesion brainstem injury or CN injury 1. If clinical signs are only in the limbs, the lesion 13. Tongue atrophy indicates either a brainstem is most likely below the foramen magnum or CN12 lesion. Deviation of the tongue can 2. If there are CN deficits, seizures, altered con- be caused by cerebral injuries sciousness, or abnormal head posture, the le- E. Spinal reflex examination sion is most likely above the foramen magnum 1. Proprioceptive reflexes. A standard grading of IV. Diagnostic testing: general the reflex is useful A. Hematology: Usually minimal changes a. Triceps reflex evaluates the radial nerve B. Biochemical tests: Alterations in blood glucose, from C7 to T2. Normally there should be a calcium, potassium, and sodium can impact ner- slight extension of the elbow vous system function. In addition, acid-base sta- b. Extensor carpi radialis reflex also evaluates tus, uremia, hyperlipidemia, hyperammonemia, C7 to T2. Normally the carpus extends and hyperviscosity can cause neurologic signs c. Biceps reflex evaluates the musculocutane- C. Urinalysis: Metabolic diseases that impact the ous nerve (from C6 to C7) nervous system—such as diabetes, renal disease, d. Patellar reflex tests femoral nerve and L4 to and liver disease—can produce changes in the L6. An exaggerated response suggests an urine upper motor neuron (UMN) lesion D. Ophthalmologic examination is warranted if there e. Cranial tibialis reflex tests the peroneal is inflammatory disease branch of the sciatic nerve from L6 to S2 E. Blood pressure measurement is warranted as 2. Nociceptive spinal reflexes are initiated by a hypertension can predispose to CNS vascular painful stimulus. Loss of the reflex suggests a disease lower motor neuron (LMN) lesion F. Thoracic radiographs and abdominal ultrasound a. Thoracic limb flexor reflex tests spinal cord are useful if inflammatory or neoplastic disease is segments C6 to T2 suspected b. Pelvic limb flexor reflex tests segments L6 G. Fecal analysis: Parasites can cause CNS disease in to S2 young animals c. Perineal reflex tests S1 to S3 H. Serology for viral or rickettsial diseases may be 3. Special reflexes indicated a. Babinski reflex is in the hindlimbs. Stroking I. Immunofluorescence can be used to identify some the plantar aspect of the metatarsus should viral diseases cause slight flexion of the toes, or no re- J. Toxicology may be utilized to identify certain sponse. A positive Babinski reflex signifies toxins UMN disease, and the toes spread apart and V. Neuroradiography and special imaging elevate A. Radiographs of the spine  CHAPTER 19 Nervous System Disorders 279 1. Used to identify bony lesions, changes in inter- 4. CSF can be tested for antibodies against infec- vertebral disc spaces tious agents 2. Provide minimal information in regard to VII. Electroencephalography (EEG) spinal cord compression A. An EEG is useful with corticocerebral lesions. B. Myelography Sedation is usually required to minimize 1. Contrast material is injected into the subarach- movement noid space B. The major disadvantage is that no information is 2. Useful for viewing extradural or intradural le- gathered regarding cause sions causing spinal cord compression VIII. Brainstem auditory evoked response tests C. Radiographs of the skull can identify fractures, hearing foramen magnum problems, and tumors IX. Electrodiagnostic examination of the motor unit D. Computed tomography (CT) provides excellent A. Needle electromyography (EMG) gives informa- imaging of bony structures tion about motor unit innervation and muscle E. Magnetic resonance imaging (MRI) provides ex- membrane ion conductance cellent imaging of brain and spinal cord B. Nerve conduction studies measure the action po- VI. Cerebrospinal fluid (CSF) collection and analysis tential conduction velocity between points along A. CSF analysis is indicated if inflammation is a motor nerve suspected C. Repetitive nerve stimulation is useful in neuro- B. CSF analysis is contraindicated if intracranial muscular junction diseases pressure is elevated D. Tensilon or edrophonium chloride test. Intrave- C. CSF collection is performed under general anes- nous (IV) administration transiently alleviates thesia. If a brain disorder is suspected, collect signs of myasthenia gravis CSF at the cerebellomedullary cistern. For spinal cord disorders, collect CSF at the lumbar space BRAIN AND CRANIAL NERVE DISORDERS D. CSF analysis 1. Gross examination I. Clinical signs a. CSF should normally be clear and colorless A. Brainstem lesions b. CSF is turbid in inflammation 1. Cranial nerve dysfunction (CN3-CN12) is c. Pink color indicates blood contamination; common yellow-orange color indicates breakdown of 2. Clinical signs involving facial expression (CN7) hemoglobin from previous hemorrhage or and mastication (CN5) are common severe elevation in CSF protein 3. Head tilt, circling, and falling are signs of ves- 2. Cytology tibular nuclei damage a. Suppurative meningitis is characterized by 4. Ascending white matter tract injury causes an increase in neutrophils and indicates ipsilateral conscious proprioceptive deficits bacterial encephalitis, meningioma, vasculi- 5. Descending UMN injury causes tetraparesis or tis in young dogs or feline infectious perito- paralysis nitis (FIP) in cats 6. Severe brainstem lesions result in altered con- b. Mixed inflammation is characterized by an sciousness and can affect cardiovascular and increase in a mixed population of cells and respiratory regulation usually indicates fungal, protozoal, or idio- B. Cerebellar lesions pathic encephalitis. It may be seen in 1. Incoordination during voluntary movements chronic bacterial infections 2. Truncal swaying and a wide-based stance c. Nonsuppurative inflammation is indicative 3. Intention tremor of the head of immune-mediated encephalitis, rickettsial 4. The menace response is absent ipsilaterally infection, and some viral infections 5. Mild pupil dilation may be present ipsilaterally d. Eosinophilic inflammation is secondary to 6. Vestibular signs and opisthotonus may be immune-mediated encephalitis, fungal or present protozoal infections, and parasite 7. Mental status is usually normal migration C. Forebrain lesions e. Increased red blood cells (RBCs) may be 1. Seizures, personality changes, and dementia due to contamination during the CSF tap can occur with both diffuse and focal but can also be due to