Neurology (Key concepts only hopefully) Flashcards
1
Q
History questions for neuro
A
- Travel (patient and herdmates)
- Environment/possible toxin/feed
- Trauma
- Herd situation
- Vaccines
2
Q
Gait localization
A
- Just make sure you know this chart
3
Q
What is the blind fold test assessing?
A
- Vestibular nerve
4
Q
Glossopharyngeal assessment
A
- Motor to pharynx and palate
- Look for dysphagia by watching them swallow and check for laryngeal hemiplegia
5
Q
Vagus assessment
A
- Signs of laryngeal dysfunction
- Slap test
6
Q
Hypoglossal assessment
A
- Motor to the tongue, so check for strength on each side
7
Q
What are the four main gait abnormalities?
A
- Ataxia
- Paresis
- Spasticity
- Dysmetria
8
Q
Gait assessment scoring
A
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
9
Q
Sacral nerve assessment
A
- Urination
- Defecation
10
Q
Peripheral vestibular disease
A
- Poll towards the lesion
- Horizontal or rotary nystagmus
- Fast phase AWAY from the lesion
11
Q
Central vestibular disease
A
- Poll may be away from the lesion
- Nystagmus can be any type
- If you see a vertical nystagmus, you should be VERY suspicious
12
Q
Other signs of vestibular disease
A
- Head tilt,
- Reluctance to move
- Nystagmus
- Circling (towards lesion)
- Leaning (lesion side down)
- Falling
- Recumbency
- Asymmetric ataxia
13
Q
Peripheral vestibular disease causing things
A
- Temporohyoid bone osteoarthropathy
- Otitis/media/interna
- Idiopathic labyrinthitis
14
Q
Central vestibular disease causing things
A
- WEE/EEE
- WNV
- EHM
- Space occupying lesions
- Parasites
15
Q
Lesions that can cause both
A
- EPM
- Trauma
16
Q
Temporohyoid osteoarthropathy signs
A
- 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)
17
Q
Diagnosis of THO
A
- Endoscopy (GP endoscopy)
- Radiographs (hard to interpret)
- CT (good, but have to recover the horse)
18
Q
Treatment and prognosis of THO
A
- Return to athleticism tends to be better with surgical correction over medial correction
- Long term survival better with surgical management
19
Q
Supportive care for THO
A
- Lubricate their eyes
- NG tube for feeding or drinking if not doing that
- anti-inflammatory medications
20
Q
Cerebellar abiotrophy - who gets it?
A
- Arabian foals
21
Q
What is the pattern of inheritance for CA?
A
- Autosomal recessive
22
Q
Clinical signs of CA
A
- 6 weeks - 4 months old when showing signs
- Intention tremors
- Base-wide stance
- Visual but lack a menace response
23
Q
Cervical Vertebral Stenotic Myelopathy - who gets type 1 vs type 2?
A
- Type 1 is big and young
- Type 2 is older and arthritic
24
Q
CVSM clinical signs
A
- Normal physical exam
- Normal mentation
- Normal CN exam
- Ataxia in all four limbs, hind limbs worse than the front
25
Diagnosis of CVSM
- Radiographs (use intervetebral ratios)
| - Myelogram (more expensive, requires general anesthesia, gold standard, horse may wake up 1-2 grades worse)
26
Treatment for CVSM
- "Basket" surgery (will likely only improve 1-2 grades)
- Time and decreased caloric intake
- Retirement
- Euthanasia
27
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
28
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
29
Treatment for EPM
- Sulfadiazine/pyrimethamine
- Ponazuril
- Diclazuril
Supportively can add NSAIDs, +/- steroids, Vitamin E, Corn oil with Marquis
30
Prognosis for EPM
- 60% of horses will improve by 1 grade
31
Equine Herpes Myeloencephalomalacia Pathophysiology
- Microthromboses of the spinal cord in some horses
| - Vaccination is NOT protective
32
Clinical signs of EHM********
- Tetraparesis*****
- Fecal and urinary retention****
- Ataxia
- May have a fever
- Incontinence
- Changes in mentation
- Ocular lesions
33
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
34
What % of horses develop EHM? What is mortality rate?
