Neurology Flashcards
Forebrain, brainstem and cerebellum functions
forebrain - recognition of special senses, behaviour
brainstem - cranial extension of spinal cord, midbrain and hindbrain and cranial nerves - reaction to environment, damage will cause depressed mentation
cerebellum - fine movement control
neuro exam - equine - behaviours
may indicate forebrain disease
seizures - specific to forebrain
head pressing
wondering
circling
changes in voice
changes in appetite
licking
aggression
yawning
blindness
neuro exam - equine - mental state
RAS and forebrain
lowered awareness
lowered conciousness
neuro exam - equine - head position
peripheral vestibular, central, cerebellar, MSK, or neuromuscular
head tilt
neck turn
cranial nerve exam - equine
1 - olfactory - can’t really test
2 - optic - sight
menace response, PLR, swinging light test - PLR needs nerve intact before chiasm, swinging light test after
3 - occulomotor - PLR, eye position and movement
4 and 6 - trochlear and abducens - eye position and movement
5 - trigeminal - sensation to face, motor to mastication muscles
7 - facial - muscles of facial expression - asymmetry, often more pronounced at muzzle, eyelid palpation may be useful
8 - vestibulocochlear - head posture, induced eyeball movement/normal vestibular nystagmus, normal gait, blindfold (exacerbates head tilt), hearing - weakness towards side of lesion
9-12 - swallowing and tongue - pull out tongue and assess for tone and symmetry, observe swallow after tongue replaced
upper motor neurone injury
spinal cord, brainstem to synapse with lower motor neurons at spinal cord
inhibit, modulate and control gait
increased muscle tone
increased reflexes
no atrophy
variable weakness
lower motor neurone injury
spinal cord grey matter and peripheral nurves
cervical - forelimbs
lumbosacral - hindlimbs
decreased muscle tone
decreased reflexes
muscle atrophy
weakness
sensory loss
motor neurone exam
ataxia - wide based stance
weakness - narrow based stance, paresis, mypometria, recumbency, postural deficits
hyperreflexia
increased muscle tone
hyporeflexia
decreased muscle tone
atrophy
cervical vertebral malformation - equine
most common spinal cord disease
initial loss of proprioception
progresses to paresis and motor weakness
to loss of sensory perception and loss of pain
ataxia - testing - equine
proprioceptive deficits
whole body or specific limb
poor coordination
swaying
excessive limb movement in swing phase
weaving
abduction
crossing limbs
stepping on themselves
signs exacerbated by tight circles, sudden stoppin, backing up, and going up and down hills
lift head so can’t watch their feet when testing
weakness (paresis) - testing - equine
hoof wear - sign of dragging toes, hypometria
generalised weakness
prefer walking to standing still - have to fix muscles to stand still
hopping
circling
trembling
buckling of weak limb
knuckling over
localised weakness - lower motor neurone or peripheral
weakness and ataxia - upper motor neurone
generalisied weakness with no ataxia - neuromuscular
tail pull - reflex - at rest tests upper motor neurone, walking tests lower
lesion localisation
C1-6 - UMN signs in both fore and hindlimbs
C7-T2 -
LMN signs in forelimb - weakness
UMN signs in hindlimb - ataxia
T3-L3 -
no forelimb signs
UMN signs in hindlimb
L4-S3 -
no forelimb signs
LMN signs in hindlimb
S3-end -
normal forelimbs and hindlimbs
classification of spinal cord deficits
1 (+) - subtle
barely detectable at normal gait, may be seen during backing, stopping, turning, swaying etc
2 (++) - mild
can be seen at normal gait but exaggerated with maneuvers
3 (+++) - moderate
prominent deficits at normal gait, can buckle and fall during maneuvers
4 (++++) - severe
spontaneous tripping and falling at normal gait, can present as complete paralysis
forelimbs often a grade lower than hindlimbs with focal cervical or brainstem lesions
hindlimb and brainstem signs
behaviour issues
seizures
blindness
coma
altered consciousness
head posture
some ataxia in conscious maneuvers
perinatal asphyxia syndrome - equine