hemorrhage due to disorders trauma. Erythrophagocytosis is an indica- 2. Diffuse disorders may cause conscious pro- tion of previous hemorrhage prioceptive deficits, stupor, coma, absent re- f. Other cells or organisms identified include sponse to pain, generalized ataxia, and bilat- tumor cells cryptococcal or fungal organ- eral miosis isms, distemper inclusions, bacteria, or 3. Focal disorders may cause circling, contralat- rickettsial organisms eral conscious proprioceptive deficits, contra- 3. Protein concentration is normally low in CSF. lateral facial sensory deficits and weakness. Disorders that increase CSF protein include en- Focal diencephalic lesions can cause lethargy, cephalitis, meningitis, neoplasia, chronic neu- altered mentation, or circling. Head and neck rodegenerative conditions, and trauma pain can result from structural lesions 280 SECTION II SMALL ANIMAL D. Manifestations of systemic metabolic alterations D. Treatment 1. Signs are usually diffuse, with alteration of 1. Corticosteroids are used to treat edema and mental status meningioma 2. Seizures may also be seen 2. Mannitol is used in those with increased intra- E. Herniation from space-occupying brain lesions cranial pressure. Furosemide will help prolong 1. If there is transtentorial herniation, clinical the effects of mannitol signs include extensor rigidity in the limbs, 3. Phenobarbital with or without potassium bro- and stupor or coma mide is indicated if seizures are present 2. If there is foramen magnum herniation, clinical 4. Lomustine may be beneficial in treating glio- signs include opisthotonus, thoracic limb rigid- mas and meningiomas ity, and severe alterations in respiration 5. Surgery may be possible, depending on II. Neoplasia usually affects middle-aged and older location animals 6. Radiation therapy consistently prolongs sur- A. Causes vival, especially for meningiomas and canine 1. The most common primary tumors in the dog pituitary tumors are meningioma and glioma (astrocytoma, glio- III. Inflammatory brain diseases blastomas, oligodendrogliomas, ependymo- A. Infectious meningoencephalitis (more common mas, and choroids plexus papillomas/ in cats) carcinomas) 1. Many agents cause inflammatory brain disease, a. Meningiomas occur mostly in dolichoce- including viral, fungal, rickettsial, and proto- phalic breeds, and gliomas occur mostly in zoal agents brachycephalic breeds 2. Diagnostic testing includes complete blood b. Meningiomas are often located in the olfac- cell count (CBC), chemistry profile, urinalysis, tory or frontal lobe radiographs, and ophthalmological evaluation 2. The most common primary tumor in the feline a. CSF analysis may be beneficial; CSF titers is meningioma; frequently multiple can be determined 3. Secondary brain tumors occur from hematoge- b. Cytologic evaluation of skin lesions, exu- nous spread or extension from surrounding dates, and aspirates may identify a pathogen tissues 3. Treatment depends on the underlying cause a. Tumors with hematogenous spread are a. Usually requires prolonged therapy hemangiosarcoma, malignant melanoma, b. Most effective if parenteral antibiotics are mammary adenocarcinoma, and pulmonary administered adenocarcinoma B. Idiopathic inflammatory brain disorders (more b. In the dog, secondary lymphoma occurs common in dogs) with the multicentric form. Multicentric 1. Granulomatous meningoencephalomyelitis malignant histiocytosis can also invade (GME) the CNS a. GME is an immune-mediated condition with c. Tumors invading by extension are usually perivascular accumulations of lymphocytes, nasal adenocarcinoma, pituitary macroade- plasma cells, and histiocytic cells. There are noma or carcinoma, and bony tumors of the disseminated, focal, and optic forms skull b. Clinical signs B. Clinical signs depend on the location and type of (1) Usually affects toy and small breeds be- tumor tween 1 and 8 years of age 1. Signs may be vague, with irritability, changes (2) Vestibular signs are common; CN5 and in behavior, pacing, and lethargy CN7 deficits may be seen. Fever, leth- 2. Signs may arise from obstruction of CSF flow argy, and anorexia may be the only clini- or from herniation. Vestibular symptoms, or cal signs seen initially cranial nerve signs may also be seen c. Diagnosis is by exclusion. A marked mono- C. Diagnosis nuclear cell inflammation is seen in the CSF 1. Laboratory testing is used to rule out other d. Prednisone may cause remission causes of nervous system signs. Adrenal func- e. Relapses are common, and patients may tion testing may reveal the presence of pitu- become refractory to treatment itary macroadenoma 2. Necrotizing encephalitis 2. Ophthalmologic examination should be done a. Similar to GME and may have an immune- to check for papilledema, which is a sign of in- mediated component. Multifocal, necrotic, creased intracranial pressure cavitating lesions are commonly seen 3. EEG may detect brain lesions or epilepsy b. Clinical signs include seizures, dementia, 4. Radiography may reveal some bony lesions or blindness, neck pain, and ataxia. Necrotiz- metastasis ing encephalitis usually occurs in toy breed 5. CT and MRI are used for more precise defini- between 9 months and 5 years of age tion of tumors c. Diagnosis is by exclusion of GME, infectious 6. CSF analysis is useful to distinguish inflamma- disease, and neoplasia. A marked mononu- tion from neoplasia clear cell inflammation is seen in the CSF  CHAPTER 19 Nervous System Disorders 281 d. Treat with prednisone and anticonvulsants. 