Exam 2 Flashcards
Testing Cranial Nerves
Olfactory (CN I)
• Do they find the treats?
Optic (CN II)
• Menace response (slowly so no air; not present in young foals)
• Pupillary light reflex (usually slow)
III, IV, VI
• Ability to move and position eye (fixed strabismus)
V, VII
• Sensory & motor of muscles of face
• Can they sense things you touch and move appropriately
• Ears, eyes, nose, mouth
VIII
• Head tilt
• Nystagmus (slow phase to side of lesion)
• Deafness – common in blue eyed paint horses (blindfold)
IX, X
• Dysphagia
XII
• Pull out tongue and see if replaces
• Unilateral muscle atrophy of tongue
Non cranial nerve portions of neuro exam
Opthalmic Exam
• Evaluate nerve ending for CN II
• Cataracts?
Gait Eval
o regular walking
o circle walking
o curb walking
o hill walking
o standing tail pull
o walking tail pull
Neck Mobility
o Head should be able to touch flank
o Head should go high & between front legs
o Palpate transverse processes manually
Identifying Sacral Nerve Damage
o Urination
o Defecation
o Tail tone
o Anal tone
o Perineal sensation
Neurologic Lesion Localization
Brain:
• mentation, behavior
Brain stem:
• cranial nerves
Cervical spinal cord:
• all four limbs
Thoracolumbar spinal cord:
• rear limbs
Sacral nerves:
• urination, defecation
Head trauma; Types of Damage, Treatment, Prognosis
Types of Damage
• Direct impact – occipital, sphenoidal, temporal bones
• Direct & contracoup impact – inner, middle ear, basilar bones, optic nerves
Treatment
• Osmotic diuretics for edema (mannitol, hypertonic saline)
• NSAIDs
• Anti-convulsants if needed
• Corticosteroids (controversial)
• Supportive care
Prognosis
• Variable
• Response to treatment best indication
• Keep them on their feet!
Head trauma; First Aid
• Is airway patent?
• What is level of consciousness?
• Pupils – size, symmetry, response
_ Bilateral nonresponsive mydriasis = grave prognosis
_ Watch for central blindness due to optic nerve trauma
• Assess motor function if standing
• Monitor respiratory patterns
Juvenile Idiopathic Epilepsy
o Autosomal dominant in (Egyptian) Arabians
o Seizure activity begins days to 6
months of age
o Seizures stop between 1 and 2 years
o Partial or full seizures, post-ictal phase
o May require medication
o Long-term prognosis excellent
Causes of Seizures
Most common
• Hepatoencephalopathy
• Trauma
• Infectious disease
• Toxins
• Intracarotid injection
Neonates
• Hypoxic-ischemic damage
• Metabolic issues
• Congenital abnormalities
• Epilepsy (only in Arabians)
Seizures; Diagnosis, Therapy
Diagnosis of Seizures
o History, signalment
o CBC, chem,
o Test for specific diseases
o CSF
o EEG, CT, MRI
(mass?)
Therapy
o Treat underlying disease
o Anti-convulsants: diazepam(acute),
phenobarbital (maintenance)
o Other anti-convulsants: potassium bromide, phenytoin, primidone
Intracarotid Injection; What? Symptoms
Accidental injection of drug into carotid artery
Symptoms
• Cortical blindness (can improve)
• Self-trauma & seizure
• Brain trauma
Equine Leukoencephalomalacia; How, symptoms, diagnosis, treatment
o Corn contaminated with Fusarium moniliforme -> toxin fumonisin B1
o Summer drought, followed by a wet period
o 3 – 4 weeks after ingestion, acute onset signs
Symptoms
• Anorexia, depression,
• ataxia, circling, blindness, head pressing
• Recumbency, seizures, death in 2-3 days
Diagnosis
• Fumonisin in feed
• CSF – xanthochromia, increased protein, pleocytosis
• Necropsy – focal liquefactive necrosis, sometimes hepatic involvement
Treatment
• Supportive
• Check other horses & remove feed
Nigropallidal Encephalomalacia; How? Symptoms
o Yellow-star thistle (Centaurea soltitialis) or Russian knapweed (Acroptilon repens)
o Some horses develop a craving; toxic in hay also
o Ingestion of large amounts over weeks to months
o Lesions in substantia nigra, globus pallidus
o Young horses most common
o No treatment/recovery
Symptoms
• Sudden onset clinical signs
• Retracted lips, continuous chewing movements
• Aimless walking, circling, ataxic, tetraparetic
• Impaired eating and drinking
• Unable to chew and propel food to pharynx
• Usually can swallow
Narcolepsy; True Vs Sleep Deprivation