in utero hypoxia or interruption of oxygen supply during birth
hypoxic lesions in multiple organs
ischemia, oedema, and reperfusion injury to various organs
dummy foals
may not be obvious until 12-24 hours
severe cases - central respiratory depression
mild - unable to latch, poor suck reflex
moderate - aimless wandering and abnormal voalisations
severe - seizure
good prognosis with nursing care - up to 2 weeks - nutrition, antibiotics, eye care, gastric ulcer medication, protection from walking into things
neonatal seizures and epilepsy - equine
trauma
sepsis
secondary to anemia, hypoglycemia, metabolic
benign epilepsy of foals - arabs up to 12 months, low seizure threshold
cerebellar hypoplasia - equine
signs at birth or within first 6 months
developmental abnormality
usually arabs
sometimes dummy foals get this as well
signs -
intention tremor
loss of fine motor control
ataxia
wide based stance
still have full strength and otherwise alert
no treatment - euthanasia
brainstem or cranial nerve disease
vestibular
facial nerve paralysis - common, associated with head collars or hitting head
ocular abnormalities - eg horners
pharyngeal/laryngeal nerve deficits - dysphagia
trigeminal neuritis - headshaking
vestibular disease - equine
usually caused by trauma or otitis media/interna
can lead to temperohyoid/stylohyoid osteoarthropathy
signs - lead towards side of lesion, ataxia, nystagmus
radiography/CT to diagnose otitis
guttural pouch endoscopy - look for changes in stylohyoid bones
dysphagia - equine
commonly associated with guttural pouch disease
less common to have neurological presentation
cranial nerves and internal carotid in guttural pouch
also lead poisoning
horners
accumulation of crud around nose from dysphagis
facial nerve paralysis - equine
commonly iatrogenic from halter
or from trauma
prolonged deficits - eye injury, keratitis/dry eye, dysphagia, feed pouching, poor performance (nostril collapse)
horners sundrome - equine
usually iatrogenic causes - extra vascular injection of irritant
loss of innervation to one side of the head
sweating to level around C2
drooping on one side
some myositis
protruding third eyelid
enophthalmus
trigeminal neuritis - equine
headshaking - abnormal, rapid, vertical head flicking (like trying to get bee out of nose)
may rub nose on ground
nostril clamping during exercise
seek shady areas
stick nose under horses tails
in severe cases may hit themselves and cause damage
grades -
0 - no shaking
1 - shaking at exercise but not enough to interfere with riding
2 - shaking at exercise too much to be safe riding
3 - shaking even at rest
diagnosis by exclusion of other causes - nothing up the nose, no nostril inflammation, check ears, teet, temperomandibular junction
treatment - nose nets, gabapentin, antihistamines, percutaneous nerve stimulation treatment (PENS - most common treatment)
spinal trauma - equine
sudden onset ataxia or recumbency
sometimes will have observed incident
often see improvement so should wait and see if they get better
can have initial improvement then worsening as scar tissue forms
most commonly atlanto-occipital-axial region, caudal cervical, or mid back (less common, needs significant force)
signs vary - ataxia and paresis to recumbency
focal or diffuse sweating
may be panicky
cervical vertebral malformation - equine
multifactorial causes - congenital and familial aspects
usually large rapidly growing horses with unrestricted diet
related to developmental orthopedic disease - may see this in other joints
ataxic with wide based stance
neck pain not common
sweating
types of lesions -
stenosis - narrowing of vertebral canal - may only be evident in one position
abnormal articular processes
subluxation on flexion or extension of neck
enlarged vertebral physeal growth regions
overriding of vertebral arch and next cudal vertebral body
proliferation of articular and soft tissues
may be able to see on radiography, CT better
management -
surgery possible but don’t really do it
early detection and dietary restrictions best