4. Treatment and prognosis depend on the under- The prognosis is poor lying cause 3. Generalized idiopathic tremors (Little White V. Brain trauma Shaker syndrome) A. Trauma can cause an increase in intracranial a. Occurs in toy and small-breed dogs with pressure leading to bradycardia, hypertension, white coat color; other breeds can be af- and pulmonary edema. A delayed consequence is fected. Usually affects dogs younger than epilepsy 6 years B. Focal signs reflect the region of the brain in- b. Clinical signs include coarse body tremors volved. Progression occurs within the first 24 to that worsen with stress, exercise, or 48 hours after an injury, so a neurologic examina- handling tion should be performed every few hours c. Differential diagnosis includes neurotoxin C. An EEG can be used to localize the brain damage exposure, seizures, and inflammatory brain D. Correct any life-threatening symptoms; elevation diseases of the head will help maintain cerebral blood flow d. Treatment is with diazepam and predni- and enhance CSF resorption. Hyperventilation sone. The prognosis is good, although will stimulate vasoconstriction and decrease in- relapses may occur tracranial pressure IV. Vascular diseases 1. Methylprednisolone sodium succinate is bene- A. Vascular encephalopathies ficial if administered immediately following the 1. Typically affects older animals. Ischemia or in- trauma farction occurs as a result of thrombosis of a 2. Mannitol and furosemide may be beneficial if blood vessel secondary to an underlying con- there is brain edema dition (e.g., hypertension, atherosclerosis, hy- 3. Hypertonic saline with hetastarch should be perviscosity, tumor emboli) used in those with hypovolemic shock and 2. Clinical signs are usually asymmetrical and head trauma cause signs of forebrain disease or vestibular 4. Use diazepam to control seizures disease 5. Monitor fluid therapy 3. Diagnosis is by diagnosing the underlying dis- VI. Metabolic brain encephalopathies order; MRI is useful in determining the extent A. The cerebrum is most often affected of the ischemia or hemorrhage B. Clinical signs include altered behavior, dementia, 4. Treatment of the underlying condition is im- and seizures portant; anticonvulsants or mannitol therapy C. Causes include osmotic and ionic imbalances, to treat brain edema may be necessary acid-base imbalance, hypoglycemia, hypoxia, B. Feline ischemic encephalopathy renal failure, and hepatic encephalopathy 1. Occurs in young to middle-aged cats, with a VII. Thiamine deficiency higher incidence in late summer. It is caused A. Deficiency in vitamin B1 is caused by improperly by a cerebral infarction of the middle cerebral formulated diets (especially all fish diets) or artery prolonged anorexia. Cats are more frequently 2. Clinical signs are of cerebral dysfunction. Sei- affected zures may be the only sign; clinical signs may B. Clinical signs include weight loss, head and neck improve over months ventroflexion, ataxia, extensor rigidity, opisthoto- 3. Rule out other causes of vascular disease and nus, coma, mydriasis, blindness, seizures, and cerebral disease; MRI may show cerebral sudden death edema C. Rule out other causes of clinical signs 4. Anticonvulsant therapy may be needed; pred- D. Treat with parenteral thiamine; supplement with nisone is not effective B vitamins for at least 2 weeks. Prognosis is good C. Necrotizing vasculitis if therapy is initiated early 1. Occurs in young (i.e, 3 to 18 months old) VIII. Neurotoxins beagles, Bernese mountain dogs, and German A. Lead poisoning shorthaired pointers. Probably immune-mediated 1. Caused by ingestion of lead-containing paint 2. Clinical signs of meningitis such as neck pain, chips, plaster board, and other building mate- stiffness, and fever are common rials. Chronic exposure may cause a chronic 3. CSF analysis shows an increase in neutrophils toxicity 4. Treat with immunosuppressive doses of corti- 2. Clinical signs include vomiting, diarrhea, costeroids. Prognosis is fair to guarded anorexia, abdominal pain, behavior changes, D. Infectious cause of vasculitis seizures, pica, vocalization, and blindness 1. Caused by fungal, protozoal, viral, or rickett- 3. Nucleated RBCs and basophilic stippling are sial agents noted on CBC. An increase in blood lead sug- 2. Head and neck pain are common, and edema gests lead poisoning results in brain swelling. Cranial nerve deficits 4. Treat with a chelating drug (EDTA; and vestibular signs may be present D-penicillamine; 2,3-dimercaptosuccinic acid). 3. Characteristics of the CSF will depend on the Give anticonvulsants if needed; treat cerebral underlying cause edema if present. The prognosis is fair to good 282 SECTION II SMALL ANIMAL B. Metaldehyde poisoning 3. Diagnosis is based on history, clinical signs, 1. Metaldehyde is a molluscide and produces se- and the absence of other disease vere metabolic acidosis if ingested 4. Discontinue administration of metronidazole, 2. Clinical signs include seizures, tremors, depres- and clinical signs usually resolve over 1 to sion, salivation, vomiting, and diarrhea. Hepatic 2 weeks failure occurs several days after ingestion G. Bromethalin poisoning 3. Diagnosis is based on history and clinical signs 1. Bromethalin is present in rodenticides and un- 4. Treat with gastric lavage and activated char- couples phosphorylation coal if within 2 hours of ingestion. Sodium 2. Clinical signs include hyperexcitability, muscle bicarbonate is used to treat acidosis; anticon- tremors, seizures, limb rigidity, nystagmus, de- vulsants may be needed. Prognosis is poor pression, ataxia, paresis, loss of deep pain, and C. Methylxanthine toxicosis (caffeine, theobromine) paraplegia 1. Dark chocolate contains more caffeine and 3. Diagnosis is based on history and clinical signs theobromine than does milk chocolate; inges- 4. Treat by inducing vomiting; give activated tion of as little as 1 ounce of baker’s chocolate charcoal if less than 2 hours after ingestion. per kilogram of body weight may be lethal Provide supportive care, and give anticonvus- 2. Clinical signs include tachycardia, cardiac ar- ants if needed. Prognosis is poor rhythmias, vomiting, polyuria, polydipsia, re- H. Ethylene glycol poisoning spiratory paralysis, cyanosis, seizures, muscle IX. Congenital malformations and anomalies tremors, ataxia, and coma A. Hydrocephalus 3. Diagnosis is based on history and clinical signs 1. Congenital disorder characterized by an accu- 4. Treat with activated charcoal, promote diure- mulation of CSF within the brain and may ac- sis, treat cardiac arrhythmias and seizures. company other congenital malformations Prognosis is fair if treatment is started early 2. Clinical signs include head pressing, dementia, D. Organophosphate and carbamate poisoning changes in behavior, seizures, altered con- 1. Actylcholinesterase is inhibited, so acetylocho- sciousness, ataxia, and visual deficits. An open line is not broken down at muscarinic and fontanelle with ventrolateral strabismus is nicotinic sites of the autonomic and somatic often present. Breeds commonly affected in- nervous systems clude Pomeranian, toy poodle, Maltese, York- 2. Clinical signs include salivation, vomiting, diar- shire terrier, Chihuahua, Manchester