- 50% of exposed horses will develop disease
| - 50% mortality rate
35
Treatment for EHM
- Supportive care
| - Sling them
36
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
37
Wildlife reservoirs
- Foxes, skunks, bats, raccoons
38
Clinical signs of Rabies
- wide variety of clinical manifestations
- Any horse with intracranial signs
- Dysphagia, weakness
- Paresthesia
- Increased salivation
39
Treatment for Rabies
- NONE
- submit all suspects post-mortem
- Contact state vet
40
EEE and WEE vectors
- Mosquitoes
- WEE may include ticks, assassin bug, and cliff swallow bug
- EEE may include nasal secretions
41
Peak EEE and WEE seasons
- June-November
42
EEE and WEE survival
- Sylvantic hosts
43
Mortality of WEE vs EEE
- WEE is 25-50%
| - EEE is 50-75%
44
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
45
Diagnosis of WEE and EEE*****
- IgM ELISA (this is how you differentiate from vaccination
- CSF shows lymphocytic pleocytosis
- Elevated TP
46
Post mortem signs of WEE and EEE
- Often normal grossly
- May see vascular changes
- Brain IHC, RT PCR, IFA, ELISA, etc.
47
Treatment for WEE and EEE
- Nonspecific
- Hydration
- Nutrition
- Ensure urination, defecation
- NSAIDs
48
Prevention of EEE and WEE******
- 2 vaccine series followed by 6month - 1 year boosters
- Mosquito control
- Want to recommend that they get their vaccinations completed
49
WNV Reservoir host
- birds and wild vertebrates
50
Clinical signs of WNV
- Weakness
- Ataxia
- Altered mentation
- Muscle fasciculations***
- CN deficits
- Recumbency
- Paralysis of 1 or more limbs
51
WNV recrudescence and prognosis
- 30% of horses can recrudesce (not correlated with a worse prognosis)
- Limb paralysis is a worse prognosis
- 30% mortality rate
52
Diagnosis of WNV
- IgM capture ELISA
| - CSF --> lymphocytic pleocytosis, elevated protein
53
Treatment of WNV
- Non-specific supportive care
- Slings can help
- Nutrition, hydration, urination, defecation
54
Prevention of WNV
- 2 vax series followed by 4 month-1 year boosters
| - Mosquito control
55
Equine leukoencephalomalacia cause
- Mycotoxin fumosin B1 (chronic ingestion)
| - Moldy corn (during GROWTH, not storage)
56
Signs of equine leukoencephalomalacia
- Incoordination
- Aimless walking
- Intermittent anorexia
- Obtundation
- CNS signs
- Progresses to delirium, hyperexcitability, belligerence, and sweating
- End stage recumbency, seizures, death
57
Nigropalladial encephalomalacia causes
- Russian knapweed and yellow star thistle
| - Takes a pretty significant amount chronically being ingested
58
Clinical signs of nigropalladial encephalomalacia
- Inability to prehend, masticate, and deglutinate
- Swallowing seems intact
- Hypertonicity of facial muscles
- Tongue may protrude or do a constant swallowing motion
59
Equine Degenerative Myeloencephalopathy (EDM) age affected
1 month - 3 years
60
Equine Motor Neuron Disease age
- Typically >2 years of age
61
Cause of EDM
- Decreased vitamin E in the diet as a foal to yearling
| - Exposure to oxidants as a foal to yearling
62
Cause of EMND
- Likely a risk of Vitamin E poor diets as well
| - Pathogenesis is still unclear
63
EDM Breed predilections
- Arabian, Thoroughbred, Morgan, Appaloosa, Standardbred, Paso Fino, Lusitanos, AQHA, Warmblood, Zebras
64
EMND Breed predilections
- Quarter Horses primarily
65
EDM signs
- Symmetric ataxia
- Weakness
- Wide-based gait
- CP deficits
- Obtunded to quiet
- 38% lose menace without loss of vision
- Pigment retinopathy
- DO NOT HAVE: muscle atrophy, CN involvement, changes in skin sensation, or changes in tail tone
