Diseases of the Bovine Central Nervous System Karl Kersting DVM, MS Food Animal Hospital, College of Veterinary Medicine, Iowa State University Ames, IA 50011 I. Diseases of the Spinal Cord - LMN signs to hind limbs, tail, bladder, A. Lower Motor Neuron (LMN) Disease anal sphincter 1. Clinical Signs 2. Diseases - Paralysis -Trauma - Areflexia/hyporeflexia - Breeding/riding injuries - Decreased muscle tone - Forced fetal extraction ( cow or calf) - Early and severe muscle atrophy - Head gate injuries - Anesthesia to specific myotomes - Parasitic 2. Diseases - Death of cattle grubs in the spinal cord - Botulism - Spinal abscesses - Organophosphate toxicity - Spondylitis (bulls) - Tick paralysis - Lymphosarcoma -Trauma - Rabies - Injection sites - Compartmental syndrome II. Diseases of the Brainstem B. Upper Motor Neuron (UMN) Disease A. Clinical signs 1. Clinical Signs 1. Cranial nerve deficits - Nuclei of Cranial nerves - Paresis - Paralysis (loss of voluntary III - XII are in the brain stem. Frequently mul­ 0 "'O movements) tiple cranial nerves involved with clinical deficit (D ~ - Normal/hyperreflexia on same side as lesion. ~ ('.") - Normal - increased muscle tone 2. Ataxia and paresis (D 00 - Late muscle atrophy 3. Depression - damage to reticular activating sys­ 00 - Decreased superficial and deep pain tem 0........ 00 ,-+- - Decreased proprioception '"i 2. Diseases B. Diseases ~ ~...... -Tetanus 1. Listeriosis 0 - Spastic Paresis 2. Thromboembolic Meningoencephalitis p - Spastic Syndrome (TEME) - Nervous Ergotism 3. Sporadic Bovine Encephalamyelitis - Dallis/Bermuda Grass Staggers (SBE) 4. Middle Ear Infections C. Mixed Spinal Cord Disease 5. Homer's Syndrome 1. Clinical Signs 6. Rabies a. Lesion of Cl - CS - UMN signs to all limbs III. Diseases of the Cerebellum - Tetra or hemiparesis - Rear limbs usually more affected than fore- A. Clinical Signs limbs 1. Ataxia b. Lesion of C6 - T2 2. Bilateral dysmetria/hypermetria - UMN signs to hind limbs 3. Base wide stance - LMN signs to fore limbs 4. Head tremor c. Lesion of T3 - L3 5. Opisthotonus - UMN signs to hind limbs 6. Nystagmus - LMN signs to segmental spinal muscles 7. NO paresis - May localize by panniculus testing d. Lesion of 1A - Cy4 B. Diseases 28 THE BOVINE PROCEEDINGS-No. 22 1. Cerebellar abiotrophy -Tumors Holsteins, Herefords 6. Vascular damage 2. Cerebellar Hypoplasia - Secondary to toxemia/septicemia, a. Inherited e.g. E. coli mastitis Herefords, Guernseys, Holsteins, Short­ 7. Hydrocephalus/Hydranencephaly horns, Ayrshires - Congenital b. Infection - Toxic - Lupines In-utero BVD infections, rarely - Infectious - Bluetongue blue tongue Classification of Bovine CNS Diseases by Age 3. Inherited Cerebellar Ataxia · Calves Youngstock Adults Jerseys, Shorthorns, Holsteins (0-2 months) (2 months-2 years) (Over 2 years) 4. Mannosidosis - cerebellar signs predominate Angus, Murray Grey, Galloway Spinal Cord Disease 5. Progressive Ataxia Trauma--------------------. Brown Swiss (Weavers), Charolais Tetanus------------------­ 6. Hereditary neuraxial edema Abscess------------------­ Herefords Spastic Paresis--------- Tick Paralysis --------- IV. Diseases of the Cerebrum and Thalamus Grubs------------ ( Often cerebrum and thalamus affected simutaneously Ergotism----------­ due to close proximity). .--------Botulism ------------.. Spastic Syndrome A. Clinical Signs Neploasia 1. Abnormal behavior 2. Depression/somnolence Brain Stem Disease 3. Coma 4. Head pressing Rabies-------------------► 0 "'O 5. Convulsions Homer's Syndrome --------------~ (D ~ 6. Ataxia Otitis Media-------------------.. ~ SBE---------------- (") 7. Opisthotonus (D 00 8. Visual deficit (cortical blindness) -------Listeriosis ----------- 00 ------TEME ---------- 0........ 00 Cerebellar Disease ,-+. B. Diseases '"i 1. Toxic ~ -Lead Cerebellar Hypoplasia ~...... 0 - Organophosphates Cerebellar Abiotrophy p - Salt poisoning Mannosidosis --------­ - Hepatoencephalopathy Inherited Cerebellar Ataxia---- 2. Metabolic N euraxial Edema - Polioencephalomalacia Progressive Ataxia - Nervous ketosis - Vitamin A deficiency Cerebral/Thalamic Disease 3. Infectious - Bacterial encephalitis/meningitis Hydro/Hydroanencephalies - Neonatal septicemia IBR - Navel ill Polio------------. - Frontal sinusitis Vitamin A deficiency - Thromboembolic Meningoencephalitis Salt Poisoning--------...... - Malignant Catarrhal Fever MCF----------- - Rabies N ervous Ketosis -IBR Bacterial Meningitis/Encephalitis -----------l► - Pseudorabies Rabies--------------------► 4. Trauma Pseudorabies ------------------► 5. Space occupying lesions Hepatoencephalopathy ------------► - Abscesses Lead---------------------. Organophosphates --------------- APRIL, 1990 29 Diagonsis and Treatment of Selected Bovine CNS Diseases - valium (.05 - .1 mg/lb. IV) - phenothiazine tranquilizers A. General Therapy for Cord Trauma - muscle relaxants 1. DMSO - 1 gm/kg as 50% solution - slow IV - Dantrolene ( 1 mg/lb. p.o. bid.) 2. Prednisone - 1-2 mg/lb. daily - Wound debridement - uterine irrigation 3. Dexamethasone - 2-5 mg/lb. IV - once - use of H202 to provide oxygen - Nursing care B. Spinal Lymphosarcoma - quiet, dark surrounding 1. Diagnosis - forced feeding and watering - Premortem demonstration of other sites of - parenteral neoplasia - use of rumen fistula -(lymph nodes, retro-orbital, etc.) - Age of cow and history of progressive rear limb E. Botulism function. 