EIM 11 Neuro Flashcards
Age predilection for grass sickness is
young, mature, 2-7yo
Risk factors for grass sickness are
grazing age 2-7 time of year - spring and early summer movement to a new property/paddock increased stocking density low serum anti-body titers against Clostridium botulinum toxins
Neuroborreliosis CS
behavioural changes, hyperesthesia, gait abnormalities, cranial nerve deficits, neck stiffness, muscle atrophy/fasciculations
Head shaking is more likely to be seen in
spring/early summer months
Geldings, thoroughbreds, younger adults (7-9yo)
The most common secondary neoplastic condition affecting the CNS of horses:
lymphoma
Leukoencephalomalacia in horses is caused by:
MOLDY CORN
Caused by ingestion of the mycotoxin fumonisin B1, a metabolite of Fusarium moniliforme
Gross - liquefactive necrosis of cerebral hemispheres
Nigropallidal Encephalomalacia is caused by:
yellow star thistle / Russian knapweed
chronic, long-term ingestion
Bilateral softening and necrosis in areas of the globus pallidus and substantia nigra
Horner’s syndrome is a collection of clinical signs associated with dysfunction of the
sympathetic nerve supply to the head and neck
Note the ’triad’ = ipsilateral ptosis, third eyelid prolapse and miosis
Third eyelid prolapse is due to enophthalmus
Sweating along the side of the face
Normal vestibular nystagmus is:
moving head side to side, eyes move slowly in the opposite direction
8th cranial nerve unilateral peripheral injury
Head tilt (poll deviation) towards the side of the lesion Horizontal nystagmus, fast phase away from side of the lesion
Guttural pouch disease can damage what near structures
Cranial nerve 9 (glossopharyngeal)
A branch of cranial nerve 10 (vagus)
Injury to the internal carotid nerve, which contains postganglionic sympathetic fibers … resulting in Horner syndrome
Which WBC type is most common in normal CSF (70-90%)
Small mononuclear cells 70-90%
Large mononuclear cells 10-30% - increase #s in axonal degeneration
Rarely may see a neutrophil – increase #s with inflammation (including meningitis, encephalomyelitis, parasitism)
Eosinophils only occasionally if there’s parasitism or other severe inflammatory process
CSF protein concentration
higher in LS than AO fluid
NORMAL range 20-124mg/dL
EHV-1 causes
mainly causes abortions, early foal deaths, and respiratory disease in young horses, and uncommonly causes myeloencephalopathy
EHV-4 causes
causes clinical disease of the respiratory tract, sporadic abortions, and has been implicated in isolated cases of myeloencephalopathy
alpha herpes viruses
EHV-1, 4, 3
gamma herpes viruses
EHV-2, 5
neurologic dz and herpes
The majority of neurologic EHV infections are infections in individuals who have have exposed before
Affected horses have higher titres at the onset of disease
The acute onset signs are a result of vasculitis, Immune complexes / type III hypersensitivity reactions
The most infectious neurotropic strains are frequently isolated from brain tissue on PM
Almost all horses are febrile at the onset of neurologic disease
IN CONTACT HORSES TO A HERPES CASE SHOULD BE ISOLATED FOR:
30 days in their current location (or until foaling if mares)
Traffic of horses and human beings on the premises should be minimized, and movement of horses onto and off of the infected premises should be suspended until at least 3 weeks after resolution of acute signs in the last clinical case or until tests show that virus transmission is no longer occurring
EMND affects
A) motor neurons in the spinal cord ventral horn cells
B) the brain stem
C) lower motor neurons
HOW LONG DOES IT TAKE TO INCREASE PLASMA VITAMIN E WITH SUPPLEMENTATION?
5000-7000 IU/horse/day for 6 weeks
goal is 2ug/ml or greater plasma conc
Horses sleep how much?
3-4 hours per day
split up into 6 phases of rest and sleep through out the night
Can horses get rem sleep in sternal?
yes if they support their head – loss of muscle tone p 608
REM sleep should compromise 15% of total sleep
If they enter while standing due to sleep deprivation they may fall
WHAT ARE GOALS OF TBI TREATMENT?
A) Delivery of oxygen to undamaged brain tissues
B) reduction of intracranial pressure
C) maintaining blood glucose concentrations of 120-140mg/dl
E) combat inflammation with NSAIDS, DMSO, Vit E
WHICH REGION OF SC INJURY MAY CAUSE “DOG SITTING”?
thoracolumbar
Which is not one of the sites that neuron 1 (first-order neuron) of the vestibular system receives impulses from?
optic nerve
T/F The cristae record movement of the head.
true
Turning the head to the left results in a horizontal nystagmus with fast phase to the ____. The accompanying slow phase is in a direction _____ body motion and allows the eyes to fix on a stationary image.
left
opposite to
Because of its proximity to the vestibular nerve where they are associated closely with the petrous temporal bone and enter the internal auditory meatus together, which nerve is commonly affected along with the vestibular nerve by a single disease process?
CN VII
With peripheral vestibular disease, there is ventral deviation of the poll
towards the affected side
With peripheral vestibular disease, there is circling
towards the lesion
With peripheral vestibular disease, there is extensor
hypotonia ipsilateral to the lesion and mild hypertonia of the extensor muscles on the contralateral side.
What distinguishes central from peripheral vestibular disease
proprioceptive deficits
Issues in what two anatomical areas can cause pathologic nystagmus?
vestibular
cerebellum
Which is believed to be the most common etiology of botulism in foals?
toxin secretion by ingested spores
Occipitoatlantoaxial malformation, cerebellar abiotrophy, and epilepsy have all been described in…?
arabian foals
Which of the following medications should be used to treat status epilepticus?
pentobarbital 2-10 mg/kg iv once
The proposed mechanism of action for IV magnesium sulfate in the treatment of HIE is…
NDMA-receptor antagonist effects, cell wall stabilization, and inhibition of free radical production
EMND clinical signs
muscle atrophy, muscle twitching, weakness, weight loss, and sweating. Affected horses may carry their heads lower than normal and lie down for longer periods
EMND diagnosis
sacrocaudalis dorsalis medialis biopsy
eNAD / EDM clinical signs
ataxia, usually onset around 6 mos
eNAD / EDM diagnosis
postmortem
biomarker of axon damage, phosphorylated neurofilament heavy subunit (pNF-H,) in serum and/or cerebrospinal fluid (CSF)
Cause of EMND
typically occurs in older horses >16 years old that have been vitamin E deficient for >18 months