66
EMND signs
- Denervation of skeletal muscles
- Weakness with muscle wasting
- Episodes of anti-gravity muscle trembling, sweating
- Elephant on a ball stance
- Weight shifting - cannot engage stay apparatus
- Sluggish PLR, horizontal pigment band
67
Risk factors for EDM
- Parent
- Living in a dry lot
- Vitamin E poor diets (heat treated pellets, stored oats, sunbaked forages, no access to green grass)
68
Protective factors for EDM
- Turn out onto green grass
69
EMND Risk Factors
- Quarter horse
- Exercising in a dirt paddock
- Cribbing, copraphagia
- Use of pelleted feed
- Use of vitamin/mineral supplement
- Diet high in carbs, low in green forage
70
DfDx for EMND
- EPM
| - CVSM
71
Diagnostics for EDM
- Rule out other neurologic diseases with similar clinical signs (EPM, CVSM)
- Plasma serum tocopherol levels
- Ophthalmic exam (pigment retinopathy)
- Histopath
72
Diagnostics for EMND
- Low serum/plasma alpha tocopherol
- May have mild increase in CK, AST initially
- Nerve biopsy (ventral branch of spinal accessory)
- Muscle biopsy (sacrocaudalis dorsal tail head)
73
EDM prevention
- Oral supplementation with the Natural RRR alpha-tocopherol
- Turnout onto green pasture
74
Treatment of EDM
- usually unsuccessful once clinical signs are present
| - May improve with 6,000+ IU/450 kg/day
75
Prognosis for EDM
- Poor for performance
| - Stabilize by 2-3 years but unlikely to imrpove
76
EMND Treatment
- RRR-alpha-tocopherol (nonracemic vitamin E)
77
Prognosis for EMND
- 40% deteriorate and are euthanized
- 40% recover but can recrudesce under heavy work
- 20% plateau and do not worsen or improve
78
Tetanus pathogenesis
- Gains access via a wound (often hard to find the wound once sick)
- Tetanolysin creates localized tissue damage
- Tetanospasmin goes to bloodstream and re-enters circulation; carried to NMJ via hematogenous spread
- Blocks the release of GABA from the inhibitory interneuron
79
Clinical signs of tetanus
- Stiff neck; trismus; rigid facial expression
- Prolapse of the nictitans membrane
- Progresses to sawhorse stance, elevated tail head, tonic muscle spasms, pharyngeal/laryngeal spasm
80
Diagnosis of tetanus
- History, clinical signs
- Can gram stain wound
- Can submit wound exudate for toxin assay
81
Treatment of tetanus****
- Can treat with penicillin and metronidazole
- Clean and debride wound
- Muscle relaxant
- Can neutralize tetanus antitoxin
- Ensure hydration, nutrition needs are
82
Risk with tetanus antitoxin
- Theiler's disease
- Equine origin product
- Don't have much to lose, since you need this if you want any chance of survival, but this is a risk
83
Prognosis of tetanus
- 75% mortality rate in horses
- Recumbency carries a poor prognosis
- Usually stabilize in 2-7 days and the nslowly improve
84
Prevention of tetanus
- Initial vax 3-6 weeks apart, then yearly booster
| - Re-booster before surgery, at time of injury
85
Botulism sources
- Wounds
- Ingestion of bacteria (more common in foals)
- Ingestion of preformed toxin in feed
86
Pathogenesis of botulism
- Hematogenous spread
| - Goes to presynaptic cholinergic nerve and inhibits ACh release by blocking the SNARE complex from docking and fusing
87
Horse sensitivity to botulism compared to people and cows
- More sensitive
88
Clinical signs of botulism
- Tongue weakness, dysphagia, lethargy, muscle weakness
- Weak facial muscles --> appears obtunded
- Stilted, hypometric gait
- Difficulty standing
- Mydriasis, decreased PLR
89
Diagnosis of botulism
- Clinical signs
- Can test GI contents, feed, wound exudate
