Non-infectious Diseases of the Nervous System Flashcards
What is the normal sleep cycle in horses? How long is their REM?
polyphasic, slow wave sleep for 3 hr/day
20-30 mins
What is the difference between sleep deprivation and narcolepsy/cataplexy?
SLEEP DEPRIVATION - lack of adequate sleep causing excessive daytime sleepiness, collapse, and unexplained abrasions of carpi and fetlocks
N/C - sleep disorder causing excessive daytime sleepiness without collapse typically due to specific triggers
What are some environmental factors that can trigger narcolepsy and cataplexy?
- predators
- raking in the herd
- housing, food
- pregnancy, lactation
- saddle, equipment
What are some medical and neurological issues that can trigger narcolepsy and cataplexy?
- orthopedic pain
- GI pain
- pleuropneumonia
- inability to lay down
- pain!
How is sleep deprivation, narcolepsy, and cataplexy diagnosed? What are the main 2 treatments?
- detailed history
- video surveillance
- CBC, biochemistry, CSF, EEE workup to rule out other issues
- provocation test with physostigmine
- NSAIDs for chronic pain
- imipramine (antidepressant)
What are seizures?
manifestations of abnormal electric activity of the brain
- epilepsy = recurrent seizures
What are signs of generalized and localized seizures?
GENERALIZED - tonic/clonic, involuntary recumbency, loss of consciousness, post-ictal blindness and depression
LOCALIZED - more subtle, may have localized post-ictal signs
What are some extracranial causes of seizures in adult horses?
- METABOLIC: hepatoencephalopathy, hypocalcemia, uremia, hyperlipidemia, estrus
- TOXIN: organophosphates, strychnine, metaldehyde
What are some intracranial causes of seizures in adult horses?
- TOXIN: moldy corn, locoweed, bracken fern, lead, arsenic, mercury, rye grass
- TRAUMA: brain injury
- VASCULAR: Strongylus vulgaris, cerebral thromboembolism, intracarotid injection
- TUMOR: neoplasia, hematoma, cholesterol granuloma
- INFECTIOUS: abscesses, rabies, arbovirus, EPM
What are 4 medical options for stopping seizures?
- SHORT TERM - Diazepam, Midazolam
- LONG TERM - Phenobarbital to effect
- potassium bromide
- LAST RESORT - Xylazine, Detomidine
What ancillary treatments are recommended for seizures?
- DMSO
- flunixin meglumine (NSAIDs)
- dextrose if hypoglycemic
What maintenance treatment is recommended for seizures?
- phenobarbital
- potassium bromide
- pregablin
- gabapentin
What happens when horses receive drugs via the carotid artery? How is this treated? How does the type of drug affect this?
drug goes to the brain causing acute seizures under needle —> horses tend to flip backwards
calm the reaction with diazepam, phenobarbital, dexamethasone, or xylazine
- water soluble = may stand within an hour, clinically normal in 1-7 days
- insoluble = acute death possible
What antibiotic may result in seizures? How do the horses react? How is this treated?
procaine penicillin —> correct injection AND accidental injection into vessel
immediate reaction - spooks, circles, snorts, bangs around stall, collapses
usually in vain - cal with Diazepam, phenobarbital, and xylazine + dexamethasone
What 4 diseases typically affect Arabian foals?
- juvenile idiopathic epilepsy
- lavender foal syndrome
- oxipitoatlantoaxial malformation
- cerebella abiotrophy
What is the etiology of juvenile idiopathic epilepsy? What clinical signs are associated? How is it diagnosed?
autosomal dominant inheritance in Egyptian lineage - foals typically grow out of it within 6 months
tonic-clonic seizures - normal between episodes
NOT lethal and not genetic test available - history and clinical signs
What is the etiology of lavender foal syndrome? What clinical signs are associated? How is it diagnosed?
autosomal recessive (LETHAL) disease in Arabian foals born with a dilute coat color
can resemble neonatal maladjustment syndrome (dummy foal) - repeat seizures with paddling and convulsions
genetic test - N/LFS carrier, LFS/LFS fatal
What in the spine affacted by oxipitoatalantoaxial malformation? What is the etiology in Arabians?