terrier, rhea, miosis, bradycardia, muscle tremors, Cairn terrier, shih-tzu, English bulldog, Boston weakness, exercise intolerance, respiratory pa- terrier, Pekingese, Lhasa apso and others. ralysis, hyperactivity, and seizures Signs are usually seen in dogs less than 1 year 3. Diagnosis is based on history and clinical signs of age 4. Treat by inducing vomiting if ingestion has 3. The primary differential diagnosis is hepatic occurred within the previous 2 hours and encephalopathy, encephalitis, and toxin there are no clinical signs. Give anticonvul- exposure sants if necessary; bathe if exposure is on the 4. Treatment with corticosteroids may be benefi- skin. Give atropine and pralidoxime chloride; cial short-term. Mannitol is indicated if there is provide support with IV fluids, nutritional sup- an elevation of intracranial pressure. Anticon- port, padded bedding. The prognosis is good if vulsants should be given for seizures treatment is early B. Lissencephaly E. Ivermectin toxicity 1. Lissencephaly is the absence of cerebral cor- 1. Normally the blood-brain barrier prevents iver- tex convolutions and thinned white matter. It is mectin from entering the CNS. A P-glycoprotein inherited in the Lhasa apso, wirehaired fox ter- pump defect in some collies, Shetland sheep- rier, and Irish setter. Some may have concur- dogs, Australian shepherds, and Old English rent cerebellar hypoplasia sheepdogs allows ivermectin to enter the 2. Clinical signs include behavior changes, de- brain. A single oral dose can be neurotoxic if mentia, seizures, and visual deficits. Clinical this defect is present signs are present at birth or within the first 2. Clinical signs include ataxia, muscle tremors, year of life tetraparesis, and coma 3. There is no specific treatment; treat with anti- 3. Diagnosis is based on history, breed, and clini- convulsants if needed cal signs C. Congenital arachnoid cysts 4. Treatment is supportive. Prognosis is good, 1. There is cystic accumulation of CSF in the sub- but recovery can take weeks arachnoid space. These can slowly enlarge and F. Metronidazole toxicity cause compression of adjacent neural tissue 1. Toxicity may be seen in the dog and cat 2. Clinical signs include seizures, paresis, behav- after more than 7 days of therapy with ior changes, and cranial nerve deficits. Signs metronidazole appear in young adults 2. Clinical signs include severe ataxia, nystagmus, 3. Diagnosis is by visualization on MRI or CT opisthotonus, seizures, and a crouched pos- 4. Treatment is by surgical fenestration of the ture in the pelvic limbs cyst wall  CHAPTER 19 Nervous System Disorders 283 D. Cerebellar hypoplasia in cats cognitive loss in older dogs (greater than 1. Caused by exposure of kittens in utero to pan- 11 years of age). Cortical atrophy and amyloid leukopenia infection plaques are common. Decreased levels of nor- 2. Clinical signs including severe ataxia, intention epinephrine and dopamine have been ob- tremors, falling, head bobbing, and loss of served in the frontal cortex menace response are observed as soon as kit- 2. Clinical signs include decreased social interac- tens start to walk tion, staring, wandering, getting lost, loss of 3. Diagnosis is based on clinical signs house training, and altered sleep cycles 4. There is no treatment 3. Diagnosis is based on history and clinical signs E. Cerebellar hypoplasia in dogs 4. Treat with selegiline, which inhibits the break- 1. May be secondary to postnatal herpesvirus in- down of dopamine and norepinephrine. Modify fection, but most cases have a genetic base. the environment, and pay attention to nutri- Affected breeds include the chow chow, Aire- tion, feeding, and exercise dale terrier, Irish setter, wirehaired fox terrier, XI. Cranial nerve disorders Boston terrier, bull terrier, Weimaraner, A. Idiopathic disorders dachshund, and Labrador retriever 1. Trigeminal neuritis 2. Clinical signs are nonprogressive and include a. Etiology is unknown. Affects middle-aged ataxia, disequilibrium, falling, intention trem- dogs ors, and an absent menace response b. Clinical signs include inability to close the 3. Treatment is not available mouth and difficulty in chewing food X. Degenerative brain disease c. Diagnosis is based on history of acute man- A. Cerebellar abiotrophies dibular paralysis 1. The cerebellum develops normally but is fol- d. Treatment is supportive; corticosteroid lowed by premature degeneration and cell therapy is not beneficial death. It is autosomal recessive in some breeds 2. Idiopathic facial paralysis or palsy 2. Clinical signs include intention tremor and pro- a. Causes gressive ataxia. Dogs are normal at birth, but b. Clinical signs include a unilateral facial clinical signs start between 4 and 10 weeks droop, decreased tear production, and in- of age ability to blink. Food, water, and saliva fall 3. Rule out other causes of progressive cerebellar out of the mouth. Cocker spaniels have an disease increased incidence 4. There is no treatment. The prognosis is poor c. Diagnosis is by ruling out other causes of B. Multiple neuronal abiotrophies facial paralysis 1. Cell loss or chromatolytic changes in multiple d. There is no treatment areas of the brain. Breeds affected include the 3. Canine idiopathic vestibular disease Cairn terrier, Kerry blue terrier, miniature poodle, a. Cause is unknown; affects older dogs and cocker spaniel, and rough-coated collie young adult cats typically 2. Clinical signs are primarily cerebellar in Kerry b. Clinical signs include head tilt, circling, fall- blue terriers, rough-coated collies, and Cairn ing, nystagmus, and anorexia. Signs gradu- terriers. Cocker spaniels have signs of both ally improve with time cerebellar and cerebral degeneration; minia- c. Diagnosis is by ruling out other causes of ture poodles have cerebellovestibular signs. clinical signs Onset of signs is usually between 4 and d. Treatment is supportive until clinical signs 16 weeks of age resolve (usually within a few weeks) 3. Differential diagnosis includes lysosomal stor- B. Hypothyroidism age disease, and inflammatory CNS disease 1. Usually causes vestibular signs, but may also 4. There is no treatment affect CN7 and CN10 C. Multisystem neuroaxonal dystrophy 2. Clinical signs are typically signs of vestibular 1. An inherited error of metabolism that results disease in swellings along regions of the axon. Breeds 3. Diagnosis is by ruling