neurology 2 Flashcards
(39 cards)
1
Q
Equine Herpes Virus
- which ones are important to us?
A
EHV 1&4 (2-3) (5-9)
2
Q
- EHV - 1 signs? why do we see these signs?
A
- Respiratory
- Abortions
- Neurologic signs
> Ischemia of neurons due to vasculitis, not neuronal infection (type III allergic hypersensitivity, immune-mediated???)
3
Q
Equine Herpes Virus
- prevalence?
- what age group is susceptible?
- transmission and nature of infection
A
- Endemic in horse population
- Most infected within first year of life
- Spread by droplets – nasal, ocular, respiratory,
reproductive - Latency – trigeminal nerve, lymphoid tissue
- Role of virus strains, latency, disease?
4
Q
EHV, neurologic signs:
- outbreaks
- morbidity and mortality
- who get this disease?
- risk factors?
- season?
A
- Virus spreads rapidly in outbreaks
- Morbidity up to 90%
- Mortality up to 40%
- Can occur at any age, rarely in foals
- Lactating & pregnant mares more susceptible
- Risk factors – age, females, fever
- More common in winter & spring
5
Q
EHV – Clinical Signs
A
- Acute onset ataxia & tetraparesis
- May be 6 – 10 days post infection
- Range: subtle signs to recumbency
- Non-specific – fever, cough, nasal discharge may occur early
- Also – anorexia, limb edema, ocular lesions
(conjunctivitis), colic
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Spinal white matter: - Ataxia, paresis, CP deficits
- Hind limbs > forelimbs, symmetric
- Urinary incontinence, bladder atonia, dysuria, scalding of legs
- Tail paralysis, decreased anal tone, decreased perineal sensation, fecal retention
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May cause more central signs: - Cranial nerve signs
- Blindness
- Vestibular signs
- Seizures
6
Q
EHV disease progression, recovery period
A
- Progression: usually 24-48 hours, then stabilize. May die or be euthanized especially if recumbent
- Need to allow months for recovery
7
Q
EHV
- Diagnosis
A
- Clinical signs
<><> - PCR
- Neuropathogenic & non-neuropathogenic strains
- Fast
- Nasal swab & blood sample (EDTA)
<><> - Serology – acute & convalescent
- > 1:256 suggests recent infection
<><> - Virus isolation
8
Q
EHV
- CSF analysis
A
- May be normal
- Xanthochromia
- Increased protein level
- May have slight increase in nucleated cell counts
9
Q
EHV
- Treatment
A
- Anti-inflammatory medication
- Fluids, nutrition
- Decompress bladder, evacuate rectum
- Sling
- Anti-viral medication – people have tried acyclovir (useless) and valacyclovir (potentially useful)
10
Q
EHV Prevention
A
- Vaccines – none are labelled for protection against neurologic disease
- Single study – suggests vaccination within 1 year increases likelihood of neuro disease 9-14x
- Herd management:
> Isolate new arrivals – 3 weeks
> Maintain distinct herd groups according to age, sex, occupation; broodmares away from others
> Minimize stress
11
Q
Ataxia Scale (Mayhew)
A
0 – Normal
1 – Subtle deficits, noted when special maneuvers performed
2 – Mild deficits, apparent all times & gaits
3 - Moderate deficits, easy to identify, all times & gaits
4 – Severe deficits, may buckle, stumble, fall
5 – Recumbent & cannot stand
12
Q
Wobbler Syndrome - possible causes in the horse?
A
- Cervical stenotic myelopathy
- Cervical static stenosis
- Cervical vertebral malformation/malarticulation
- Cervical vertebral dynamic instability
- Aberration in cartilage & bone metabolism
- Trauma
- Degenerative joint disease
13
Q
Wobbler Syndrome signalment
- age, breeds, sex, etc…
- who gets this? factors?
A
- Age – months to years
- Breed – any
> Many TB, STB, QH
> Older horses – Warmbloods, any breed - Sex – male > female
- Fast growing young horses – part of developmental orthopedic diseases.
