Neuro Flashcards
tension headache presentation
generalised, bilateral
non-pulsatile
tight band, pressure like
can radiate to neck and shoulders
episodic, chronic
tension headache ix
none specific to tension headaches
normal neuro exam
pericranial or neck muscle tenderness possible on examination
is a recent fall a red flag
yes for subdural haemorrhage
what do you need to be aware of when prescribing analgesia for headaches
medication overuse headaches (aka rebound headaches)
cluster headache presentation
unilateral
episodic
sudden onset
excruciating pain
lacrimation, rhinorrhea, partial Horner’s
cluster headache ix
no ix specific for cluster headaches.
MRI- exclude anything more sinister
ESR - exclude giant cell arteritis
pituitary function tests - exclude pituitary adenoma
cluster headache mx
acute
-subcutaneous sumatriptan
-high dose, high flow O2
prophylaxis
-verapamil (CCB)
migraine presentation
unilateral
comes on gradually
pulsating, throbbing
4-72 hrs
exacerbating: activity, stress, phonophobia, photophobia
relieving: quiet, dark room
associated symptoms:
aura. n+v, visual changes, tingling, numbness, migraine interferes with current activities
migraine ix
mostly ix of exclusion
- MRI - exclude smth more sinister
- ESR - exclude giant cell arteritis
- LP - haemorrhage, meningitis
migraine mx
conservative:
- headache diary
- avoid triggers
- relaxation techniques (CBT, mindfulness)
acute:
- simple analgesia
- triptans
- consider anti-emetic
prophylaxis:
- propanolol
- topimarate
- amitryptiline
DO NOT GIVE OPIATES
trigeminal neuralgia presentation
unilateral pain along trigeminal distribution
paroxysmal, lasting seconds, recurrent episodes
stabbing, shooting pain, like electric shock
exacerbated by moving jaw
risk factors for trigeminal neuralgia
increased age
female
multiple sclerosis
management of trigeminal neuralgia
1st
acute - anticonvulsants (eg carbamazepine)
long term - microvascular decompression or ablation surgery
raised ICP headache presentation
bilateral, gradual, throbbing
vomiting
confusion
worse in mornings
severe pain
papilloedema
Cushings triad - increased systolic BP, irregular breathing, bradycardia
raised ICP Ix
urgent CT head
never do lumbar puncture, can cause brainstem herniation
raised ICP mx
management of risk factors
analgesia
treat underlying cause
what layers of brain does meningitis affect
arachnoid and pia
causes of meningitis
bacteria - e.coli, h.influenzae, strep pneumoniae, neisseria meningitidis, listeria monocytogenes
virus - enteroviruses, HSV, VZV, HIV
tuberculosis
meningitis signs and symptoms
meningism: neck stiffness, photophobia, headache
fever
n+v
seizures
malaise
hypotension
tachycardia
Kernig’s sign
Brudzinski’s sign
petechial non-blanching rash
meningitis Ix
obs
VBG
lumbar puncture (most important)
2 sets of blood cultures
CT head before LP
CSF analysis in bacterial meningitis
appearance - cloudy
cells - increased neutrophils (polymorphs)
glucose - reduced
protein - increased
CSF analysis in viral meningitis
appearance - clear
cells - increased lymphocytes (mononuclear)
glucose - normal
protein - normal/increased
CSF analysis in TB meningitis
appearance - fibrin web
cells - increased lymphocytes (mononuclear)
glucose - reduced
protein - increased
meningitis mx
at GP: benzylpenicillin IM & urgent referral to hospital
at A&E: broad spec ABs (ceftriaxone IV, benzylpenicillin IM) acyclovir if viral
targeted ABs
consider dexamethasone
manage close contacts
complications of meningitis
hearing loss
sepsis
impaired mental status
encephalitis causes
viral: HSV 1-2, CMV, EBV, HIV, measles