prognosis poor for riding the horse once disease advanced
cauda equina syndrome - equine
affects sacrococcygeal spinal cord segments - to bladder, rectum, anus, tail and perineum
incontinence
flaccid anal, perineal and tail tone
penile prolapse
weakness and paresis of pelvic limbs
causes -
trauma - breeding
infectious - polyneuritis equi, EHV-1
toxic - sorghum
rare congenital abnormalities
neoplasia
EHV-1 management
localise lesion
rule out other causes
history of respiratory signs or abortion
isolate
can recover with good nursing carer
better prognosis if not recumbent - if down for more than 24 hours then prognosis poor
may see residual deficits for a year
can cause cauda equina syndrome
peripheral nerve and neuromuscular disease - equine
localised weakness - peripheral nerve
diffuse weakness - neuromuscular
abnormal hind limb gait - shivering and stringhalt
generalised tetany - tetanus
prognosis depends on degree of damage to the nerve -
neuropraxia - loss of function only - may resolve in 14 days
axonotmesis - severence of axons - 6 months
neurotmesis - severence of entire nerve fibre - prolonged or permanent loss of function
scarring and fibrous tissue can lead to permanent worsening of nerve injury
brachial plexus injury - shoulder and carpus involvement
radial nerve - more albow
sweeney - suprascapular nerve trapped
support other limbs to prevent weight bearing laminitis
equine motor neurone disease
neuromuscular
generalised weakness
trembling
hungry
weakness but not ataxia
shifting weight
reluctance to stand still
elevation of tail head
diagnosis -
signs
mild muscle enzyme increase
low serum vitamin E
muscle biopsy of tail head muscle - atrophy
retinal lipopigment deposits
treatment - vitamin E supplement, physio
often not fixable
botulism - equine
clostridium botulinum - contaminated feed, water, or in ingesta of suckling foals
blocks acetylcholine at presynapses
flaccid paralysis of skeletal muscle
classic tongue paralysis –> respiratory depression
stringhalt - equine
hyperreflexia in hindlimb -
classic stringhalt - unilateral
toxic stringhalt - bilateral
can recover from classic form - take off pasture, takes about 18 months
tetany - equine
distressed face
flared nostils
elevated tail head
stiffness
third eyelid pulled across
clostridium tetani
entrance through wound
muscles continuously contracting, often elicited by sound, light and touch
poor prognosis
can try antitoxins
toxin increases necrosis at wound site of entry
sections of the vetebrae
C1-C5 - neck
C6-T2 - cervical intumescence - thoracic limbs
T3-L3 - thoracolumbar - trunk
L4-S3 - lumbosacral intumesence - pelvic limbs
Cd1-end - tail
toxins that cause seizures
xylitol
raisins
chocolate
alcohol
cannabis
stage of seizure
pre-ictal - altered behaviour
ictal - actual seizure - lack of response to external stimuli, involuntary urination
post-ictal - disorientation
post seizure exam
temperature - hyperthermia –> more seizures
neuro exam - check for deficits (over 5 mins or cluster seizures can cause lasting brain damage), check for signs of CNS neoplasia
gait - any signs of weakness or ataxia
categorising neuro lesions - 5 finger rule
localisation - location in CNS
lateralisation
pain/non painful
progression - progressive/stable/improving
onset - chronic/acute/peracute
ddx for seizures
toxins
idiopathic epilepsy
thromboembolism
neoplasia - meningioma, glioma, lymphoma
haemorrhage - increased intracranial pressure
immune mediated
meningitis - bacterial, viral, protozoan (neospora)
trauma
hydrocephalus - big head chihuahua
liver disease - and any metabolic disease affecting the liver
pancreatic disease - insulinoma
diagnostics for seizures
MRI - mass
bloods -
liver - liver enzymes - bile acid stim, albumin, bilirubin, clotting
pancreas - blood glucose
anemia
serology - specific disease testing
c reactive protein - raised if lots of inflammation
CSF tap - neutrophilia and bacteria in spinal fluid - bacterial meningitis
treatment - idiopathoc epilepsy
consider frequency and length of seizures
cluster seizures particularly bad
diazepam - reduces electrical seizure in brain when already having seizure
phenobarbitol - takes 3 weeks to work properly, hepatotoxic
potassium bromide - alongside other drugs, lots of side effects
once on them have to stay on forever
all options have side effects - sedation, liver toxicity, ataxia, PUPD, weakness, behaviour changes
ddx vestibular syndrome
otitis
neoplasia
encephalitis
antibiotic reaction
thiamine deficiency
head trauma
hypothyroidism
idiopathic vestibular disease
head tilt towards side of lesion
fast phase nystagmus away from side of lesion
IVDD - hansen type 1
nucleus pulposus broken out of disc completely
acute and explosive onset
around age 2
mostly at thoracolumbar junction
painful
over time - haemorrhage, necrosis, infarcation
most common sausage dog type
IVDD - hansen type 2
bulge of disc but not complete break out
usually at only one site
more chronic
painful - neck pain more apparent than lower back
can lead to nerve root compression - very painful, radiating down nerve
older dogs
terriers, dalmation, GSDs
IVDD - cervical myelopathy
wobbler syndrome
large and giant breeds
weakness and ataxia, first seen in pelvic limbs
lameness and stiffness in thoracic limbs
neck pain and stiffness - more obvious than lower back
weird posture - wobbly back legs
reduced proprioception
2 types -
disc associated - middle aged dobermans - hypertrophy of annulus (abnormally shaped disc)
bone associated - youn great danes - bone malformation and osteoarthritis, multiple levels often affected (overgrowth of bone around spinal cord)
handling can cause ongoing damage
IVDD - grading
1 - painful, no neuro deficits
2 - painful, wobbly but ambulatory
3 - non ambulatory but in tact motor function if needed
4 - no motor function, in tact deep pain
5 - no motor and deep pain gone
IVDD - management
conservative - cage rest, anti-inflammatories, analgesia, bladder management
grades 1-2 or if surgery not possible
surgery -
fenestration - more simple, prophylactic to prevent further, doesn’t penetrate spinal canal
decompressive surgery - enter spinal canal to remove extruded material
fibrocartilaginous embolism
large breeds + mini schnauzers and shelties
sudden onset vocalisation - acute pain
knuckling, weakness, collapse - one or more limbs, progressing for first 24 hours
cause - piece of fibrocartilage goes intramedullary and causes acute vascular injury and embolism
medical management - NSAIDs, steroid
can’t operate
absence of deep pain is a poor prognostic sign
cen develop ascending damage - can’t be treated
chronic degenerative radiomyelopathy
chronic
hind limb dysfunction
pain
wobbling
loss of proprioception
scuffing toes
(similar to ALS in humans)
usually progress to non-ambulatory in a year
large breeds
need CT and MRI to diagnose
lots of differentials - hip dysplasia, disc disease, spinal tumours
atlanto-axial instability
young, toy breeds
cervical pain - ddx for hansen 1 IVDD
lesion at C1-C5 - all 4 legs, can cause tetraplegia and respiratory distress
usually acute trauma from fall or RTA
keep neck supported
management -
mild - medical - rest, NSAIDs, 6-8 week neck brace
severe - surgery - high risk of complications
Neoplasia - spinal
primary - meningioma, glioma, nerve sheath tumours (forelimb problems, axillary pain), lymhoma
secondary - rich cancellous bone site, common for mets - first sign of neoplasia can be spine fracture
hypervitaminosis A
cats fed too much liver - chronic
lethargy
poor coat - stiff so don’t want to groom
constipation
anorexia
stiffnedd/reluctance to move
new bone formation around spine, compresses spinal cord and nerve roots
makes movement difficult and painful
discospondylitis
infection of disc and vertebral endplates
hematogenous spread - bite wounds, foreign bodies, surgical site infection
middle aged large breeds
gradual onset
pain
stiffness
ataxia
sometimes paresis
pyrexia
ataxia in chronic cases
management - cage rest, antibiotics, NSAIDs,
surgery - decompress, debride and collect samples
prognosis fair to good but poor if fungal infection