True
• Hereditary, rare
• Spontaneous collapse, daytime sleepiness
• May be triggered by specific events
Sleep Deprivation
• Limited recumbent sleep – likely very common
• Pain associated with recumbency
• Environmental factors
• Social-behavioral factors
Peripheral Vs Central Traumatic Lesions
Peripheral
• Head tilt toward lesion
• Nystagmus fast phase away from lesion
Central
• Head tilt away from lesion
• Nystagmus any direction
Temporohyoid Osteoarthropathy Pathogenesis, Diagnosis, Treatment, Prognosis
Pathogenesis
• May begin w/ middle ear infection
• May be primary noninfectious arthritic condition
• Hyoid bone fuses ->
• Any movement can cause breakage ->
• Fracture affects CN VII & VIII deficits
OR
• Acute seizures & death
ALSO
• May have CN IX & X signs (dysphagia)
Diagnosis
• Endoscopy of guttural pouch
• Rads
• CT or MRI
Treatment
• standing basihyoid- ceratohyoid disarticulation
• NSAIDs, +/- antibiotics may help
• Treat corneal ulcer if present
Prognosis
• Most stabilize & improve over 6-12 mo
• Risk of bilateral dz
• Risk of new Fx
Cerebellar Abiotrophy; who?, Symptoms, Diagnosis, Prognosis
o Arabian foals
o Autosomal recessive
o Premature death of purkinje cells
Symptoms
• 6-4wks old
• Intention tremor of the head
• Symmetric ataxia
• Hyperextension of the limbs
• Base-wide stance
• Lack of menace reflex?
• Visual with normal
Diagnosis
• Presumptive based on signs
• Genetic testing
• Histology
Prognosis
• No treatment available
Occipitoatlantoaxial Malformations; Basics, Diagnosis, Treatment
o Congenital malformation
o Arabian horses; autosomal recessive;
o DNA test available for one form
o Neurologic signs result from spinal cord compression
o Onset of signs birth - 6months
Diagnosis
• Confirm with imaging (radiographs, CT, MRI)
Treatment
• No available treatment
Cervical Vertebral Stenotic Myelopathy; Type I Vs Type II
Type I
• Developmental disease in young, fast-growing horses (<2 years of age)
• Most common at C3, C4, C5
• Often young, fast-growing, male horses
• Nutritional imbalances in Cu, Ca, P may play a role
• Concurrent OCD?
Type II
• Older horses with
degenerative
joint disease
• Most common at
C5, C6, T1
• Especially
common in Warmblood breeds
Cervical Vertebral Stenotic Myelopathy; Common name, Pathophysiology, Clinical Signs, Treatment, Prognosis w/ Sx
o “wobblers”
Pathophysiology
• Multiple sites of compression may be present
• Can occur as far caudally as C7 – T1
• May present with acute onset after relatively minor trauma
• Compression may be “static” or “dynamic”
Clinical Signs
• Primarily Upper motor neuron – ataxia, general proprioceptive deficits
• Usually symmetric signs
• Pelvic limbs usually more severely affected if lesion is C1 – C5
• Thoracic limbs may be same or worse if C6 – T1
• May be worse with flexion or extension of the neck (dynamic)
Treatment
• Surgery – “basket” stabilization
• Restricted energy and protein diet
• Time – turn out and wait
Prognosis w/ Sx
• 80% improve one neurologic grade
• 40% improve two grades or more
• Up to 1 year for full recovery
Cervical Vertebral Stenotic Myelopathy; Diagnosis
Rads
Minimal Sagittal Ratio
• minimum sagittal diameter of the spinal canal divided by the maximum sagittal diameter of the vertebral body
• Narrow = <52% at C3/4, C4/5, C5/6
and/or <56% at C6/7
Myelogram
• Best method for definitive diagnosis
• Neutral, flexed, & extended views
• 50% or greater reduction in width of dorsal and ventral dye columns directly opposite each other
Equine Degenerative Myeloencephalopathy; Basics, Predisposing Factors, Diagnosis, Prognosis, Treatment
o Diffuse degenerative neurologic disease
o Classically described as symmetrical ataxia, proprioceptive deficits all four limbs in young horses (6 months to 2 years of age)
o Pigment retinopathy in some affected Warmblood horses
Predisposing Factors
• Genetic predisposition + environmental factors
• Insufficient Vit E in diet especially early in life (lack of fresh green grass)
Diagnosis
• Difficult antemortem
• Measure serum Vit E (may be normal)
• Plasma and CSF phosphorylated neurofilament heavy chain (new / accuracy?)
