Equine neurology: central and peripheral Flashcards
What conditions may lead to collapse due to failure of the muscles in the horse?
- Exercise induced collapse
- Other metabolic disorders of muscles
- Electrolyte abnormalities interfering with conduction
What is idiopathic hypersomnia in horses?
Inappropriate sleep in standing adults
Describe the characteristics of idiopathic hypersomia in horses
- Rapid or slow onset of recumbency
- No REM
- Wake spontaneously
- May cause trauma
- May be triggered by specific stimuli
- Epistaxis may be seen
Explain the cause of idiopathic hypersomnia in horses
- Is not a neurological condition, is due to lack of sleep
- Sleep deprivation can be due to: thoracolumbar pain, bilateral lameness, behavioural/herd dynamic issues
What are teh common consequences of head trauma in the horse?
- Often involve vestibular and facial nerves leading to head tilt
- Brain injuries lead to seizures, coma, recumbency, blindness
What conditions is DMSO used for in the horse?
PAS, EHC, EPM, WNV and trauma
Outline the management of head trauma in horses
- Need to control seizures if present
- Consider lfuid status/nutrition
- Patience
- May require decompressive craniotomy
- Corticosteroids: no evidence for benefit or negative effect
- DMSO: little evidence
- Mannitol: reduces ICP
Evaluate the use of DMSO in the treatment of head trauma in the horse
- Osmotic diuretic so reduces ICP
- Stabilises lysosomes
- Free radical repair
- Little evidence base
- No immunosuppressive effects as seen in corticosteroids
Describe the assessment and management of a down horse with suspected spinal injury
- Give time
- Lesion localisation important
- Determine prognosis
- Request second opinion before euthanasia where possible
- Need to manage recumbent horse - nutrition, turning, prevention of co-morbidities
List the indications for euthanasia as a result of spinal injury
- Recumbent for >5days
- Worsening clinical signs
- Muscle pathology (myoglobinuria)
- Colic, uncontrollable pain
What approach (in terms of euthanasia) should be taken for a horse that has suffered:
a: pelvic fractures and is recumbent
b: Wobbler’s syndrome (grade 5)
c: Hind limb paralysis/paresis following spinal fractures
d: neuritis of cauda equina
e: non responsive neuropathy of one or more peripheral nerves
f: recumbent non responsive post trauma
g: laminitis, non-responsie
h: lameness associated with prolonged periods of recumbency
a: Immediate euthanasia, no second op. required
b: Immediate euthanasia, no second op. required
c: Immediate euthanasia, no second op. required
d: Second opinion required prior to euthanasia
e: Second opinion required prior to euthanasia
f: Immediate euthanasia with second opinion
g: Second opinion required prior to euthanasia
h: second opinion required prior to euthanasia
Give a peripheral cause of neurological diseases that falls into the “degenerative” category
Equine grass sickness (NB could also be inflammatory/infectious)
Give a peripheral cause of neurological diseases that falls into the “anomalous” category
- Hyperkalaemic period paralysis
- Polysaccharide storage myopathy
Give a peripheral cause of neurological diseases that falls into the “metabolic” category
Synchonous diaphragmatic flutter aka Thumps
Give a peripheral cause of neurological diseases that falls into the “nutritional” category
Equine motor neurone disease
Give a peripheral cause of neurological diseases that falls into the “neoplastic” category
Mediastinal neoplasia (Horner’s syndrome)
Give a peripheral cause of neurological diseases that falls into the “inflammatory-infectious” category
- Guttural pouch empyaema
- Vestibular disease
Give a peripheral cause of neurological diseases that falls into the “inflammatory-inflammatory” category
Polyneuritis equi
Give a peripheral cause of neurological diseases that falls into the “idiopathic” category
- Equine recurrent laryngeal neuropathy
- Shivering
- Stringhalt
Give a peripheral cause of neurological diseases that falls into the “toxic” category
- Botulism
- Tetanus
Give a peripheral cause of neurological diseases that falls into the “trauma” category
- Postanaesthetic neuropathies
- Facial nerve damage
Describe the typical appearance of unilateral facial nerve dysfunction
- Ipsilateral ear paralysis
- Droopy ipsilateral eyelid
- Ipsilateral muzzle paralysis (nose deviates to the contralateral side )
Describe the apperance of vestibular disease in horses
- Head tilt and circle in ipsilateral direction
- Nystagmus “fast phase” away from lesion
- May be exacerbated by blindfolding as may be compensating with vision
Describe the common underlying cause of vestibular disease in horses
- Ear disease
- E.g. trauma: basisphenoid fracture due to rearing and falling backwards
- Or otitis media/interna: may also lead to facial nerve paralysis and Horner’s, infection in guttural pouch may progress to otitis media
What is polyneuritis equi?