- If you give feed, takes them long time to eat it
90
Treatment of botulism
- EARLY administration of anti-toxin
- Minimal efficacy in recumbent horses
- Clinical signs may progress for 12-24 hours post administration
- Prophylactic antimicrobials for aspiration pneumonia
91
Prognosis of botulism
- 7-14 days for resolution of dysphagia
- 1 month for resolution of full limb strength
- Poor prognosis once recumbent
92
Prevention of botulism
- BoNT/B vaccine available for endemic areas
| - 3 part initial series administered 4 weeks apart
93
Idiopathic epilepsy risk factors
- Egyptian Arabian heritage
94
Age of onset for Idiopathic epilepsy of Arabian foals
- 2 months typically
95
Clinical signs for Idiopathic epilepsy of Arabian foals
- NO pre-ictal period
- WHole body myotonus seizures
- Collapse
- Opisthotonus
- Seizures last about 1 minute to <5 minutes
- PROFOUND post-ictal period (obtunded, cortical blindness, lack of bond, loss of interest in suckling for days)
96
Treatment for idiopathic epilepsy of Arabian foals
- Diazepam to stop active seizing
| - Long term phenobarbital q12 hours
97
Phenobarbital monitoring
- Monitor phenobarbital levels if possible
- Monitor liver values
- Can taper if seizure free for 3 months
98
Prognosis for Idiopathic epilepsy of Arabian foals
- GOOD!
| - Seizures usually stop by 1 year of age
99
Adult partial seizures
- No loss of consciousness
| - Facial twitching, running in circles, self-mutilation
100
Generalized seizures
- Loss of consciousness --> collapse
| - Tonic-clonic muscle activity
101
Status epilepticus
- Generalized seizures >5 min duration
102
Aural period of seizures
- Pre-seizure period in an adult
| - Restless, anxious
103
Ictal period
- True seizure activity
104
Post-ictal period
- Lasts minutes to days
| - Obtunded, disoriented
105
Most common causes of seizures in adults
- Brain trauma
- Hepatoencephalopathy
- Toxicity
- Mass including pituitary adenoma
106
Diagnosis of seizures
- Careful documentation
- Complete PE, CBC, Chem, Liver functions
- Cardiac eval (could be another problem completely)
- CSF analysis
- MRI
- EEG
107
Treatment of adult seizures
- Diazepam emergently
- Phenobarbital SID to start
- Possible potassium bromide
108
Prognosis of seizures
- May begin phenobarbital taper if seizure free for 6 months
- Must counsel client that they probably shouldn't ride a horse that has had a seizure
109
Most common cause of head injury
- Poll injury after flipping over
110
Two parts of head trauma injury
- Immediate damage: mechanical disruption (shearing forces that can lead to blindness)
- Secondary damage is delayed, swelling, bleeding, hypoxia
111
Clinical signs of head trauma
- Altered mentation
- Altered CN exam
- Bleeding from ears, nose, mouth
112
Treatment for head trauma
- Steroids
- Mannitol, hypertonic saline (decreasing intracranial pressure)
- Prophylactic antibiotics if fracture, bleeding
113
Narcolepsy cataplexy breeds
- American Miniature Horse
- Lippizzaner
- Shetland pony
- Fell pony
114
Initial phase of Narcolepsy/cataplexy
- Head lowers, flaccidity of lips
| - Progresses to staggering, buckling, stertor, ataxia
115
Evidence of Narcolepsy/cataplexy on a physical exam
- Scabs, callouses on the dorsal aspect of the fetlock
116
Rule outs for narcolepsy-cataplexy
- Acute collapse
- Sleep deprivation
- Vagal syndrome
117
Diagnosis of narcolepsy-cataplexy
- Physostigmine (can cause colic or acute death if given IV)
- Can resolve clinical signs with atropine for 24 hours
118
Treatment of narcolepsy-cataplexy
- Tricyclic antidepressant imipramine