out other causes of ves- affected include the rottweiler, Jack Russell tibular disease, and documentation of hypo- terrier, Chihuahua, bullmastiff, Labrador re- thyroidism triever, collie-sheepdog mixed breed, and 4. Treat with thyroid supplementation domestic shorthaired cat C. Neoplasia 2. Clinical signs are cerebellar in origin; cerebral 1. CN5 neoplasia signs are seen in the Labrador retriever a. Neurofibromas or schwannomas are most 3. Differential diagnosis includes other congenital common in middle-aged to older dogs cerebellar disorders, or inflammatory, meta- b. Slow progression of temporal and masseter bolic, or toxic disorders muscle atrophy followed by facial sensory 4. There is no treatment loss is observed D. Cognitive dysfunction c. MRI is the diagnostic method of choice 1. Neurodegenerative disorder of the forebrain d. Surgery is difficult; radiation therapy may with gradual onset and progression of slow progression 284 SECTION II SMALL ANIMAL 2. CN8 neoplasia behavior and/or motor activity, followed by a a. Neurofibromas or meningiomas may affect change in behavior or orientation CN8. In addition, other tumors may extend B. Obtain a thorough history. Include information on into or invade the nerve vaccination status, pedigree, travel history, medi- b. Clinical signs include vestibular signs, cations given, and previous medical and surgical Horner syndrome, and other cranial problems neuropathies C. Obtain as much data about seizure episodes as c. MRI is the diagnostic method of choice possible. Include duration, time between seizures, d. Usually not possible to remove the tumor type of seizures, and behaviors surrounding the D. Congenital sensorineural deafness seizure 1. Caused by postnatal cochlear hair cell and D. Evaluate current behaviors and document spiral ganglion degeneration; occurs in many changes dog breeds. Also occurs in white cats with IV. Diagnosis blue eyes A. Dogs 2. Clinical signs include unilateral or bilateral 1. In dogs younger than 1 year, seizures are usu- deafness in very young puppies ally secondary to developmental, metabolic, or 3. There is no treatment inflammatory disorders 2. In dogs between 1 and 5 years of age, seizures are usually idiopathic, although some may re- SEIZURES sult from a congenital disorder I. Definitions 3. If older than 5 years of age, seizures are usu- A. An epileptic seizure is caused by abnormal activ- ally due to structural disorders (brain tumor), ity in the cerebral cortex or metabolic diseases B. Epilepsy is the chronic disorder characterized by B. Cats: Idiopathic epilepsy is rare; almost all cats recurrent epileptic seizures have an underlying cause of seizures C. Status epilepticus is a continuous seizure that C. Diagnostic approach lasts more than 30 minutes 1. Idiopathic epilepsy is likely if: D. Clinical stages a. There is greater than 4 weeks between 1. Prodrome stage is the period before the onset seizures of a seizure. Altered behavior may be noted b. The dog is a large breed dog during this stage c. Seizures start between the ages of 1 and 2. The aura is the initial phase of a seizure 5 years 3. The ictal phase is the manifestation of the seizure 2. Secondary epilepsy is likely if: 4. The postictal phase is the period immediately a. There is less than 4 weeks between seizures after the seizure. Altered behavior may be b. The first seizure is a focal seizure noted c. Seizures start before 1 year of age or after E. Seizure types 7 years of age 1. Generalized convulsions are most common d. There is an abnormal neurological 2. Automotor seizures (psychomotor seizures) examination are characterized by abnormal behaviors and 3. Seizures attributable to a metabolic disorder motor signs such as aggression, howling, ex- are likely if: cessive barking, fly-biting behavior a. There are signs of systemic illness 3. Focal seizures originate from a focal lesion in b. There is less than 4 weeks between seizures the cerebral cortex. Focal motor seizures may D. Diagnostic testing manifest as facial twitching, or twitching of 1. Minimum database includes CBC, biochemistry limb muscles profile, urinalysis, thoracic radiographs, and 4. Clustered seizures refers to two or more sei- blood pressure. Serum bile acids may be war- zures within 24 hours ranted if portosystemic shunt is suspected II. Causes 2. MRI is best for diagnosing an intracranial A. Normally there is a balance between excitatory disorder or neoplasia and inhibitory neurotransmission. With epilepsy, 3. CSF examination should be performed if an there is more excitatory neurotransmission inflammatory process is suspected B. Idiopathic epilepsy implies that there is no under- 4. Other diagnostic tests may be indicated if lying brain lesion present toxins, insulinoma, or infectious diseases are C. Secondary epilepsy occurs owing to a structural suspected lesion in the brain V. Treatment D. Cryptogenic epilepsy is due to a presumed struc- A. The goal of therapy is to decrease or eliminate tural lesion that has not been identified (previous seizure activity with minimal side effects of head trauma, hypoxic events, vascular events, medication postencephalitis) B. Treatment should be started when there have III. Clinical Signs been two or more seizures within 6 months, there A. Epileptic seizure should be suspected if there have been two or more cluster seizures within is an incident of a sudden onset of abnormal 12 months, there has been an episode of status  CHAPTER 19 Nervous System Disorders 285 epilepticus, there is evidence of an intracranial F. New antiepileptic drugs disease, or a seizure has occurred within one 1. Felbamate is used alone week of a trauma 2. Gabapentin is used in dogs with hepatic dis- C. Phenobarbital administration ease. Also used in cats 1. Maximal absorption occurs within 4 to 8 hours G. Drugs not used for routine therapy in the dog after oral administration 1. Phenytoin (Dilantin) causes hepatotoxicity and 2. Most is metabolized by the liver has very rapid elimination 3. Phenobarbital induces the hepatic P450 2. Diazepam (Valium) can cause withdrawal sei- system in the dog but not the cat. This zures, and tolerance develops very quickly will decrease the elimination half-life in H. Hospital emergency treatment for seizures the dog 1. Emergency therapy should be given if status ep- 4. IV treatment can achieve therapeutic concen- ilepticus is present, if a single