Non-suppurative neuritis of the proximal spinal, cranial sensory, motor nerveroots and sacral nerves. Can progress to proliferative granulomatous perineuritis
Describe the pathogenesis of polyneuritis equi
- Demyelination of teh sacrococcygeal roots of the caudal equina
- May be secondary to viral disease, autoimmune in some cases, unknown if viral or bacterial
- Anti-p2 myelin anitibodies
Describe the clinical signs of polyneuritis equi
- Occasionally cranial nerve disease (head tilt)
- Tail, anal penile, perineal, areflexia and atonia
- Require analgesia
- Surrounded by areas of hypersensitivity
- EMG dhows denervation potentials
What is a key differential for polyneuritis equi?
Spinal fracture
Outline the treatment of polyneuritis equi
- Prognosis is hopeless, no recovery
- No improvement with steroids or gold salts
- Nursing, in particular re. bladder required
- Analgesia
What is equine grass sickness?
Generalised dysautonomia affecting primarily theenteric nervous system
Compare acute, subacute and chronic equine grass sickness based on survival time
- Acute: die rapidly
- Subacute: survive >2 days
- Chronic: survive >7 days
Describe the epidemiology of equine grass sickness
- Young male on pasture, no prev. exposure to EGS
- Change of pasture in previous 2 weeks
- Cool, dry weather, frost
- Previous cases on same pasture
- Seasonal bias for April to July
List the gastrointestinal signs of Equine grass sickness
- Abdominal pain
- Nasogastric reflux
- Dysphagia
- Empty looking abdomen, very dry faeces
What causes the abdominal pain seen in Equine grass sickness?
- Ileus due to myenteric neuronal degeneration (loss of parasympathetic control)
- Dehydration of colonic contents (impaction)
- Liver pathology
Explain the cause and effects of nasogastric reflux in equine grass sickness
- Loss of lower oesophageal sphincter tone and ileus
- “vomit” through nose
- Can lead t oesophageal ulcers
Explain the cause and effects of dysphagia in equine grass sickness
- Loss of parasympathetic control to pharynx (CN IX)
- Unable to swallow
List the non-GI clinical signs of equine grass sickness
- Tachycardia
- Ptosis
- Rhinitis sicca (snuffles)
- Muscle fasciculations and weakness (narrow based stance)
Explain the cause and effect of tachycardia in equine grass sickness
- Loss of vagal control, increased sympathetic outflow
- Heart rate often higher than expected for degree of pain or hypovolvaemia of patient (HR>100)
Explain the cause ptosis in equine grass sickness
- PSNS dysfunction to CN III/VII (suply to levator palpebrae superioris, levator anguli oculi)
- Mullers muscle (sympathetic innervation)
- Non-specific debilitating disease
Explain the cause and effect of rhinitis sicca in equine grass sickness
- Loss of PSNS supply to mucosal glands of nasal mucosa
- Seen in late subacute/chronic disease
- Dry crusty nasal discharge, poor prognostic sign
Compare the pathology in acute and chronic equine grass sickness
- Localised to ileum in chronic
- Generalised intestinal pathology in acute
Describe and evaluate the best diagnostic test for equine grass sickness
- Ileal biopsy
- requires laparotomy (midline/flank): decreases survival
- May see neuronal degeneration within ganglia, depletion of ganglia, vacuolation
List the differential diagnoses for dysphagia in the horse
- Equine grass sickness
- Botulism
- Lead toxicity
- Anatomical pharyngeal abnormalities e.g. sub-epiglottic cyst, cleft palate
- Foreign body (pharyngeal, oesophageal)
- Guttural pouch disease
- Neurological disease (EPM, rabies, EEE, WEE, trauma)
Outline the aspects of treatment of equine grass sickness
- Nursing care
- Analgesia
- Management of each clinical sign
Describe the nursing care required for equine grass sickness
- Feeding: small feeds every 30-60mins, hand feeding, hand grazing, varied diet
- Appetite stimulation: diazepam 0.02mg/kg IV BID-TID (nt as successful as in cats)
- Prokinetics e.g. cisapride
Describe analgesia in the management of equine grass sickness
- Promotes voluntary feeding, reduces pain associated with swallowing and abdominal pain
- Oesophageal/gastric ulceration - H2 blockers, sucralfate
What is the prognosis for equine grass sickness?
50% recover, 50% of those normal within a year, rest have ongoing problems with colic etc.