non-viral: bacterial meningitis, TB, malaria, listeria, lyme disease, legionella
encephalitis presentation
viral prodrome
can have signs of meningism
headache
altered mental state
encephalitis Ix
EEG
LP
Blood (FBC, LFT, culture)
CT/MRI
encephalitis Mx
give acyclovir to all pts with suspected encephalitis
then give appropriate antiviral or antibiotic according to underlying aetiology
stroke definition
sudden onset focal neurological deficit of presumed vascular origin lasting more than 24 hrs
types of stoke
haemorrhagic
ischaemic
stroke symptoms
acute onset
limb weakness/numbness
facial droop
dizziness
loss of coordination and balance
speech difficulties
visual changes
ACA stroke associated signs
contralateral hemiparesis (legs > arms)
behaviour changes
MCA stroke associated signs
contralateral hemiparesis (arms > legs)
contralateral hemisensory loss
apraxia
aphasia
quadranotopias
PCA stroke associated symptoms
contralateral homonymous hemianopia
visual agnosia
cerebellar dysfunction signs
DANISH
Dysdiadochokinesia
Ataxia (gait and posture)
Nystagmus
Intention tremor
Slurred, staccato speech
Hypotonia/heel-shin test
stroke Ix
urgent within 1hr:
- non contrast CT head to rule out haemorrhage
ROSIER score - risk of stroke in emergency room
serum glucose - hypoglycaemia may mimic stroke
u&e - exclude hyponatraemia
cardiac enzymes to exclude MI
FBCs - anaemia or thrombocytopenia prior to initiation of thrombolysis or anticoagulants
ECG - monitor vital signs
CT angiogram
carotid doppler
stroke mx
once haemorrhage excluded, initial treatment depends of time from symptom onset
<4.5 hrs - thrombolysis (IV alteplase)
then give aspirin 300mg oral
> 4.5 hrs or thrombolysis contraindicated- aspirin 300mg oral
all pts should be referred to stroke unit MDT
swallowing assessment - aspiration pneumonia, choking
secondary prevention of stroke
300mg PO of aspirin for 2 weeks
then
AF pts: DOAC/warfarin prophylaxis
non-AF pts: (1st line) clopidogrel lifelong (2nd) aspirin + dipyrimadole + antihypertensive/glucose control/atorvastatin
score used to estimate stroke risk in TIA pts
ABCD2 score
score 4+ refer to stroke specialist
transient ischaemic stroke mx
300mg aspirin
if within 7 days of episode: specialist review within 24 hrs
if after 7 days of episode:
specialist review within 7 days
secondary prevention
clopidogrel 75mg o.d
+ high intensity statin (atorvastatin)
+ BP control with antihypertensive if necessary
vessels affected in extradural haematoma
middle meningeal artery underneath pterion
extradural haematoma signs and symptoms
head trauma > loss of consciousness > lucid interval > headache, decreased GCS, symptoms of raised ICP
extradural haematoma ix
urgent non-contrast CT head - lemon shape
maybe MRI
extradural haematoma mx
surgical emergency
refer to neurosurgery for burr hole or craniotomy
blood vessels affected in subdural haematoma
bridging veins
RF for subdural haematoma
head trauma and falls
elderly
alcoholics
anticoagulation
classification of subdural haematoma
acute - within 72 hrs (younger pts, trauma)
subacute - 3-20 days (worsening headache, elderly)
chronic - after 3 weeks (headache, confusion)
subdural haematoma signs and symptoms
gradual continuous headache
fluctuating consciousness
confusion
personality changes
symptoms of raised ICP
subdural haematoma ix
urgent non-contrast CT head
- banana shape
subdural haematoma mx
depends on size and presenting symptoms
A to E approach and neurosurgery referral
small (<10mm) + no significant neurological dysfunction - observe
large (>10mm) or significant neurological dysfunction - Burr hole or craniotomy