seizure lasts more trations rapidly than 5 minutes, if there is more than one seizure 5. Serum monitoring per hour, or more than 3 seizures per day a. Trough concentrations of serum phenobar- 2. Use diazepam to stop seizure activity and a bital should be monitored after reaching a long-acting drug to prevent further seizures steady state I. At home emergency treatment for seizures b. After starting treatment, monitor at 1. Diazepam is rapidly absorbed when given rectally 2 weeks, 45 days, 3 months, 6 months, and 2. Administer when a seizure first starts, up to 1 year. Then monitor at 6-month intervals 3 times per day c. Monitor if status epilepticus or cluster sei- zures occur or if there are more than two SPINAL CORD DISORDERS seizures between monitoring times d. Adjust dosage based on desired concentra- I. Causes tion and actual concentration, not accord- A. Anomalies are usually recognized when the ing to body weight animal starts to walk. Some worsen with time and e. If a peak level measurement is desired, mon- cause progressive worsening of clinical signs itor at 4 to 6 hours post-pill B. Degenerative disorders may be inherited, includ- f. Monitor CBC and chemistry profile at least ing lysosomal storage disorders, spinal muscular every 6 months atrophy, and hereditary ataxia. Other degenera- 6. Adverse effects tive disorders are age-related and include cervical a. Sedation and lethargy commonly occur, but spondylomyelopathy, intervertebral disc disease, this is usually transient and dissipates after lumbosacral stenosis, and mucopolysaccharido- a few weeks sis in cats b. Polyuria, polydipsia, and polyphagia may C. Trauma can be from an external source (hit by occur. Weight gain is also common car) or internal source (disc herniation) c. Alkaline phosphatase commonly elevates, D. Inflammation or infection and thyroid hormone concentrations may 1. Bacterial infection is usually secondary to in- be depressed fection of surrounding tissues d. Hepatotoxicity may develop, and the effi- 2. Viral infection includes rabies, canine distem- cacy over time may be gradually diminished per virus, FIP, and feline immunodeficiency vi- D. Refractory epilepsy rus (FIV) 1. Seizures have continued or worsened over 3. Fungal myelitis occurs with cryptococcosis, 3 months even though phenobarbital concen- blastomycosis, histoplasmosis, and coccid- trations appear adequate iodomycosis 2. Status epilepticus has occurred, or hepatotox- 4. Rickettsial causes include ehrlichiosis and icity is present Rocky Mountain spotted fever E. Bromide therapy 5. Protozoal causes include Neospora caninum, 1. Oral bromide is used in addition to phenobar- and toxoplasmosis bital and decreases the number and severity of E. Immune-mediated disorders occur in young dogs seizures in many dogs (commonly boxers), and signs are typically neck 2. Monitor bromide levels at 1 month, 3 months, stiffness, hyperesthesia and fever. GME is also an and 6 months after starting therapy. Then immune-mediated disorder monitor every 6 months after that F. Toxins include strychnine and tetanus 3. Bromide can be used without phenobarbital if G. Vascular disorders can result in ischemia of the there is hepatic disease, if there have been no spinal cord with dysfunction seizures for more than a year, or the quality of H. Neoplastic causes include astrocytoma, ependy- life is unacceptable on both phenobarbital and moma, hemangiosarcoma, lymphoma, and other bromide, and there have been no seizures for tumors. Tumors can be intramedullary or extra- more than 3 months medullary 4. Bromide therapy is not recommended in cats II. Clinical signs due to a high prevalence of respiratory A. Hyperpathia is the exaggerated response to a problems painful stimulus. Hyperpathia occurs when nerve 286 SECTION II SMALL ANIMAL roots or dura adjacent to the spinal cord are 3. Infection should be treated with antibiotics involved that cross the blood-brain barrier, such as B. Proprioceptive deficits and ataxia occur early in trimethoprim-sulfonamide, refampin, metroni- spinal cord disease dazole, penicillins, quinolones, clindamycin, 1. Injury to CP tracts causes knuckling and cephalosporins. Discospondylitis is usu- 2. Injury to unconscious proprioception (UP) ally caused by Staphylococcus but may be tracts causes ataxia in limbs caudal to the caused by other organisms. Treat with an ap- lesion propriate antibiotic C. Paresis (weakness) can result from injury to UMN 4. Immune-mediated disorders are treated with or LMN tracts immunosuppression. Prednisone is used in 1. UMN injury causes weakness in limbs caudal combination with other immunosuppressive to the lesion, and LMN injury causes weakness agents in limbs at the level of the injury 5. Toxicities, such as tetanus, are treated with 2. UMN injury causes increased extensor muscle a combination of penicillin, tetracycline, tone when recumbent or metronidazole with tetanus antitoxin, 3. LMN injury causes decreased spinal reflexes, chlorpromazine, diazepam, and decreased muscle tone, and muscle atrophy phenobarbital D. Nociceptive (pain) loss 6. Neoplasia is difficult to treat as most chemo- 1. Injury to ascending nociceptive tracts in the therapeutic agents do not cross the blood-CSF spinal cord results in depressed or absent pain barrier. Lomustine does penetrate the CNS and from stimuli caudal to the injury can be used in conjunction with prednisone to 2. Lack of deep pain sensation indicates severe treat CNS lymphoma spinal cord injury B. Surgical treatment E. CP loss occurs first, followed by UP loss, UMN, 1. The primary goal is to decompress the spinal then nociceptive loss as lesions worsen cord and stabilize the vertebral column F. Intramedullary lesions cause symmetrical clinical 2. The decision to perform surgery is based signs; extramedullary lesions cause asymmetrical on the progression of clinical signs and signs that are usually ipsilateral to the lesion the likelihood that surgery will be III. Diagnosis beneficial A. History: Progression of symptoms, signalment, 3. Surgery is most beneficial if it is performed and nature of onset are most important early in the course of the disease B. Lesion localization by evaluation of clinical signs C. Nursing care is very important and includes ther- is important as some diseases target specific mal applications of cold and hot packs, muscle areas of the spinal cord massage, limb