Neurology (Key concepts only hopefully) Flashcards
History questions for neuro
- Travel (patient and herdmates)
- Environment/possible toxin/feed
- Trauma
- Herd situation
- Vaccines
Gait localization
- Just make sure you know this chart
What is the blind fold test assessing?
- Vestibular nerve
Glossopharyngeal assessment
- Motor to pharynx and palate
- Look for dysphagia by watching them swallow and check for laryngeal hemiplegia
Vagus assessment
- Signs of laryngeal dysfunction
- Slap test
Hypoglossal assessment
- Motor to the tongue, so check for strength on each side
What are the four main gait abnormalities?
- Ataxia
- Paresis
- Spasticity
- Dysmetria
Gait assessment scoring
0 = Normal 1 = Difficult to detect, very subtle 2 = Deficits detectable with maneuvers but difficult to detect when going in a straight line 3 = Deficits obvious in a straight line 4 = stumbles, at risk for falling 5 = recumbent, unable to rise
Sacral nerve assessment
- Urination
- Defecation
Peripheral vestibular disease
- Poll towards the lesion
- Horizontal or rotary nystagmus
- Fast phase AWAY from the lesion
Central vestibular disease
- Poll may be away from the lesion
- Nystagmus can be any type
- If you see a vertical nystagmus, you should be VERY suspicious
Other signs of vestibular disease
- Head tilt,
- Reluctance to move
- Nystagmus
- Circling (towards lesion)
- Leaning (lesion side down)
- Falling
- Recumbency
- Asymmetric ataxia
Peripheral vestibular disease causing things
- Temporohyoid bone osteoarthropathy
- Otitis/media/interna
- Idiopathic labyrinthitis
Central vestibular disease causing things
- WEE/EEE
- WNV
- EHM
- Space occupying lesions
- Parasites
Lesions that can cause both
- EPM
- Trauma
Temporohyoid osteoarthropathy signs
- Early: reluctance to chew, head shaking, ear rubbing, facial hyperesthesia, reluctance to take the bit
- Late: Facial nerve paralysis and signs of peripheral vestibular disease (Sudden onset; asymmetrical)
Diagnosis of THO
- Endoscopy (GP endoscopy)
- Radiographs (hard to interpret)
- CT (good, but have to recover the horse)
Treatment and prognosis of THO
- Return to athleticism tends to be better with surgical correction over medial correction
- Long term survival better with surgical management
Supportive care for THO
- Lubricate their eyes
- NG tube for feeding or drinking if not doing that
- anti-inflammatory medications
Cerebellar abiotrophy - who gets it?
- Arabian foals
What is the pattern of inheritance for CA?
- Autosomal recessive
Clinical signs of CA
- 6 weeks - 4 months old when showing signs
- Intention tremors
- Base-wide stance
- Visual but lack a menace response
Cervical Vertebral Stenotic Myelopathy - who gets type 1 vs type 2?
- Type 1 is big and young
- Type 2 is older and arthritic
CVSM clinical signs
- Normal physical exam
- Normal mentation
- Normal CN exam
- Ataxia in all four limbs, hind limbs worse than the front
Diagnosis of CVSM
- Radiographs (use intervetebral ratios)
- Myelogram (more expensive, requires general anesthesia, gold standard, horse may wake up 1-2 grades worse)
Treatment for CVSM
- “Basket” surgery (will likely only improve 1-2 grades)
- Time and decreased caloric intake
- Retirement
- Euthanasia
Equine Protozoal Myeloencephalitis Pathophysiology
- Sarcocystis neurona (protozoa) ingested by the horse after ingesting opossum feces
- Travels to the CNS and does whatever signs it wants
Diagnostics for EPM
- Serology (only tells you exposure in some areas; upwards of 90% of horses have been exposed)
- CSF antibody titers are gold standard (but if you have blood in the CSF, can cause a positive, so would want to follow up with CSF to serum ratios)
- Necropsy
Treatment for EPM
- Sulfadiazine/pyrimethamine
- Ponazuril
- Diclazuril
Supportively can add NSAIDs, +/- steroids, Vitamin E, Corn oil with Marquis
Prognosis for EPM
- 60% of horses will improve by 1 grade
Equine Herpes Myeloencephalomalacia Pathophysiology
- Microthromboses of the spinal cord in some horses
- Vaccination is NOT protective
Clinical signs of EHM**
- Tetraparesis*****
- Fecal and urinary retention**
- Ataxia
- May have a fever
- Incontinence
- Changes in mentation
- Ocular lesions
Biosecurity for EHM
- CONTACT your state vet
- nasal swabs, buff coats from affected horses
- STOP TRAFFIC AT THE BARN
- BID rectal temperatures
- Quarantine if necessary
What % of horses develop EHM? What is mortality rate?
- 50% of exposed horses will develop disease
- 50% mortality rate
Treatment for EHM
- Supportive care
- Sling them
Rabies Pathophysiology
- Local replication of rabies in the muscle
- Binds to ACh receptors and travels to the CNS via peripheral nerves
- Replicates in the brain and goes down to salivary glands
Wildlife reservoirs
- Foxes, skunks, bats, raccoons
Clinical signs of Rabies
- wide variety of clinical manifestations
- Any horse with intracranial signs
- Dysphagia, weakness
- Paresthesia
- Increased salivation
Treatment for Rabies
- NONE
- submit all suspects post-mortem
- Contact state vet
EEE and WEE vectors
- Mosquitoes
- WEE may include ticks, assassin bug, and cliff swallow bug
- EEE may include nasal secretions
Peak EEE and WEE seasons
- June-November
EEE and WEE survival
- Sylvantic hosts
Mortality of WEE vs EEE
- WEE is 25-50%
- EEE is 50-75%
Initial clinical signs of WEE and EEE
- Mild fever, stiffness
- 1-3 weeks later progresses to mild fever and obtundation
- Further progresses to cerebrothalmic signs, compulsive walking, hyperesthesia
- Recumbency and death eventually
Diagnosis of WEE and EEE*****
- IgM ELISA (this is how you differentiate from vaccination
- CSF shows lymphocytic pleocytosis
- Elevated TP
Post mortem signs of WEE and EEE
- Often normal grossly
- May see vascular changes
- Brain IHC, RT PCR, IFA, ELISA, etc.
Treatment for WEE and EEE
- Nonspecific
- Hydration
- Nutrition
- Ensure urination, defecation
- NSAIDs