- Multifactorial
> Genetic
> Nutrition – high protein & calories, micromineral imbalance (Cu, Zn)
> (Trauma)
14
Q
Onset & Progression of wobblers
A
- Often insidious
- May be acute
- Vague lameness
- Progression over months, wax & wane
- Spontaneous recovery uncommon
15
Q
wobblers presenting complaints and clinical signs
A
- Clumsiness or stumbling when move out of stall
- Rider – looseness or “losing the back end” on turns
- Reluctance to change leads
- Stumble & fall
<><><><><> - Spinal ataxia
- Spastic gait
- Conscious proprioceptive deficits
- Weakness
- Hind limbs > forelimb signs (C1-C5)
> Why? pelvic tracts of spinal cord more superficial - Forelimb signs more pronounced (C6-T2)
> Why? brachial plexus and thoracic tracts more superficial here
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Degree of difference - if there is a difference between fore and hind limbs with Wobblers, it will only be ~1 degree, important because if we have a horse will multifocal disease we will see a difference of more than 2 grades
16
Q
Wobbler - Radiographs
A
- Vertebral canal stenosis
> Intraventricular sagittal ratios
=> Min. canal diameter and max. vertebral body diameter
=> C3-C6 <50%
=> C7 <52% - Degenerative joint disease, OCD, malformation
- Physeal flaring (caudal, ventral canal)
> “ski jumps” - Caudal extension of the caudal laminae
- Angulation between vertebral bodies
17
Q
Wobblers Dx
A
- Neurologic evaluation
- Spinal radiographs, myelogram
- Rule out other diseases
> EPM, EHV-1, EDM
> Space-occupying lesion (cyst, abscess, tumor)
> Aberrant parasite migration
18
Q
wobblers Tx
A
- Rest, stall restriction
- Anti-inflammatory medication
- Ultrasound-guided joint injections (may help with pain associated with arthritis)
- (Feed restriction) > if you detect this early in life
- Surgery (?) > invasive, difficult, many complications…
19
Q
Equine Protozoal Myeloencephalitis
- pathogen? hosts?
A
- Sarcocystis neurona, (Neospora hughesi)
<><> - Definitive host – opossum
> Didelphis virginiana
> Sexual reproduction in intestine, shed oocysts
<><> - Intermediate host
> Unknown – asexual reproduction → sarcocysts
> Skunk, raccoon, domestic cat, armadillo
> Horse – aberrant intermediate host (CNS)
20
Q
EPM - Pathogenesis
A
- Fecal – oral contamination (water, feed)
- Ingestion
- Parasite locates to CNS
> brain, spinal cord
> Not peripheral nerves or nerve roots - Found in neuronal cells, mononuclear cells, endothelial cells
21
Q
EPM clinical signs? differential and how to tell them apart?
A
- Depends on extent & distribution
- Can present with any CNS signs
- Usually spinal ataxia (often resembles Wobbler syndrome)
> EPM more likely if there is notable asymmetry
> Also if large disparity between forelimb and hind limb signs
> Also if there is muscle loss
22
Q
EPM diagnosis
A
- Rule out other diseases
- Detect S. neurona specific antibodies – serum, CSF
- Serology – depends on geographic area. Up to 90% positive in some areas. Only means exposure.
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Tests: - Western blot
- IFA - indirect fluorescent antibody (react w S. fayeri)
- SAG testing
23
Q
EPM Treatment? considerations?
A
Sulfadiazine-pyrimethamine
- V rarely - blood dyscrasia, neonatal or reproductive problems
- Pyrimethamine interferes with dihydrofolate reductase
> Do NOT supplement w folic acid during treatment
> Stop pyrimethamine therapy
> Can supplement with folinic acid
<><>
Ponazuril (give loading dose) – was currently on back order
<><>
Diclazuril – Protazil (Merck Animal Health, USA)
<><>
Toltrazuril
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- Anti-inflammatory medication > Parasite die-off
- Vitamin E – antioxidant
24
Q
EPM prognosis, prevention?
A
Prognosis:
– guarded, do not know extent of neural damage; need to see response to treatment
> Moderate to severe signs – 60% improved at least 1 grade
> 10-20% may recover completely
<><><><>
Prevention: try to inhibit the opossums from getting into feed
> Avoid possum feces in feed.
25
Equine Degenerative Myeloencephalopathy (EDM)
- who is affected? age, breed, sex?
- Age: Young horses <1 year up to 3 years of age
- Breeds: Many
> Horses, ponies, donkey, Przewalski, zebra
> Heritability strongly suggested in Morgan, Appaloosa, Lusitano
> More common in some familial lines
- Sex: no predilection
- How common is it? > a big question still.
26
EDM
- etiology??