manipulations, hydrotherapy, fre- C. Minimum database includes CBC, biochemistry quent evacuation of the bladder, padded bedding, profile, and urinalysis to assess overall health. and daily baths Specialized tests may be warranted based on V. Prognosis findings A. Based on clinical signs D. Electrodiagnostic tests such as EMG, nerve veloc- 1. The more severe the clinical signs, the poorer ity studies, or nerve root studies may be helpful the prognosis but require referral to a 2. The longer the duration of spinal cord injury, specialist the poorer the prognosis E. Imaging techniques B. Based on cause 1. Plain spinal radiography is good for evaluation 1. Anomalies have a nonprogressive course, and of bony lesions but does not give good infor- prognosis depends on the extent of injury mation regarding spinal cord compression 2. Degenerative disorders have a guarded or poor 2. Myelography may be useful but is invasive and prognosis requires longer anesthesia times 3. Trauma 3. MRI is useful for imaging the spinal cord and a. With fractures, if the spinal cord is intact, other soft tissues surgery can be beneficial if performed 4. CT is preferred if bony lesions are being within a few hours of injury evaluated b. Extramedullary compressive lesions have F. CSF analysis is the test of choice for diagnosing a better prognosis than intramedullary inflammatory spinal cord disease lesions IV. Treatment 4. Infection has a guarded prognosis unless a A. Medical therapy specific cause can be identified and treated. 1. Degenerative disorders causing compression Discospondylitis has a fair to good prognosis of the spinal cord are treated primarily with if treatment is instituted early glucocorticosteroids at antiinflammatory doses 5. Meningitis and myelitis 2. Spinal cord trauma should be treated a. Immune-mediated meningitis has a good immediately after injury with large doses of prognosis if treated appropriately corticosteroids. Glucocorticosteroids are bene- b. Granulomatous encephalitis has a guarded ficial for about the first 2 to 3 days to poor prognosis  CHAPTER 19 Nervous System Disorders 287 6. The prognosis for vascular disorders depends E. Inflammatory and immune-mediated disorders on the severity of the neurologic deficits 1. Toxoplasma gondii and Neospora caninum can 7. Neoplasia is associated with a poor prognosis cause inflammation of peripheral nerves overall 2. Acute polyradiculoneuritis (coonhound paraly- sis) is a common peripheral nerve disorder a. Frequently observed in hunting dogs 1 to PERIPHERAL NERVE DISORDERS 2 weeks after exposure to a raccoon I. Neuropathy refers to functional disturbances in the b. Pelvic limb weakness rapidly progresses to peripheral nervous system. Polyneuropathy refers to tetraparesis. Response to pain is often involvement of several nerves exaggerated II. Clinical signs typically include weakness and muscle c. Differential diagnosis includes botulism, tick atrophy. Self-mutilation may occur paralysis, myasthenia gravis, and protozoal III. Principles of diagnosis infection A. History and physical examination are most d. Treat with supportive care important F. Idiopathic disorders can affect any breed of B. Elevations of creatine phosphokinase, lactic dog or cat, causing insidious or acute onset of dehydrogenase, and aspartate aminotransferase weakness suggest a muscle disorder G. Traumatic injury C. Needle EMG can record activity in skeletal muscle 1. Common cause of weakness D. Muscle and nerve biopsies may help with the 2. Prognosis is better when the nerve is injured diagnosis close to the muscle it innervates IV. Treatment is typically supportive 3. Brachial plexus avulsion is common in road A. Prevent decubital ulcer formation traffic injuries or when animals jump from B. Prevent tendon and muscle contraction with moving vehicles physical therapy a. Treat with physical therapy to prevent mus- C. Maintain nutrition cle contraction. Prevent abrasions D. Make sure that there is complete evacuation of b. Regrowth of injured nerves may take the urinary bladder months. Amputation should be considered V. Specific peripheral nerve disorders if there is self-mutilation or little return to A. Anomalous, inherited, and congenital disorders function after 6 months 1. These disorders are noted prior to 1 year of age, and diagnosis is based on clinical signs MUSCLE AND NEUROMUSCULAR and signalment. An inherited or congenital dis- JUNCTION DISORDERS order should be suspected in any young dog or cat with signs of peripheral nerve disease I. Causes 2. Specific breeds that may be affected by recog- A. Hereditary disorders nized inherited disorders include German 1. Canine dystrophin-deficient muscular dystrophy shepherd dogs, Tibetan mastiffs, boxers, point- a. Similar to Duchenne muscular dystrophy of ers, longhaired dachshunds, Brittanys, rottwei- humans lers, Leonberger dogs, Alaskan malamutes, dal- b. Most commonly in males matians, golden retrievers, Birman cats, and c. Breeds predisposed include golden re- Norwegian Forest cats triever, Irish terrier, Samoyed, rottweiler, 3. Globoid cell leukodystrophy is caused by a de- Japanese spitz, and Labrador retriever ficiency of -galactocerebrosidase d. Evident by about 10 to 12 weeks of age, and 4. Glycogen storage disease in Norwegian Forest clinical signs include stunted growth, weak- cats occurs due to a deficiency in a glycogen ness, muscle atrophy branching enzyme e. Serum creatine kinase levels are markedly 5. Other storage diseases affecting peripheral elevated nerves include hyperchylomicronemia in cats, 2. Feline dystrophin-deficient muscular dystrophy Niemann-Pick disease, and GM2-gangliosidosis a. Lethal condition of young male cats B. Metabolic and endocrine disorders b. Clinical signs include skeletal muscle hyper- 1. Diabetes mellitus can cause limb weakness trophy, glossal hypertrophy and dysfunc- (more pronounced in the pelvic limbs) tion, and excess salivation 2. Hypothyroidism can be associated with c. Serum creatine kinase levels are markedly weakness, muscle wasting, and reduced spinal elevated, and there is lack of dystrophin in reflexes skeletal muscles C. Nutritional disorders are uncommon. Vitamin B 3. Other muscular dystrophies deficiency can induce neuropathy a. Muscular dystrophy with merosin D. Neoplastic disorders (laminin -2) deficiency has been reported 1. Nerve sheath tumors and lymphoma are most in a mixed-breed