Neurology Flashcards
What abnormality is indicated with abnormal states of wakefulness (mentation)?
Abnormal cerebral function
How to induce somnelence in a foal (without chemical sedation)
Madigan squeeze (usually only works once)
Signs of cerebellar disease
Intention tremor (incompatible with life)
Disease indicated with a head tilt
Vestibular
Testing optic nerve function
Menace response (blink = facial nerve and withdrawal = central processing e.g. cerebral and cerebellar, learned and not present for first 14 days of life)
Pupillary light reflex (direct and consensual, oculomotor nerve/III)
What is this horse suffering from?
Anisocoria
What can ptosis be a clinical sign for?
Neurological (oculomotor control) or ocular pain
Cranial nerve associated with horizontal nystagmus
III and VI
Cranial nerve associated with vertical nystagmus
III and IV
Cranial nerves responsible for facial sensation
Trigeminal
Cranial nerve for palpebral/corneal sensation
Trigeminal/V
Cranial nerve for facial expression
Facial nerve
What cranial nerve dysfunction is this horse suffering from?
Left facial nerve dysfunction
What cranial nerve dysfunction is this horse suffering from?
Vestibulocochlear/8
Function of glossopharyngeal nerve
Sensory, taste (posterior 1/3)
Motor to tongue (extrinsic muscle)
Motor to pharynx
How to test hypoglossal nerve function
Controls intrinsic muscles of tongue and pharynx so give animal food
Testing spinal reflexes
Panniculus reflex
Anal tone
Tail tone
Foot placement (may just be obedient/sluggish horse)
Scale for gait assessment in neurological cases
Mayhew ataxia scale
Spinal ataxias with normal mentation
Cervical Vertebral Compressive Myelopathy (CVCM)
Equine Herpes Virus (EHV-1)
Equine protozoal myeloencephalopathy (EPM)
Vitamin E related ataxias
Differentiating ataxia from lameness
Irregularly irregular vs regularly irregular
Ataxia evaluation on walk (more obvious) vs lameness on trot
Spinal ataxia
Proprioceptive deficits
Crossing, abduction, circumduction, knuckling (ascending pathways)
Foot dragging, stumbling (descending pathways)
Is ataxia an abnormality of ascending or descending tracts?
Refers specifically to proprioceptive deficits (ascending tracts/sensory) but they run so close to UMN tracts (descending tracts/motor) that normally both occur simultaneously
Vestibular ataxia
Head tilt, leaning, falling to one side, wide base stance
Cerebellar ataxia
Loss of modulatory effect of cerebellum
Wide base stance
Dysmetria (hyper/hypo)
No proprioceptive deficits
No weakness
Dysmetria
Inability to control the distance, speed, and range of motion necessary to perform smoothly coordinated movements
Vitamin E related ataxias
Equine degenerative myeloencephalopathy/axonal dystrophy (EDM)
Equine Motoneuron disease (weakness)
Why does compression of spinal cord lead to more proprioceptive deficits than motor deficits?
Sensory/ascending pathways are more superficial in spinal cord (deeper pressure required for motor deficits)
What disease does ‘Wobbler’s syndrome’ refer to?
Cervical vertebral compressive myelopathy/CVCM
Most common non-infectious neurologic disease condition in horses
CVCM/wobbler’s
Clinical presentation of Wobbler’s
Moderate to severe ataxia (inability to perform, unsafe)
Typically diagnosed early in life (<4yo), but can manifest later in life (OA)
Factors in Wobblers (multifactorial disease)
Genetic predisposition
Dietary imbalances
Rapid growth rates
Clinical signs of wobblers
Ataxia, weakness and spasticity
Generally symmetrical deficits, sometimes asymmetric (OA)
Truncal sway, crossing and interferences when turning, hindlimb pivoting
Diagnosis of wobblers
Radiograph (intervertebral ratios on good laterolateral)
Radiographic myelography (dorsal contrast column, total dural diameter, DCC reduction)
CT myelography and MRI (transverse plane images, better definition of tissues, anaesthesia risk)
(Strongest diagnostic test is post mortem, others have low sensitivity/specificity)
What does a walking tail pull assess?
Upper motor neurone
What does a standing tail pull assess?