- occipitus: base of skull
- atlas: C1
- axis: C2
OAAM1 autosomal recessive mutation
What are the most common clinical signs associated with OAAM?
- abnormal head neck carriage +/- torticollis, extension
- brainstem compression: hyperreflexia, hypertonia, weakness, ataxia
- reluctance to move head/neck
- click or crepitation on palpation
- tetraplegia, tetraparesis
- stillbirth, sudden death
How is OAAM diagnosed?
IMAGING - fused skull base, atlas, and axis
What are 2 causes of cerebellar abiotrophy in Arabians
autosomal recessive mutation causes…
- degeneration after the formation of the cerebellum
- apoptosis of Purkinje cells
When do clinical signs of cerebellar abiotrophy in Arabians? What is seen?
1-6 months of age
- intention head tremor
- ataxia: dysmetria, spasticity, goose stepping
- wide-based stance
- unable to rise
- startle easily, may fall
- lack of menace
What is shivers? In what horses is it most common?
chronic progressive equine movement disorder of unknown etiology related to cerebellum abnormalities
- Draft horses
- Warmbloods
- tall horses, M > F
What 5 clinical signs are associated with shivers?
- difficulty walking backwards
- hyperflexed limb postures
- tremors during backwards movement
- muscle atrophy, decreased strength
- problem picking up feet for farrier
What 4 movements are associated with shivers?
- hyperextension
- hyperflexion and abduction
- shivering hyperflexion
- shivering forward flexion
What pathology is associated with equine shivers?
end terminal neuroaxonal degeneration within the deep cerebellar nuclei
What is eNAD/EDM?
Equine Neuroaxonal Dystrophy / Equine Degenerative Myeloencephalopathy - abdnormal neurons within brainstem and spinal cord
What is the environmental trigger for eNAD/EDM? What does this cause?
lack of vitamin E from pelleted feed, dry lots, overcrowding, insecticides, and wood preservative
- ataxia
- lack of antioxidants
- lipid peroxidation
- demyelination
When do clinical signs of eNAD/EDM appear? What is seen?
1-12 months —> can be older!
- acute/insidious symmetric ataxia (pelvic > front)
- trunk and limb paresis, wide based posture
- hypometria
- 2 beat gait possible
- reduced slap test, cervicofacial, cutaneous trunci
- depression, obtunded
How is eNAD/EDM diagnosed?
NO ANTEMORTEM DX
- vitamin E low in 3 samples within 24 hrs
How is eNAD/EDM is treated? How does it progress?
slow progression of vitamin E (1-2 IU/kg) to help for stabilization —> water soluble d-alpha-tocopherol
stabilizes over 2 year, horse is not suitable for riding or breeding
What are the 2 types of cervical vertebral myelopathy? What causes each?
TYPE 1 = C1-C6 in young horses with dynamic proximal flexion and distal extension; developmental
TYPE 2 = static C5-T1 in young to middle aged horses; degenerative osteoarthritis
(Wobbler Syndrome)
What are genetic, physical, and dietary risk factors associated with development of Wobblers?
GENETIC - rapidly growing male geldings (stallions), large breeds (TB. WB, TWH)
PHYSCIAL - rapid growth, large size, osteochondrosis dissecans
DIETARY - high protein, caloric intake, Cu/Zn
What are the most common clinical signs associated with CVM (Wobbler syndrome)?