- genetic basis, but also:
- Problem with Vitamin E
> Deficiency (feed, dry lots)
> May be inability to handle Vit E once absorbed
> Analyze feed levels of Vit E (α-tocopherol)
> Analyze blood levels of Vit E(α-tocopherol)
=> (point in time measurement; may not reflect past levels)
27
EDM - clinical signs, differentials
- Clinical signs – symmetric spinal ataxia
- Diagnostic Rule outs: Wobbler Syndrome, EPM
28
EDM - treatment, prevention
- Treatment – not likely to be effective
- Prevention !!!
- Supplement Vit E (natural > synthetic)
> Especially if familial problem, stored feed, lack of pasture, (exposure to insecticides, wood preservatives)
29
Equine Motor Neuron Disease
- what is this?
- anatomy affected?
- signalment?
- risk factor?
- Acquired neurodegenerative disease, sporadic (ALS-like); systemic oxidative stress
- Ventral horns, gray matter of the spinal cord & select brainstem nuclei
- Age: adult horse (2-27 years of age)
- Vitamin E deficiency – lack of pasture, dry lots, dried feed, pelleted feed
30
EMND - clinical signs
- Weakness – profound
> Stand camped under
> May rest against solid objects
> Head & neck may droop
> NO ataxia or neurologic deficits
- Muscle atrophy
- Trembling in anti-gravity muscles
- Sweating
- Frequently shift weight
> Inability to use the stay apparatus
- Recumbency
- Raised tail head (muscle atrophy, fibrosis of the dorsal coccygeal muscles)
- Note: Eyes – retinal pigmentopathy (40%)
> Ceroid lipofuscinosis
> Black/brown/yellow deposits tapetal/non-tapetal junction, reticulated/mosaic
31
EMND - diagnostics
- CK & AST – may be mildly to moderately elevated if rapid progression
- CSF – protein may be elevated; ncells– normal
- Electromyography
- Muscle biopsy – sacrocaudalis sacralis m. (tail head) – atrophy of type 1 myocytes in response to denervation (high sensitivity, low specificity)
- Nerve biopsy – spinal accessory nerve, medial belly of the sternocephalicus m.
32
Polyneuritis equi
- what is this?
- what is affected?
- cause?
- cells?
- Cauda Equina Syndrome
- Progressive granulomatous polyradiculoneuritis
- Cranial nerves & other spinal nerves – less
common
- Cause?? (unknown) – allergic, autoimmune, viral associated, other
- Infiltration of macrophages & Tc cells
33
Polyneuritis equi
- signs, outcomes
- Progressive paralysis of tail, bladder, rectum, anus, penis
- May have initial hypersensitvity & hyperesthesia esp. tail head; leads to desensitization of tail head, perineum,
caudal thighs, caudal rump
- May lead to hind limb ataxia, muscle atrophy
34
Polyneuritis equi
- Cranial nerves affected (often asymmetric):
- Cr. V – motor branch
- Cr. VII
- Cr. VIII
- Others > III, IX, X, XII
35
Polyneuritis equi - Differential dx
– fracture, subluxation, EHM, rabies, sorghum toxicity, other infectious diseases
36
Polyneuritis equi diagnostic tests, treatment, prognosis
- CSF
> Mononuclear pleocytosis
> Lesser increase in neutrophils
- Abnormal EMG
- (Increased P2 myelin basic protein)
- Treatment – anti-inflammatory dose corticosteroids, symptomatic treatment
- Prognosis – hopeless (may sustain for months)
37
Epilepsy - types, who gets them, what we see?
Primary – idiopathic
- Heritable conditions:
- Juvenile idiopathic - line of Egyptian Arabians (respond well to treatment, may outgrow)
- Arabian Lavender foal syndrome
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- Secondary – other disease processes
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- Abnormal, synchronous electrical discharges
- Spontaneous, paroxysmal, involuntary movements
- Generalized or partial
38
Epilepsy - dx, tx
- Diagnostics – many to determine, rule out primary disease
<><>
Treatment
- Diazepam
- Phenobarbital
- Potassium bromide – this is in addition to phenobarbital
39
Narcolepsy/Cataplexy
- what is this?
- signs?
- Dx, ddx
- tx
- Excessive sleepiness
- Paradoxic form of sleep
- Rapid eye movement (REM) sleep
- May involve muscle weakness, recumbency
- Diagnostic rule outs: chronic sleep deprivation, seizures
- Diagnosis – signs, EEG, physostigmine provocation (central acting cholinesterase inhibitor)
- Treatment – transient improvement with atropine; other: imipramine (cataplexy)??