Lower motor neurone
Medical treatment of wobblers in young horses
NSAIDs +/- steroids (acute phase)
Diet restrictions (limit overnutrition with protein/starch, maintain correct Ca:P, avoid excess copper)
Medical treatment of wobblers in adult horses
NSAIDs +/- steroids
Mesotherapy and exercises
Intra-articular facet joint injection (OA)
Surgical treatment of wobblers
Ventral interbody vertebral fusion
What level of improvement is seen with surgical treatment of wobblers?
1-2 grades
Clinical signs of equine herpes virus causing spinal ataxia
Previous respiratory disease 6-10d prior (intermittent cough, serous nasal discharge, conjunctivitis)
Symmetric ataxia ± weakness (bladder distension/urinary incontinence, poor anal tone, recumbency)
Inconsistent fever
Chorioretinitis
Usual progression of equine herpes virus
Respiratory disease 6-10 days prior (primary replication, replicates in LNs, establishes in trigeminal ganglia/respiratory lymphoid organs, secondary replication in secondary organs e.g. pregnant uterus, CNS, eye)
Stabilisation over 24 hours
Majority of horses fully recover
Diagnosis of equine herpes virus causing spinal ataxia
Signalment (high risk e.g. movement, resp. disease)
Nasopharyngeal swab PCR
Whole blood PCR
Serology (complement fixation test if unvaccinated)
CSF tap (often unrewarding, xanthochromia and increased protein)
Treatment for equine herpes virus
Prevent spread (isolate, monitor temperatures, 21 days movement restriction, biosecurity)
Valacyclovir 30mg/kg q 8h for 48h, then 20mg/kg q12h
Low-molecular heparin SC
NSAIDs/Steroids? (Treat respiratory disease early enough = less fever = less viraemia = lower likelihood of neurological disease)
Infectious agent in equine protozoal myeloencephalopathy
Sarcocystis neurona (and Neospora hughesi)
Key features of equine protozoal myeloencephalopathy
Definitive host opossum
Horse only aberrant host
Migration of schizonts and merozoites to CNS
N. hughensi transplacental too?
USA and South America most common (S. neurona prevalence 10-90%, N. hughesi prevalence 10%)
Ingestion of contaminated feed (concentrate/hay/grass)
Seropositive ≠ aetiology
Clinical signs of equine protozoal myeloencephalitis
Any possible neurological sign/insidious or acute
Asymmetric ataxia with/without cranial nerve deficits (VIII, VII, X)
Weakness and muscle atrophy (gluteus, biceps femoris, epaxial musculature)
Poor anal tone, “cauda equina syndrome”
Diagnosis of equine protozoal myeloencephalitis
Challenging but intrathecal production of antibody (S.neurona): SAG
Serum: CSF ratio< 1
Do not trust serum + results in areas of high prevalence
Routine CSF analysis often unrewarding: high protein and high WBC rare
Clinical signs + area with opossums
Response to treatment?
Post-mortem: histopathology confirmation
Treatment of equine protozoal myeloencephalitis
Pyrimethamine and sulfadiazine (90 days treatment)
Diclazuril/ponazuril (60 day treatment)
NSAIDs/Steroids acute severe stages
Long term Vitamin E supplementation
Relapse in 10% of cases
Prevention of EPM
Avoid exposure to opossum faeces
Daily administration of low dose Ponazuril/diclazuril/Nitazoxanide
Diffuse degenerative disease of the equine spinal cords and caudal portion of the brainstem and primarily affects young horses (<1yo), but can take longer to diagnose (<5yo)
Equine degenerative myeloencephalopathy/axonal dystrophy
Clinical signs of equine degenerative myeloencephalopathy/axonal dystrophy
Insidious onset of symmetric spasticity, ataxia, and paresis
Pelvic limbs are usually more severely affected than the thoracic limbs
Some horses will have decease menace response , lethargy or behavioural changes
Long-term poor performance
Cause of equine degenerative myeloencephalopathy
Low Vit E<2ug/ml but non responsive to treatment
Prevention of equine degenerative myeloencephalopathy
Supplementation in following circumstances:
Some breed lines might be predisposed (QH?)
Areas with Low VitE
Last month pregnancy and nursing period
Fast phase of nystagmus away or towards lesion side?
