Neurological exam of the horse and neuro diseases Flashcards
What does hypermetria, intetion tremors and weakness point towards
Cerebellar lesion
What is the first question to ask during neurological exam
Are there are cranial nerve signs present
What virus can have neurological and respiratory presentations
Equine herpes virus
What localisation would blindness, dementia, seizure, mild ataxia point towards
forebrain
What location would gait CN signs, gait deficits, tetraparesis and altered consciousness point towards
Brainstem
If we see tail/bladder paralysis, perineal hyperalgesia what localistion of lesion does this point towards
Sacral
What behavioural abnormalities might we see with forebrain disease
Yawning
Wandering
Psychosis
Circling
Head pressing
Seizures
What are some possible causes of forebrain dysfunction
Trauma to head
Hyponatraemia, hypoglycaemia
Hepatic encephalopathy hyperammoniaemia
Toxicity
Space occupying lesions
Intracarotd drug administration
How quickly will a horse react to an intra carotid drug injection
Immediately off the needle
How can we classify seizures
Either generalised or focal
Then focal split into simple focal or complex focal +/- secondary generalisation
Difference between simple focal and complex focal seizures
Complex focal has impaired consciousness
Signs of a generalised seizure
Loss of consciousness
Tonic clonic contraction
Limb paddling
Loss of continenance
Jaw clamping
WHen might strabismus be normal
NEwborn foals
What CN dysfunction causes a ventrolateral strabismus
CN III oculomotor nerve
What CN dysfunction causes a medial strabismus
CN VI
What CN dysfunction causes a dorsal strabismus
CN IV
Pathway for pupillary light response
Photoreceptors –> optic enrve –> optic chiasm with 90% decussation –> contralateral optic tract –> visual cortex + some to pretectal nuclei to prasymp CN III nuclei for pupil constriction (some crossing back here hence consensual response)
Which nerve is responsible for pupil constriction in PLR
CN III
Difference between dazzle response and PLR
Dazzle response uses a higher level of response with rostral colliculi but sitll subcortical
ONly gone in very bad disease
What do we expect to see with the swinging light test
Both pupils constrict with more constriction when light moved to contralateral eye
PAlpebral reflex
Touch medial canthus; stimulates CNV trigeminal sensory branch
Get blink response via Facial nerve motor
What is important to remember about the menace response
IT is learned; absent for a few days
What might a slow, abnormal menace indicate
cerebellar disease since cerebellum has a role in coordination and smoothing the menace response
What nerve controls head position and if there is a lesion which way does it go
VEstibulocochlear
Fall towards side of lesion
What are classic signs of facial nerve paralysis
Ear droop on that side
Eyelid droop
Muzzle twisted towards normal side
What is the cervicofacial reflex
Tap neck at C1-C2 and look for grimace from the corner of the mouth; tests C1/C2 nd CNVII
What would an animal with proprioceptive defects look like when walked; esp with head raised to move line of sight
Excessively floaty forelimbs
What disease would be shown up when horse blindfolded and asked to move
Proprioceptive defects with vestibular disease
What does it mean about deficits if proprioception is abnormal at rest vs when moving
If abnormal at rest = conscious deficits
If when moving = unconscious proprioceptiv deficits
Grades 0-5 ataxia
0 = normal
1 = mild neuro deficits only under special circumstances e.g walking in circles
2 = mild neuro deficits at all times/giats
3 = moderate deficits at all times
4 = severe deficits with tendency to buckle, stumble, trip, fall
5 = recumbent
Basic signs with UMN lesion
Paresis
Hyperreflexia
Basic signs with LMN lesion
Paralysis/paresis
Neurogenic muscle atrophy
Loss of reflexes
What would we see with gait at C-C5 lesion
UMN signs in fore and hindlimbs with hindlimbs looking worse
Wha would we see with C6-T2 lesion
LMN signs in forelimbs
UMN signs in hindlimbs
So forelimbs look ‘worse’
What would we see with T3-L3 lesion
Normal forelimbs, UMN signs to hind lims
What would we see with L4-S1 lesoni
Normal forelimbs
LMN signs to hindlimbs
What would we see with sacral/caudal lesions
Normal forelimbs
Normal or LMN signs in hing limbs
Cauda eqiune sign e.g bladder issues
What is coup and contrecoup
Where the brain is shaken inside the skull causing acceleration decelleration injuries which cause bruising and swelling to cranial and caudal aspects of the brain