dog and in several cats. common, producing signs of a neuropathy Affected animals are young, with muscle 2. Insulinomas have also been associated with weakness and atrophy. Serum creatine neuropathy kinase is moderately elevated 288 SECTION II SMALL ANIMAL b. Muscular dystrophy with sarcoglycan defi- (1) Common in dogs, also occurs in cats ciency has been identified in a few breeds (2) Associated with autoantibodies against of dog. Serum creatine kinase concentra- nicotinic nicotinic acetylcholine recep- tion is markedly elevated, and there is an tors on postsynaptic membrane of neu- absence of sarcoglycan in skeletal muscle romuscular junction. This leads to im- 4. Hereditary myopathy of Labrador retrievers paired neuromuscular transmission and a. Autosomal recessive weakness b. Clinical signs include progressive muscle b. Masticatory muscle myositis selectively weakness, exercise intolerance, and gait affects the masticatory muscles abnormalities c. Extraocular muscle myositis is localized to c. Varying morphologic features have been extraocular muscles noted on muscle biopsies d. Polymyositis 5. Central core-like myopathy (1) Generalized inflammatory myopathy as a. Great Danes a result of cell-mediated immunity b. Excitement causes episodes of body trem- (2) Associated with malignancies, systemic ors and collapse lupus erythematosus, and immune- 6. Nemaline rod myopathy has been reported in mediated arthritis several cats and one dog. Characterized by 2. Metabolic disoders mild weakness, tremors, reluctance to move, a. Lipid storage myopathy and progressive muscle atrophy. Nemaline b. Malignant hyperthermia syndrome rods are present within myofibers c. Electrolyte imbalances, particularly potas- 7. Familial canine dermatomyositis sium and calcium a. Collies and Shetland sheepdogs. Autoso- d. Endocrine disorders such as hypothyroid- mal dominant in collies ism, hyperadrenocorticism, and hypoadre- b. Severe dermatitis on face, ears, extremities nocorticism over bony prominences, and tail tip e. Neoplastic disorders. Thymoma has been c. Inflammatory myopathy of masticatory associated with myasthenia gravis and muscles and muscles distal to elbow and polymyositis stifle f. Parasitic disorders (especially Neospora 8. Glycogen storage disorders caninum, and Ehrlichia canis) a. Rare g. Viral disorders (feline calicivirus, FIV) b. Muscle weakness is minor compared with h. Toxic or drug-induced disorders (neurotox- other clinical symptoms ins from ticks, Clostridium botulinum toxin, 9. Myotonia congenital organophosphate insecticides) a. Chow chow and miniature schnauzers; i. Ischemic disorders (thromboembolism and also cats vascular occlusion) b. Clinical signs include difficulty rising, mus- II. Clinical signs cle stiffness, bunny-hopping gait; affects A. Muscular weakness is the most common clinical puppies sign c. DNA test available B. Gait abnormalities 10. Mitochondrial myopathy C. Paralysis or paresis a. Clumber spaniels and Sussex spaniels with D. Localized signs such as regurgitation, dysphagia, a pyruvate dehydrogenase deficiency dysphonia, dyspnea b. Exercise intolerance with metabolic acido- III. Diagnosis sis, excessive elevation of lactic acid and A. History and physical examination are most impor- pyruvate tant. Proprioception and pain are usually intact in 11. Hypertonicity syndrome motor unit disorders a. Identified in Cavalier King Charles spaniel, B. Perform routine laboratory tests to identify under- English springer spaniel, soft-coated whea- lying disorders. Other tests such as lactate, thyroid ton terrier, and border terrier hormone concentrations, adrenal function tests, b. In Cavalier King Charles spaniels, clinical ANA titer, and serologic tests may be indicated signs appear between 3 to 7 months of D. Specialized tests such as edrophonium chloride age. Exercise or excitement precipitate challenge test, electrodiagnostics, muscle biopsy, pelvic and thoracic limb hypertonicity and carnitine quantification may be helpful c. Treat with clonazepam E. Radiography should be performed to rule out un- 12. Congenital myasthenia gravis derlying disorders such as megaesophagus, neo- a. Jack Russell (Parson Russell) terriers, plasia, aspiration pneumonia, thymoma English springer spaniels, and smooth fox IV. Treatment terriers A. Generalized myasthenia gravis b. Deficiency in muscle acetylcholine receptor 1. Anticholinesterase drugs are most commonly B. Acquired neuromuscular disorders used for treatment 1. Autoimmune disorders 2. Corticosteroids are used if there is a negative a. Acquired myasthenia gravis response to edrophonium chloride testing, and  CHAPTER 19 Nervous System Disorders 289 anticholinesterase treatment does not improve Supplemental Reading muscle strength 3. Azothioprine or cyclophosphamide can be Fenner WR, March PA. Diagnostic approach to neurologic used for refractory cases disease. In Birchard SJ, Sherding RG, eds. Manual of 4. Management megaesophagus by feeding Small Animal Practice, 3rd ed. St Louis, 2006, food and water with the animal in an upright Saunders, pp. 1233-1248. position. Have animal remain upright for Luttgen PJ, Cudden PA. Disorders of the spinal cord. In at least 10 minutes after feeding. Anticholin- Birchard SJ, Sherding RG, eds. Manual of Small Animal esterase drugs should be given 1 hour before Practice, 3rd ed. St Louis, 2006, Saunders, pp. 1294-1303. feeding March PA. Diseases of the brain and cranial nerves. In B. Focal myasthenia gravis Birchard SJ, Sherding RG, eds. Manual of Small Animal 1. Manage by elevating food and water Practice, 3rd ed. St Louis, 2006, Saunders, pp. 1249-1276. 2. Lower doses of anticholinesterase drugs may Podell M. Seizures. In Birchard SJ, Sherding RG, eds. control regurgitation Manual of Small Animal Practice, 3rd ed. St Louis, 2006, C. Immune-mediated inflammatory myopathies Saunders, pp. 1277-1293. 1. Masticatory muscle myositis: Treat with Shell LG. Peripheral nerve disorders. In Birchard SJ, immunosuppressive doses of Sherding RG, eds. Manual of Small Animal Practice, glucocorticoids 3rd ed. St Louis, 2006, Saunders, pp. 1304-1314. 2. Polymyositis: Treat with immunosuppressive Shelton GD. Disorders of muscle and neuromuscular doses of glucocorticoids junction. In Birchard SJ, Sherding RG, eds. Manual of 3. Lipid storage myopathy: Treat with Small Animal Practice, 3rd ed. St Louis, 2006, L-carnitine Saunders, pp. 1315-1324.