subarachnoid haemorrhage risk factors
polycystic kidney disease
alcohol
smoking
hypertension
signs and symptoms of subarachnoid haemorrhage
pain in back of head
thunderclap headache
meningism signs
subarachnoid haemorrhage ix
urgent non contrast CT head
- look for hyper-attenuation around circle of Willis
if CT head normal, lumbar puncture
- xanthochromia and oxyhaemoglobin
subarachnoid haemorrhage mx
same as haemorrhagic stroke
refer for neurosurgical evaluation
nimodipine to prevent delayed cerebral ischaemia
review anticoagulant medication
epilepsy triggers
there may be no triggers
lack of sleep
alcohol
flashing lights
stress
epilepsy signs and symptoms
before
- strange feeling in stomach
- strange smells or taste
- visual disturbances
during
- tongue biting
- incontinence
- jerking movements
after
- slow recovery
- post-ictal headache
- post-ictal confusion and drowsiness
- post-ictal myalgia
frontal lobe epilepsy presentation
motor symptoms
jacksonian march
post-ictal flaccid weakness
involuntary actions
temporal lobe epilepsy presentation
aura (epigastric discomfort)
automatisms
hallucinations
parietal lobe epilepsy presentation
sensory disturbances (pain, tingling, numbness)
occipital lobe epilepsy presentation
visual phenomena
tonic-clonic seizures phases
tonic phase - muscles stiff
clonic phase - quick rhythmical jerking of limbs
absence seizures presentation
brief staring episodes lasting 5-10 seconds
LOC but posture may be maintained
common in children
may be mistaken for not paying attention
epilepsy Ix
EEG
bloods to identify cause
glucose - hypoglycaemia
fbc - infection
u+e - electrolyte disturbances
serum prolactin - post-ictal transient elevation
CT,MRI to identify potential lesion
clinical diagnosis made after 2+ unprovoked seizures occurring >24 hrs apart
epilepsy mx
focal
- carbamazepine
- lamotrigine
generalised
1st - sodium valproate
2nd - carbamazepine
avoid sodium valproate in women of childbearing age
lamotrigine preferred
side effects of antiepileptics
psychiatric disturbances
weight gain
carbamazepine - neutropenia and osteoporosis
lamotrigine - Stevens-Johnson syndrome
what are dissociative seizures
resemble epileptic seizures but no biological correlate
suspect if prolonged duration and history of abuse, psychological precipitants
mx often involves psychotherapy
status epilepticus definition
seizure lasting > 5 mins or repeated seizures without recovery or regain of consciousness in between
medical emergency
status epilepticus triggers
non adherence to medication
alcohol abuse
overdose and drug toxicity
status epilepticus mx
secure airway
- high flow o2
iv access and monitoring
IV lorazepam or PR diazepam
- repeat after 10 mins if seizure doesn’t stop
IV phenytoin
refer to ICU
epilepsy complications
sudden unexpected death in epilepsy (SUDEP)
behavioural problems
fractures from seizures
complications from drugs
Guillain-Barre syndrome aetiology
autoimmune process attacking myelin surrounding peripheral nerves
30% cases after gastroenteritis infection caused by Campylobacter jejuni
Guillain-Barre syndrome signs and symptoms
gastroenteritis
URTI
peripheral neuropathy
-ascending paraesthesia and pain
-symmetrical limb weakness
-hypotonia
- flaccid paralysis
-altered sensation/numbness
-fasciculations
can cause respiratory paralysis
Miller-Fischer syndrome (25% of cases)
- opthalmoplegia
- areflexia
- ataxia
Guillain-Barre syndrome Ix
definitive diagnosis
- nerve conduction studies
spirometry
lumbar puncture
- increased protein
- normal glucose and WCC
bloods