• Definitive diagnosis requires necropsy
Prognosis
• Poor
Treat
• Supplement Vit E Non racimic (better for prevention)
Equine Motor Neuron Dz; Basics & Clinical Signs
o Risk peaks at about 16 years of age
o Typically seen in horses that have been vitamin E deficient for > 18 months
o Horses usually have not had access to fresh green grass pasture
o Affects lower motor neurons
o Associated muscles atrophy
o Lesion similar to amyotrophic lateral sclerosis (Lou Gehrig’s disease)
Clinical Signs
• Excellent appetite
• Muscle wasting, weightloss
• Abnormal stance
• Weakness, trembling, recumbency
• Paraphimosis
• Ocular lesions
Equine Motor Neuron Dz; Diagnosis, Treatment, Prognosis
Diagnosis
• History, clinical signs
• Mild to moderate increases in CK
• Low plasma vitamin E
• Biopsy of sacrocaudalis dorsalis medialis muscle
Treatment
• Move to new environment
• Vitamin E as described for EDM
Prognosis
• W/ treatment
• 40% improve
• 40% stabilize
• 20% progress
Suprascapular Nerve Injury; aka, acute vs chronic
o AKA Sweeney
Acute traumatic injury
• Outward rotation of the shoulder
Chronic Traumatic Injury
• Visible atrophy
Radial Nerve Paralysis; How? Clinical SIgns
o Trauma around elbow due to lateral recumbency or humeral fx
Clinical Signs
• Can’t flex shoulder or extend limb
• Dorsum of hoof on ground
• Not weight bearing
EPM Life Cycle, Predisposing factors, Diagnosis
Life Cycle
o Definitive host eats meat (OPO) ->
o Sporocyst in feces ->
o Horse eats feces on accident ->
o Sarcocyst encysts in muscle
Predisposing Factors
o 1-5 years old
o Racing or showing
o Spring, summer, fall
o Wildlife, especially opossums
o Wooded terrain surrounding the farm
o Previous EPM on the farm
o Recent adverse health event
Diagnosis
o Serum:CSF titer ratio <100 STRONGLY correlates w/ EPM
o PE
o Neuro exam
o Rule out other diseases
o Detection of IgG in serum & CSF (only shows exposure)
o Necropsy
EPM Clinical Signs
o May be >1 year after infection
o Encited by stress, preganancy, decreased immunity, steroid use
Spinal Cord
• Ataxia, asymmetry, atrophy
Brain
• Depression, Blindness, Circling, Recumbency
EPM Treatment
Sulfadiazine + pyrimethamine
• >3mo
• 70% improve
Ponazuril
• 28 days
• 60% improve
Diclazuril
• Top dress for feed
• 28 days
• 67% improve
o Supportive care
o NSAIDs
o Vit E
o Levamisole
No response in 30 days is poor prognosis
EHV-1 Vs EHV-4
EHV-4
• Respiratory dz
EHV-1
• Neuro dz
• abortion
Equine Herpes Transmission, Pathogenesis
Transmission
• Shed via nasal secretion & aerosol
• Sniffing aborted fetuses
• Horses as young as 11 days can be infected despite maternal Abs
Pathogenesis
• Replication n respiratory tract ->
• Local lymph nodes w/ in hours ->
• Cell associated viremia ->
• Latency ->
• Travel / stress ->
• CNS endothelial cells ->
• Vasculitis & reactive thrombosis
Equine Herpesvirus Myeloencephalopathy; Basics, Clinical Signs, Diagnosis
• All ages accept young
• Pregnant/nursing mares highly susceptible
• Incubation 2-10days
• May be associated w/ abortion or resp dz
• Biphasic fever may come prior to neuro signs
Clinical Signs
o Rapid onset
o Ataxia worse in hindlimbs
o Bladder paralysis (dribbling urine)
o May have central or CN signs
Diagnosis
o PCR or isolation of nasal secretions or buffy coat
Equine Herpesvirus Myeloencephalopathy; Treatment, Prognosis, Prevention
Treatment
o NSAIDs
o Heparin
o Support rectal/bladder function
o Soft bedding
o Support sling
Prognosis
o Fair-good if standing
o Poor if recumbent
o Months to recover
o Some have residual effects
Prevention
o Separate horses into small groups
o Minimize stress
o Isolate new arrivals
o Vx does not prevent neuro dz (may decrease nasal shedding)