Identify the poor prognostic factors for equine grass sickness
- Surgery (hence make a clinical diagnosis)
- Dysphagia
- Colic
- Ponies (vs cobs)
- Rhinitis
Explain the significance of equine grass sickness relating to other horses
- EGS thought to be related to pasture toxin
- Often several cases from same pasture
- Horses exposed to EGS less likely to develop the condition
- Naiive animals most likely to be affected
What is equine motor neuron disease (EMND)?
Spontaneous neurodegenerative disease with insidiuous onset preogressing over one to several months
Describe the cause of equine motor neuron disease
- Associated with vit E/Se deficiency
- Oxidative damage of peripheral nerves leading to weakness and other sigsn
What is an “elephant on a barrel” stance pathognomic of in horses?
Equine motor neuron disease
Describe the clinical signs of equine motor neuron disease
- Weight loss + ravenous appetite
- Symmetrical neurogenic muscle atrophy (LMN signs)
- Triceps, biceps, quadriceps atrophy
- Fine fasciculations adn coarse trembling
- Frequent recumbency
- Wekaness
- Worse standing than walking
- Continuously shift weight on hindlimbs, unabe to lock stifles
- Excessive sweating
- Low head carriag
- Tail elevation
- Short strided gait
- No ataxia
- Black teeth (highly suggestive, but not pathognomic)
Which methods are used in the diagnosis of equine motor neuron disease?
- Clinical signs
- Muscle biopsy
- Blood biochem and haematology
- EMG
- Retinal examination
Describe the results on muscle biopsy that would indicate equine motor neuron disease, and state which muscle is used
- Sacrocaudalis dorsalis medialis muscle used (top of tail head)
- Shows severe denervation, atrophy and fibrotic contraction
Describe the results on retinal examination that would indicate equine motor neuron disease
Mosaic pattern of brown pigment in the tapetal fundus (lipofuscin deposition)
Describe the pathology that occurs with equine motor neuron disease
- No gross lesions, but may see pale vastus muscle
- Neuronal degeneration with depletion of motoro neurons in the ventral horns of the spinal cord
- Axon degeneration in ventral roots and peripheral nerves
- Neurogenic muscle atrophy of type 1 muscle fibres
- Lipopigment deposition in capillaries of spinal cord
How does the neurogenic muscle atrophy of type 1 fibres that occurs in EMND relate to the clinical signs?
- Cannot lock stay apparatus, so cannot stay standing for long periods of time
- No issues at walk or trot so see constant shifting and recumbency, but no ataxia when moving
Outline the treatment for equine motor neuron disease
- Unrewarding
- Vit E supplementation-
- Green grass
- Euthanasia
Discuss the prognosis of EMND
- Poor, may show minimal slow improvement
- Will always remain weak and thin
Explain how vitamin E deficiency may lead to EMND
- Inadequate access to green pasture
- Vit E protects membranes by scavening free radicals and preventing peroxidation of lipid membranes
Describe idiopathic head shaking in horses
- Vertical movements of head in repeated fashion
- May rub nasal areas on legs
- Occasionally strike out at muzzle while ridden
Discuss the causes of idiopathic head shaking in horses
- Multifactorial, not consistent between horses
- Behavioural/stereotypical component
- Allergic rhinitis
- Photic
- Trigeminal stimulation
Describe the diagnosis of idiopathic head shaking in horses
- Frustrating
- Rule out obvious causes such as trauma, foreign body
- Assess response to therapy e.g. cyproheptadine, carbemazepine, steroids, sunglasses if photic
- Perinerualanalgesia (infraorbital nerve)
Describe the treatment of idiopathic head shaking in horses
- Depends on underlying cause
- Medical therapy: cyproheptadine, carbamazepine, steroids
- Physical therapy: nose nets, fly shields
- Surgery (nerve compression)
What is cauda equine neuritis?
Rare and sporadic disease in horses that involves the nerves on the cauda equina
Which cranial nerves are affected in cauda equina neuritis?
CN VII, VIII, and rarely V
What causes cauda equina neuritis?
Likely autoimmune or post infectious origin (herpes, adenovirus)
Which group of horses is most affected by cauda equina neuritis?
Adult females
Describe the clinical signs of cauda equina neuritis
- Tail paralysis, incontinence, gait deficits
- Cranial nerve deficits
Describe the progression of cauda equina neuritis
- Inflammation starts in intradural portion fo the nerve root (lymphoplasmacytic)
- Inflammation continues in the extradural portion forming large “masslike” lesions (granulomatous)
Describe the method for the diagnosis of cauda equina neuritis and the prognosis
- Compatible clinical signs
- CSF shows non-suppurative pleocytosis and elevated total protein
- Post mortem
- Prognosis poor