- anti-ganglioside antibody in Miller-Fisher variant
Guillain-Barre syndrome mx
IV immunoglobulin (IVIG)
cord compression signs and symptoms
motor
- limb weakness
-UMN symptoms below level of lesion
-LMN symptoms at level of lesion
sensory
-sensory loss below a specific level
-back pain
autonomic
- constipation
- urinary retention
- erectile dysfunction
cord compression Ix
definitive diagnosis - MRI
may use CT
bloods- FBCs, u&e, calcium, ESR, immunoglobulin electrophoresis (multiple myeloma)
urine- Bence Jones proteins (multiple myeloma)
radiculopathy cause
compression of nerve at or near the nerve root as it exits the spinal cord
signs and symptoms of radiculopathy
LMN symptoms for muscles innervated by this spinal root
dermatomal pattern of pain, numbness
eg sciatica
management of radiculopathy
physiotherapy and NSAIDs
Lasegue’s sign
pain in the distribution of the sciatic nerve is reproduced on passive flexion of the straight leg at the hip between 30-70 degrees
types of hydrocephalus
obstructive
- stenosis of cerebral aqueduct or intraventricular foramina
- posterior fossa lesions compressing 4th ventricle
communicating
- decreased CSF absorption
- increased CSF production
normal pressure
- idiopathic chronic ventricular enlargement without significantly elevated CSF pressure
- triad: urinary incontinence, cognitive impairment, gait apraxia (wet, wacky and wobbly)
hydrocephalus ex vacuo
- ventricular expansion secondary to brain atrophy such as in Alzheinmer’s
signs and symptoms of hydrocephalus
acute onset
- features of raised ICP
- n+v
- headache
- papilloedema
chronic onset
- cognitive impairment
- unsteady gait
- double vision
- CN palsies
in children
- sunset eyes
- skull enlargement
hydrocephalus Ix
1st line - CT/MRI head
CSF analysis from ventricular drain
management of hydrocephalus
ventriculoperitoneal shunting to drain CSF
multiple sclerosis types
relapsing remitting (RR) ms
or primary progressive MS
both turn into secondary progressive MS
multiple sclerosis signs and symptoms
optic neuritis
motor weakness
sensory disturbance
fatigue
hemiparesis/hemisensory loss
Lhermitte’s sign
multiple sclerosis diagnosis
- absence of alternative diagnosis
- dissemination in time (DIT)
- dissemination in space (DIS)
methods:
clinical history and examination
MRI
CSF
electrophysiology (VEPs)
antibodies associated with myasthenia gravis
autoantibodies against AChR at NMJ
some pts may have anti-MuSK antibodies
gland associated with myasthenia gravis
thymus gland !
thymic hyperplasia (70%)
thymoma (10%)
myasthenia gravis symptoms
muscles fatigue with use:
ptosis
diplopia
dysarthria
dysphagia
+/- SOB
fatigable muscles
normal reflexes
mysathenia gravis ix
bloods
- anti-AChR and anti-MuSK autoantibodies
- some patients are seronegative
EMG
CT/MRI to check for thymomas
Lambert Eaton Myasthenic Syndrome pathophysiology
autoantibodies against presynaptic VGCC at NMJ
Lambert Eaton Myasthenic Syndrome symptoms
muscle weakness improves with use
- difficulty walking
- weakness in upper arms and shoulder
- similar symptoms to MG
- autonomic: dry mouth, constipation, incontinence
- hyporeflexia
Lambert Eaton Myasthenic Syndrome associations
small cell lung cancer - paraneoplastic
autoimmune
Lambert Eaton Myasthenic Syndrome Ix
CT/MRI of chest for cancer detection should be performed
bloods for autoantibodies
EMG
CT/MRI to check for thymomas
motor neurone disease pathophysiology
build up of ubiquitinated proteins in the cytoplasm
death of corticospinal tracts
MND symptoms and signs
progressive muscle weakness
dysphagia
shortness of breath