1. Diagnosis - CBC usually normal, only 15% leukemia - Clinical signs - BLY + titer is not confirmatory, but a negative - dysphagia titer usually rules out disease - bloating - Postmortem confirmation by necropsy - flaccid paralysis - downers 2. Treatment - respiratory arrest - Terminal disease - may see herd outbreaks - Current interest in chemotherapy - may resemble lead toxicity, rabies or milk fever - Corticosteroids - Confirmed by isolation of botulism toxin from - Asparaginase (Elspar) GI contents or feed - Electromyography will demonstrate neuro­ C. Spinal Hypoderma muscular blockade 1. Diagnosis - History of pica in cattle - History of recent pour-on or ivermectin 2. Treatment 0 "'O therapy in late fall or winter - Antitoxin - CDC & University of Pennsylvania (D - Alert, "dog-sitters" - Expensive ~ ~ - Acute onset - Supportive care (") (D - CSF: increased protein, neutropils, eosinophils 00 - Anticholinesterases (neostigmine) 00 2. Treatment - provide transient improvenent 0........ 00 - General therapy for cord trauma ,-+- - Increased mortality '"i 3. Prognosis - poor ~ F. Organophosphate Toxicity ~...... 0 D. Tetanus 1. Diagnosis p 1. Diagnosis - Clinical signs - Based solely on clinical signs: - muscarinic - stiff gait - tetany -salivation - sardonic smile -lacrimation - elevated tail head -sweating - erect ears -diarrhea - prolapsed 3rd eyelid -colic - History of recent injury, surgery or -miosis parturition -dyspnea (bronchospasm) 2. Treatment - cattle are rewarding patients -nicotinic - Penicillin -skeletal muscle tetany followed by paresis - Antitoxin -central - is of limited value in neutralizing preexisting -hyperesthesia toxin -stupor - massive doses - 300,000 units q 12 h for 3 -convulsions are rare treatments -History of exposure - intrathecal administration of 50,000 u -Test for cholinesterase activity in blood or tissue - Sedation (delta pH test) - chloral hydrate (1 oz./500 lb. p.o.) -blood cholinesterase levels of 25% or less of 30 THE BOVINE PROCEEDINGS-No. 22 normal are diagnostic I. Homer's Syndrome 2. Treatment 1. Diagnosis - Atropine - .25 mg/lb. - repeat as needed - Clinical signs - 2-PAM - 10 mg/lb. - ipsilateral miosis - Activated charcoal for oral exposure - ipsilateral ptosis - Shampoo for dermal exposure - ipsilateral dry muzzle - ipsilateral facial warmth G. Listeriosis - Concurrent nasal carcinoma 1. Diagnosis - History of balling gun injury or perivascular - Clinical signs accident - stupor 2. Treatment - head pressing - Symptomatic - circling - unilateral facial paralysis ( drooped lip & ear, dry J. Otitis media eye) 1. Diagnosis - head deviated, not necessarily tilted - Clinical signs - fever + /- - head tilt, +/-aural discharge - History of : - circling - silage of poor quality - ataxia - recent freeze - febrile - flooding - History of: -CSF - recent respiratory disease (Pateurella sp. a - increased protein frequent isolate) - increased WBC, mainly mononuclear cells - ear sucking in calves - Postmortem 2. Treatment - Brainstem microabscesses - Antibiotics - Organism notoriously difficult to culture - Systemic 0 "'O 2. Treatment -Topical and DMSO (D ~ - oxytetracycline - 5 mg/lb. IV - Antiinflammatory therapy ~ - penicillin - 25,000-30,000 u/lb. (") - Banamine (D 00 -Aspirin 00 H. Thromboembolic Meningoencephalitis - Corticosteroids 0........ 00 ,-+- 1. Diagnosis '"i - Clinical signs K. Polioencephalomalacia ~ ~...... - acute onset } 1. Diagnosis 0 - recumbency & coma similar to a stroke - Clinical Signs p - paresis and ataxia - usually less than 1 year old - febrile - ataxia - nystagmus - head pressing - Fundic exam - cortical blindness (pupils respond to light) - retinal hemorrhage and exudate -coma -CSF - convulsions - increased protein - Response to thiamine - increased WBC, mainly neutrophils - Decreased erythrocyte transketolase activi1ty - Concurrent synovitis and lameness, pneumonia - Increased blood pyruvate levels or CNS disease in other animals -CSF - Postmortem - normal to increased protein - Hemorrhagic infarcts of CNS -especially - markedly increased pressure brainstem and cerebral cortex - Postmortem 2. Treatment - Polioencephalomalacia -