Away
Acquired progressive neurodegenerative disease that affects neurons in brain and spinal cord (LMD)
Equine motor neuron disease
Trigger for equine motor neurone disease
Vitamin E deficiency for longer than 18 months
Risk factors for equine motor neuron disease
Excess copper and no access to green forage
Equine motor neuron disease clinical signs
Generalized weakness (slow gait, dragging toe, base-narrow stance)
Shifting weight between limbs
Muscle fasciculations of anti-gravitatory muscles (T>P)
Generalized sweating
Neurogenic muscle atrophy (Type I fibres)
Pigmentary retinopathy
Diagnostics for equine motor neuron disease
Low Vit E in serum <2ug/,l
Confirmatory: sacrocaudalis dorsalis medialis muscle (tail) shows myelinated axons degeneration
Post mortem: loss of motor neurons from ventral horn spinal cord
Treatment of equine motor neuron disease
Vitamin E (water dispersible better): 5000-7000 IU/day for 3 months
Involuntary sudden violent repetitive movements of the head dorso-ventrally, horizontally or rotatory
Head shaking
Presentations of headshaking
Nose rubbing on stationary objects /floor/scratching
Lower head carriage
Snorting, sneezing, snoring
Excessive nasal discharge
Most common cause of head shaking
Idiopathic
Symptomatic head shaking
Cause can be found and withdrawal permanently removes the problem
Top cause of persistent head shaking
Trigeminal nerve/V mediated: facial/head noxious sensations
Signalment for head shaking
Young geldings 5-12yo
Pleasure horses and sport horses
April-summer
95% during ridden exercise, 53% during lunging, 26% when turnout in pasture and 12% stabled
Triggers for head shaking
Photic (bright light, photoperiod, cystic corpora nigra, floaters in posterior/anterior chamber)
Allergic (rhinitis)
Sinusitis, otitis (Trombicula autumnalis), GP mycosis
Structural: skull fractures, dental disease, THO, TMJ (hyperesthesia)
Bit bridle
Diagnostic plan for head shaking
Aim is to identify potential triggers:
Physical exam/environment/ management
Ocular exam
Dental exam
Upper airway endoscopy including GP
Nerve blocks (infraorbital and maxillary)
Skull x-rays/CT
Otoscopy
Medical treatment of head shaking
Cyproheptadine 0.3mg/kg PO BID
Carbamazepine (4mg/kg)
Gabapentin (25mg/kg q 8h)
Steroids (inhaled)
Magnesium sulphate 40mg/kg)
Antihistamine drugs
Melatonin 4 mg/kg BW, q6h
Nose nets
Ocular sunglasses
Bridles bit
Surgical management of head shaking
All have poor response
(Infraorbital neurectomy with cryotherapy, chemical sclerosis, caudal compression of infraorbital nerve)
Other therapies for head shaking
EquiPENNS (percutaneous nerve stimulation)
Electro-acupuncture
Spectrum of CND disorders characterized by episodes of excessive sleepiness, muscular weakness and REM onset sleep
Narcolepsy
Episodes of collapse due to lack of regular resting/sleep
Sleep deprivation
Reasons for sleep deprivation
Chronic arthritis
Chronic pain
Fear to environment
Narcolepsy cause
Dysfunctional orexin system: hypocretins 1-2 and hypothalamic GABA neurons
Familiar in several breeds
Clinical signs of sleep deprivation and narcolepsy
Staggering, lowering the head and neck, buckling of the thoracic limbs, kneeling posture, flaccidity of lips
Unexplained abrasions wounds (knees, lips)
Kneeling when tightening the girth
Diagnosis of sleep deprivation or narcolepsy
Age, recent changes in environment, stable, barn, premises, wild life
Concurrent disease: arthritis: back, hocks, carpus, PPID
Quality of bedding, tight rungs in winter
True narcolepsy: rule out differentials
Treatment of sleep deprivation and narcolepsy
Bute-trial
Thick bedding
Large stable
Inside barn
Remove rugs
Progressive, chronic neuromuscular disease in horses characterized bygait abnormalities when backing up, trembling of the tail while held erect, trembling of the thigh muscles and a flexed and trembling hind limb when held
Shivers
Cause of shivers
Damage of the deep cerebellar nuclei (function is fine-tune of planned movements, flexion and extension activated at the same time)
Clinical signs of shivers
Backing manoeuvre: hyperextension of hindlimbs
Inability of picking up the hind limbs: offers contralateral limb, hyperextension
Normal ambulation otherwise: walk forward, trot, cantering, performing
Key features of shivers
Normally starts around 5 years of age
Normally progressive and performance limiting
Rule out other conditions: upper fixation of patella, stifle OA, sacro-iliac pain
Prognosis of shivers
Guarded, no treatment