What effect can be seen over 1-2 weeks after coup contrecoup with head trauma
Loss of vision due to optic nerve twang during swinging and slow degeneration
What happens in a rectus capitus muscle avulsion
caused by hyperextension of neck
Muscle can rip off temporal bone causing huge haemorrhage, nose bleed
Why might we choose to take CSF from the lumbosacral space after a head injury
Because there is a risk of cerebellar herniation if the ICP is raised and atlanto-occipital puncture is done
Things to consider in approach to head trauma (treatment)
CT best
Manage seizures
Reduce intracranial pressure if needed; hypertonic saline
NSAIDs
Vit E
Steroids
O2 if needed
How to manage seizures in a horse
Diazepam, phenobarbital, KBr
Signs of hyperammonaemia causing cerebral oedema
Yawning
Dullness
Wandering
Head pressing
Aggression
What two things can cause hyperammonaemia
Liver disease
Intestinal disease
Approach to dealing with hyperammonaemia
Deal with underlying disease
Add lactulose to convert ammonia to ammonium salt so less is absorbed
Antimicrobials to change gut slora
Why do horses with equine motor neuron disease look worse when standing than walking
Because the postural type 1 muscles are most affected since these have higher oxidative requirement
Aetiology of equine motor neuron disease
Vitamin E deficiency causing oxidative neuronal damage and neurogenic muscle atrophy
= neurodegenerative disease causing LMN signs
What things can lead to vitamin E deficiency in equine motor neuron disease
Dietary: lack of access to fresh pasture
INability to absorb vit E due to GI tract disease
Excess dietary copper
Treatment and prognosis of equine motor neuron disease
Treat with non-synthetic vitamin E suppleentation
40% improve a lot, 40% stabilise and 20% deteriorate
= guarded prognossi
Diagnosis of equine motor neuron disease
Muscle biopsy for neurogenic atrophy
Can measure vitamine E serum concentration but this is not specicifc
Clinical signs of equine motor neuron disease
Weakness and muscle atrophy
Narrow base stance
WEight shifting
Pigment retinopathy
What is polyneuritis equi
Granulomatous infiltration of extradural cauda equina
Signs = tail/anus/perineum/bladder/rectum paralysis as with caudal equine syndrome
+ cranila nerve signs
Poor prognosis
What cranial nerve signs are esp common with polyneuritis equi
facial nerve, trigeminal, vestibular signs
What is temporohyoid osteoarthropathy
Degenerative change at the temporohyoid articulartion; due to osseous proliferation at the joint and then pathological fractures of petrous temporal bone
–> Causes damage to vestibulo-cochlear (+/- facial nerve)
What are some possible aetiologies of temporohyoid osteoarthropathy
Spread of infection from middle/inner ear
Non-septic degenerative joint disease
Trauma
Clinical signs of temporohyoid osteoarthropathy + diagnosis
Vestibulocochlear nerve dysfunction: head tilt, nystagmus, dizziness, ataxia, dysphagia
Facial nerve dysfunction: asymmetry, corneal ulcers from exposure keratopathy
Diagnosis = seeing endoscopic thickening of articulation of sytohyoid bone in dorsal guttural pouch
[+ could do CT; or DV plain X-ray and compare the two sides]
Treatment of temporohyoid osteoarthropathy
Anti-inflammatories
+/- antibiotics
Surgical ceratohyoidectomy
What is Horner’s syndrome and what are the signs
Interruption of the sympathetic innervation to face
Lesion can be anywhere on pathway e.g neck, guttural pouch, cranial thorax
Signs = sweating, miosis, ptosis
What is shivers
Muscular condition of unknown origin where limbs with shivering flexed hindlimb posture
Progressive with no treatment; can progress to forelimbs
3 post-anaesthetic neuro complications and their signs
Facial neve paralysis: muzzle deviated away from lesion, may see corneal ulcers due to exposure keratitis (reduced saliva and tear production)
Radial nerve paralysis: dropped elbow and unable to bear weight
Spinal cord malacia; dog sitting with flaccid paralysis caudal to lesion after GA
Whta is the cause of cervical vertebral stenotic myelopathy in young vs old horses and which areas are affected
Young horses: malformation of vertebral canal/ligaments/cervical vertebrae
–> Affects mid cervical spine
Old horses: osteoarthritic change of articular process joints
-> Affects caudal cervical spin
What is static vs dynamic cervical vertebral stenotic myelopathy
Static = where there is compression in a neutral position
Dynamic = compression when the head is flexed/extended
Why are hindlimbs affected first in cervical vertebral stenotic myelopathy