- symmetric ataxia
- UMN paresis and hing dysmetria
- circumduction pelvic limbs
- toe dragging (flexor paresis)
- decreased resistance on tail pull (extensor paresis)
- hypometric, stiff component
- neck pain
How do horses with CVM (Wobbler syndrome) respond to walking in a straight line, over a curb, in a circle, and backing? How do they respond to a tail pull?
variable stride length with low arc, dragging, and circumduction
lack of proprioception, hit step
spasticity, circumduction, overreaching
wide base, leaning, dragging, slow protraction
extensor paresis = decreased resistance
What are some rule causes of CVM (Wobbler)?
- angular deformity of vertebrae
- malalignment between vertebrae
- stenosis of vertebral canal
- flare/epiphysitis caudal vertebral epiphysis of vertebral body
- extension of the dorsal aspect of the vertebral arch
- abnormal ossification of the vertebral process
- DJD of the vertebral process
How is CVM (Wobbler syndrome) diagnosed?
(laterolateral) plain radiographs - anatomical structures, decreased diameter of the vertebral canal
- sagittal ratio
CVM, sagittal ratio:
compare smallest diameter of vertebral canal to the width of the vertebral body
CVM, sagittal ratio:
Other than plain radiographs, how is CVM (Wobbler syndrome) diagnosed?
- positive contrast myelography for surgery done under GA, shows dural diameter reduction of 20%
- CT, MRI, scintigraphy highlight smaller abnormalities
- cervical vertebral canal endoscopy
What medical treatments are available for CVM (Wobbler syndrome)?
- stall rest to avoid additional trauma
- dietary management: restricted proteins and energy
- corticosteroids
- NSAIDs
- DMSO
better for younger horses waiting for surgery
What are the 2 surgical treatments used for CVM (Wobbler syndrome)?
- veterbral interbody vertebral fusion with a Cloward Bagby Basket and threaded titanium implant
- dorsal laminectomy
fuse vertebra and restrict movement
What is thought to cause cauda equina syndrome?
possibly autoimmune or infectious etiology results in progressive granulomatous polyganglioradiculoneuritis and cytotoxic T cells and macrophage infiltration of the cauda equina
What are 5 clinical signs associated with cauda equina syndrome? What causes them?
- dysuria, tail rubbing
- hyperesthesia
- desensitization and paresis of tail, bladder, and rectum
- urine overflow, fecal retention
- ataxia, atrophy
destruction of somatic and autonomic LMN and sensory neurons at the level of the nerve roots and dorsal root ganglia
What must be ruled out before diagnosing cauda equina syndrome? What 3 diagnostics are used?
trauma (radiographs!), EHM, rabies, sorghum toxicosis
- CSF: moderate pleocytosis
- EMG: denervation
- high circulating antibodies against P2 myelin - not commercially available, not specific
What parts of the nervous system are affected by equine motor neuron disease? What does this result in?
motor neurons in the spinal cord ventral horn and brain stem
generalized neuromuscular weakness and neurogenic muscle atrophy
What is the most common cause of equine motor neuron disease? What risk factors contribute to this?
lack of antioxidants
- absence of pasture or good quality hay
- heat treated pellets
- dirt lot
What horses are most commonly affected by equine motor neuron disease? What clinical signs are seen? What clinical sign is uniquely missing?
adults, around 9 y/o
- weight loss despite good appetite
- muscle wasting of tricepts, quadriceps, and gluteal muscles
- trembling, patchy sweating
- narrow-based stance, shifting weight
- low head carriage, elevated tail head
- walks better than standing with gait abnormalities
NO ATAXIA
How is equine motor neuron disease diagnosed? What can be biopsied?
- CBC/chem: mildly elevated CK and AST, low vitamin E
- EMG, absorption tests
- fundic exam - lipofuscin deposition
MUSCLE - sacrocaudalis dorsalis medialis
NERVE - ventral branch spinal accessory nerve = neuronal degeneration and loss, muscle denervation atrophy
How is equine motor neuron disease treated? What is prognosis like?
- dietary changes
- vitamin E: water soluble alpha-tocopherol
poor for returning to performance, guarded for life
EDM vs EMND:
