Neurology Flashcards

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1
Q

Forebrain, brainstem and cerebellum functions

A

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

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2
Q

neuro exam - equine - behaviours

A

may indicate forebrain disease

seizures - specific to forebrain
head pressing
wondering
circling
changes in voice
changes in appetite
licking
aggression
yawning
blindness

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3
Q

neuro exam - equine - mental state

A

RAS and forebrain

lowered awareness
lowered conciousness

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4
Q

neuro exam - equine - head position

A

peripheral vestibular, central, cerebellar, MSK, or neuromuscular

head tilt
neck turn

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5
Q

cranial nerve exam - equine

A

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

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6
Q

upper motor neurone injury

A

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

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7
Q

lower motor neurone injury

A

spinal cord grey matter and peripheral nurves

cervical - forelimbs
lumbosacral - hindlimbs

decreased muscle tone
decreased reflexes
muscle atrophy
weakness
sensory loss

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8
Q

motor neurone exam

A

ataxia - wide based stance
weakness - narrow based stance, paresis, mypometria, recumbency, postural deficits
hyperreflexia
increased muscle tone
hyporeflexia
decreased muscle tone
atrophy

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9
Q

cervical vertebral malformation - equine

A

most common spinal cord disease
initial loss of proprioception
progresses to paresis and motor weakness
to loss of sensory perception and loss of pain

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10
Q

ataxia - testing - equine

A

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

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11
Q

weakness (paresis) - testing - equine

A

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

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12
Q

lesion localisation

A

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

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13
Q

classification of spinal cord deficits

A

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

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14
Q

hindlimb and brainstem signs

A

behaviour issues
seizures
blindness
coma
altered consciousness
head posture
some ataxia in conscious maneuvers

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15
Q

perinatal asphyxia syndrome - equine

A

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

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16
Q

neonatal seizures and epilepsy - equine

A

trauma
sepsis
secondary to anemia, hypoglycemia, metabolic

benign epilepsy of foals - arabs up to 12 months, low seizure threshold

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17
Q

cerebellar hypoplasia - equine

A

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

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18
Q

brainstem or cranial nerve disease

A

vestibular
facial nerve paralysis - common, associated with head collars or hitting head
ocular abnormalities - eg horners
pharyngeal/laryngeal nerve deficits - dysphagia
trigeminal neuritis - headshaking

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19
Q

vestibular disease - equine

A

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

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20
Q

dysphagia - equine

A

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

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21
Q

facial nerve paralysis - equine

A

commonly iatrogenic from halter
or from trauma

prolonged deficits - eye injury, keratitis/dry eye, dysphagia, feed pouching, poor performance (nostril collapse)

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22
Q

horners sundrome - equine

A

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

23
Q

trigeminal neuritis - equine

A

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)

24
Q

spinal trauma - equine

A

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

25
Q

cervical vertebral malformation - equine

A

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

26
Q

cauda equina syndrome - equine

A

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

27
Q

EHV-1 management

A

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

28
Q

peripheral nerve and neuromuscular disease - equine

A

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

29
Q

equine motor neurone disease

A

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

30
Q

botulism - equine

A

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

31
Q

stringhalt - equine

A

hyperreflexia in hindlimb -
classic stringhalt - unilateral
toxic stringhalt - bilateral

can recover from classic form - take off pasture, takes about 18 months

32
Q

tetany - equine

A

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

33
Q

sections of the vetebrae

A

C1-C5 - neck
C6-T2 - cervical intumescence - thoracic limbs
T3-L3 - thoracolumbar - trunk
L4-S3 - lumbosacral intumesence - pelvic limbs
Cd1-end - tail

34
Q

toxins that cause seizures

A

xylitol
raisins
chocolate
alcohol
cannabis

35
Q

stage of seizure

A

pre-ictal - altered behaviour

ictal - actual seizure - lack of response to external stimuli, involuntary urination

post-ictal - disorientation

36
Q

post seizure exam

A

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

37
Q

categorising neuro lesions - 5 finger rule

A

localisation - location in CNS
lateralisation
pain/non painful
progression - progressive/stable/improving
onset - chronic/acute/peracute

38
Q

ddx for seizures

A

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

39
Q

diagnostics for seizures

A

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

40
Q

treatment - idiopathoc epilepsy

A

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

41
Q

ddx vestibular syndrome

A

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

42
Q

IVDD - hansen type 1

A

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

43
Q

IVDD - hansen type 2

A

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

44
Q

IVDD - cervical myelopathy

A

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

45
Q

IVDD - grading

A

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

46
Q

IVDD - management

A

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

47
Q

fibrocartilaginous embolism

A

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

48
Q

chronic degenerative radiomyelopathy

A

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

49
Q

atlanto-axial instability

A

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

50
Q

Neoplasia - spinal

A

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

51
Q

hypervitaminosis A

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

52
Q

discospondylitis

A

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

53
Q
A