Because the spincerebellar tracts are more peripherally located so they are compressed first
What is the classic history/signalment for young horses with cervical vertebral stenotic myelopathy
= after a period of recent rapid growth
First sign is reduced proprioception which progresses to paresis or spasticity
Diagnosis of cervical vertebral stenotic myelopathy
CT best
Myelography/plain radiographs
Take flaexed and neutral positions because dynamic lesions may only be noticed when neck is flexed
Compression normally visible from dorsoventrally
Conservative management of CVSM
Anti-inflammatories
Restrict diet in younf horses
Restrict exercise
Clinical signs of tetanus
Third eyelid protrusion
Saw horse rigid stance
Raised tailhead
Lockjaw
Dysphagia
Miosis
Hyperaesthesa
How does tetanus work
Clostridim tetani contaminated wounds and produces tetanospasmin and tetanolysin toxins
Tetanospasmin undergoes haematogenous spread then retrograde transport up peripheral nerves to inhibtiory interneuros and prevents synaptic release of GABA
Get spastic paralysi s
Treatment of tetanus
Give antitoxin
Clean and debride wound, make it aerobic to eliminate C tetani
Antibiotics; use metrnodazole
Tetanus toxoid vaccine (at distal site to anti-toxin)
Control muscle spasm: methocarbamol, diazepam, alpha 2 agonist sedation
Nursing care
Vaccine protocol for tetanus
Vaccinate at 6 months with 2 vaccines 4 weeks apart
Boost in last trimester to protect foal
When might we give tetanus antitoxin as tetanus prevention
For risk periods e.g any unvaccinated horse where wound/castration/abscess noticed
What are the possible ways to get botulism
Ingesting spores so toxin produced in GI tract
Infection of wound with C botulinum
Ingestion of pre-formed toxin in forage (spoiled food)
Pathogenesis of botulism
Haematogenous spread of toxin, binds to NMJ terminal and blocks ACh release causing flaccid paralysis
Pathogenesis of equine herpes myeloencephalitis
Ubiquitous EHV1 enters resp epithelial cells –> lymphocytes/monocytes –> lymphatics/blood –> dissemination
Have. background of respiraotry disease then sudden onset of neurosigns
Signs with equine herpes myeloencephalitis
Ataxia esp in hindlimbs
Bladder distension/incontinence, penile protrusion, flaccid tail and anus
Treatment for equine herpes myeloencephalitis
Supportive care with NSAIDs, nrusing
Antivirals; valacyclovir, gangiclovir 1
Why do we not use acyclovir in horses
Low bioavailability and poor effect
Prognosis for equine herpesvirus myeloencephalitis
50-70% survival
May have neuro deficits for life
How does vaccination help with equine herpesvirus myeloencephalitis
Decreases overal environmental load of EHV1
BUT does not protect against EHV myeloecenpahtiis
What is west nile virus
Flavivirus not currently in UK but with potential to come here as we have mosquito vector
Which species are amplifier hosts for west nile virus and which are dead end
Birds are amplifiers
Horses are dead end
Clinical signs of west nile virus
Most show no signs
Dullness, facial paralysis, dsphagia, muscle fasciculations, hyperexcitabiltiy. ataxia, recumbency
What is neuroborreliosis and what are the clinical signs
Disease due to borrelia burgdorferis which is transmitted by ixodes ticks
Causes muscle atropgy/weight loss, CN dysfunction ataxia, shifting lameness, pyrexia, joint effusio
Why must we take care with diagnosing Lyme disease from serology
ARound 1/3 of healthy horses are seropositive so may not be relevant to signs
As well as antibody titre what can we do to help diagnose neuroborreliosis
Use silver stain on joint effusion fluid and look for spirochaetes
Treatment of neuroborreliosis
MOnths long tetracyclines; starting with IV oxytet and moving to oral doxy
What type of virus is rabies
lyssavirus
Incubation time and clinical signs of rabies
INcubation = 2 weeks to several months
Signs: ataxia, pyrexia, colic, lethargy, self-mutilation, aggression
= fatal
What is equine protozoal myeloencephalitis
Protozoal disease from sarcocystis neurona and Neospora nughesia
affects white and grey matter at any CNS site
See atypical lameness, can get seizures, ataxia, dyphaia
NOT in UK
Why is monitoring horses important to assess western/eastern/venezualean equine encephalitis rsisk to human health
Horses are sentinel hosts so can be used to predict risk to humansS
Signs of western/eastern/venezualean equine encephaliti
Pyrexia, dullness, cirlcing/head pressing, dysphagia, paralysis, death
What causes western/eastern/venezualean equine encephaliti
Togavirus
Primary reservoir in birds/rodents