sparing of oculomotor, sensory and autonomic function
wasting of thenar muscles
wasting of tongue base
upper neurone symptoms
- spasticity
- hyper-reflexia
- clonus
-positive Babinski’s sign
lower neurone symptoms
- hyporeflexia
- hypotonia
- muscle atrophy
- fasciculations and fibrillations
Parkinson’s pathophysiology
loss of dopaminergic neurones in substantia nigra
misfolded alpha synuclein builds up
Lewy bodies and Lewy neurites
drugs that cause parkinsonism
drugs that lower dopamine like antipsychotics and antiemetics
parkinsonian triad
resting tremor
rigidity
bradykinesia
6 Ms of Parkinsons
Monotonous hypotonic speech
Micrographia
Marche a petit pas
Misery
Memory loss
hypomiMesis
diagnosis of parkinsons
clinical diagnosis
Atypical Parkisonisms
Multiple system atrophy
- early autonomic and cerebellar features
- Papp-Lantos bodies
Progressive supranuclear palsy
- early postural instability and vertical gaze palsy
Corticobasal degeneration
- alien limb phenomenon
Vascular Parkinsons
- legs particularly affected
- gait worse than tremor
Lewy Body Dementia
- early dementia + visual hallucinations
Huntington’s disease pathophysiology
autosomal dominant inheritance
mutation of huntingtin gene (HTT)
expansion of CAG trinucleotide
atrophy of the striatum (caudate and putamen)
Huntington’s signs and symptoms
motor
- chorea
- athetosis
- dysphagia
- ataxia
cognitive
- depression
- personality changes
- lack of concentration
- dementia
Huntington’s Ix
CAG repeat testing
MRI
Huntington’s CAG repeat testing analysis
< 29 repeats: normal range
29-34: pt will not develop disease but next generation is at risk
35-39: some pt may develop disease, next gen at risk
40+: pt will develop disease
types of dementia
Alzheimer’s
Frontotemporal
Vascular
Lewy body
dementia pathophysiology
buildup of abnormal amyloid precursor protein (APP)
normally this breaks down into alpha and gamma secretase but in dementia breaks down into beta and gamma secretase which is resistant to degradation
this causes:
- extracellular amyloid plaques
- phosphorylation of tau
- intracellular neurofibrillary tangles
- leads to build up of abnormal APP
- degeneration of ACh neurones
5 As of Alzheimers
Amnesia
Anomia
Apraxia
Agnosia
Aphasia
(+/- depression and paranoid delusions)
Alzheimer’s ix
clinical diagnosis
- CSF: high tau, low beta amyloid
- CT, MRI, PET, SPECT
- brain tissue required for definitive diagnosis
MMSE
Addenbrooke’s cognitive assessment
MOCA
frontotemporal dementia (Pick’s disease) pathophysiology
tauopathy
involves tau. not amyloid beta.
frontal and temporal lobes affected
pick bodies - hyperphosphorylated tau protein
death within 5-10 yrs
frontotemporal dementia signs and symptoms
onset 40-60yrs
personality change
disinhibition
overeating- prefer sweet foods
emotional blunting
relative preservation of memory
Vascular dementia pathophysiology
CVS risk factors, female
sx similar to Alzheimer’s
location-specific deficits
affects small and medium vessels
step-wise progression
Wernicke’s encephalopathy pathophysiology
thiamine deficiency
Wernicke’s encephalopathy risk factors
alcoholism
malnourishment
bariatric surgery
dialysis
Wernicke’s Encephalopathy Ix
bloods (serum albumin, vit B1, LFTs)
ECG
CT
neuropsychology
Wernicke’s Encephalopathy signs and symptoms
triad: ataxia, eye signs, confusion
alcoholism
malnourishment
Wernicke’s Mx
medical emergency
likely give Pabrinex (B1)
Wernicke’s vs Korsakoff’s
Wernickes’s:
- acute
- confusion
- cerebellar and eye signs
- reversible
Korsakoff’s:
- chronic
- alert
- amnesia and confabulation
- irreversible?
