Neuro big topics Flashcards
define TIA
transient, reversible neurological phenomenon lasting <24 hours with complete clinical recovery
causes of TIA
thromboembolism from carotids
cardioembolism
hyperviscosity
define amaurosis fugax
retinal artery embolism, causing sudden transient loss of vision in one eye
DDx TIA
hypoglycaemia
migraine aura
focal epilepsy
TIA Ix
carotid doppler CT brain (existing infarcts) Echocardiogram (cardiac cause of embolism) Erythrocyte sedimentation rate serum glucose
scoring system to estimate risk of stroke following TIA?
ABCD2 1 age >60 1 BP >140/90 clinical features 2 unilateral weakness 1 speech disturbance w/o weakness duration 1 10-59 mins 2 >60 mins 1 diabetes
treatment of TIA
control risk factors:
- blood pressure (antihypertensive regimen)
- cholesterol (statins)
- diabetes
- stop smoking
antiplatelets
- clopidogrel + aspirin
carotid endarterectomy
driving
- avoid for 1 month
- inform DVLA
effects of anterior cerebral artery stroke?
front and medial cerebrum superior humunculus thus:
- leg weakness/sensory disturbance
- gait apraxia
- incontinence
- drowsiness
- akinetic mutism (damage to cingulate gyrus)
- face SPARING
effects of middle cerebral artery stroke?
most common artery affected
- contralateral arm and leg weakness/sensory disturbance
- hemianopia (optic radiation)
- aphasia - difficulty comprehending (wernicke’s area in dominant temperoparietal lobe) and formulating speech (broca’s area in dominant frontol lobe)
- facial DROOP
- visuospatial disturbance
effects of posterior cerebral artery stroke?
- contralateral homonymous hemianopia with macular sparing
- cortical blindness
- visual agnosia (cant interpret what seeing)
- prosopagnosis (cant recognise faces)
- colour naming and discrimination
effects of poster circulation stroke?
supplies brainstem, cerebellum and occipital lobes
- motor deficits (hemiparesis/facial paresis)
- dysarthria (slow/slurred speech)
- vertigo
- nystagmus
- dysdiadochokinesia
- altered consciouness
investigations for stroke?
- urgent CT/MRI brain
to distinguish ischaemic and haemorrhagic - serum glucose
- coagulation tests
treatment of ischaemic stroke
thrombolysis (IV alteplase) if <4.5 hours after onset of symptoms –> alteplase = tissue plasminogen activator
risk management
- antiplatelets: aspirin + clopidogrel
- statins
- AF –> warfarin
- BP
post-stroke referral:
- speech and language therapy
- physio
- occupational therapy
risk factors for stroke? modifiable and non-modifiable
modifiable:
- HYPERTENSION
- smoking
- lack of exercise
- obesity
- diabetes
- hyperlipidaemia
non-modifiable
- ethnicity (black/asian)
- age
- male
- family history
- atrial fibrillation
what must always be excluded in DDx for stroke?
hypogycaemia
contraindications of thrombolysis in stroke?
- past CNS bleed
- > 4.5 hours since symptom onset
- seizures at presentation
- uncontrolled blood pressure
- recent lumbar puncture
What might be the cause of crossed signs? ie left arm weakness and right mouth droop
BRAINSTEM LESION
- crossed signs not involving brainstem would require 2 separate cortical lesions on both hemispheres
- facial involvement suggests lesion abve spinal cord
- CNs affected on same side as lesion (LMN signs), and corticospinal tract affected before it decussates at medulla (UMN signs)
LMN CN7 palsy (Bell’s palsy) vs UMN CN7 palsy (stroke)?
bells palsy = LMN lesion thus NO forehead sparing
stroke = UMN CN7 lesion this FOREHEAD SPARING
primary and secondary causes of haemorrhagic stroke?
primary:
- hypertension (Charcot-Bouchard aneurysm –> affects basal ganglia)
- lobar (cerebral amyloid angiopathy)
secondary:
- metastases/tumour
- arteriovenous malformation
- anticoagulants (warfarin)
treatment of haemorrhagic stroke
control BP –> B-blocker
warfarin antidote –> beriplex
cause of subarachnoid haemorrhage?
rupure of circle of willis due to:
- saccular/Berry aneurysm rupture
- arteriovenous malformation
risk factors subarachnoid haemorrhage?
smoking alcohol hypertension family history polycystic kidney disease
signs and symptoms of subarachnoid haemorrhage?
symptoms:
- sudden onset thunderclap headache
- vomiting
- seizures
- photophobia
- drowsiness
signs:
- kernig’s sign
- neck stiffness
- sentinel headache
investigations of subarachnoid haemorrhage?
- CT brain –> star-shaped blood pooling, hydrocephalus
- lumbar puncture (wait 12 hours) –> xanthochromia
DDx subarachnoid haemorrhage?
meningitis
migraine
management of subarachnoid haemorrhage?
refer all to neurosurgeon
nimodipine (CCB to control BP)
endovascular coiling
patho of parkinsons and histological features?
degeneration of dopaminergic neurones on substantia nigra pars compacta
associated with lewy bodies
features of parkinsons
1) pill-rolling tremor, worse at rest, unilateral
2) rigidity
3) bradykinesia (slow to initiate movement, monotonous hypophonic speech, micrographia)
4) postural instability
- gait (reduced arm swing on one side, shuffling)
premotor features of parkinsons
- anosmia (reduced smell sense)
- depression
- REM sleep disorders
- urinary urgency
- constipation
- visual hallucinations
management of parkinsons
early:
- ropinirole (dopamine-2 agonist)
- selegiline (monoamine oxidase-B inhibitor)
late:
- co-beneldopa (levodopa with decarboxylase inhibitor)
subtypes of motor neurone disease
- amyotrophic lateral sclerosis –> UMN + LMNs affected
- progressive bulbar palsy –> UMN + LMNs of CN 9-12
- primary lateral sclerosis –> UMNs affected
- progressive muscular atrophy –> LMNs affected
key features of MND
- muscular atrophy
- UMNs and LMNs both affected
- paralysis
- loss of motor control
- preservation of mental awareness
- NO sensory/sphincter disturbance (vs MS and polyneuropathies)
- NO eye movement involvement (vs MG)
pathology of MND
degeneration and loss of neurones in motor cortex, CN nuclei and anterior horn cells
diagnostic investigations for MND
1) electromyography/nerve conduction studies
2) clinical features
- increased creatinine kinase
- lumbar puncture
diagnostic criteria for MND
el escorial
treatment of MND
- riluzole (antiglutaminergic)
localisation of lesions:
- cortical lesion
- internal capsule
- brainstem
- spinal cord
- cortical lesion = contralateral weakness over large area
- internal capsule = complete contalateral hemiparesis
- brainstem = bilateral weakness, involves CN, bulbar involvement
- spinal cord
what is amyotrophic lateral sclerosis
events in the ALS-frontotemperal dementia locus
archetypal patient
- over 40
- stumbling gait
- foot drop
- proximal myopathy
- weak grip
- weak shoulder abduction (cant wash hair)
- speech/swallowing –> aspiration pneumonia
UMN signs:
- spasticity
- brisk reflexes
- upgoing plantars
LMN signs:
- wasting
- tongue fasciculations
- hypotonia
patho of multiple sclerosis
discrete plaques of demyelination at multiple CNS sites due tp CD-4 T-cell mediated immune response, leading to axonal loss and progressive symptoms (relapsing and remitting)
key features of MS
ALWAYS UMN AFFECTED
optic involvement
- unilateral optic neuritis
brainstem lesions:
- diplopia
- vertigo
- nystagmus
- facial numbness
- swallowing difficulty
spinal cord involvement
- abnormal gait
- bladder dysfunction
- numbness/tingling in limbs
- spastic leg weakness
- Lhermittes = electric shock feeling down spine/limbs
Uhthoffs = symptoms worsened by heat/exercise
risk factors of MS
family history
human t-lymphotropic virus-1
decreased vitamin D exposure (temperature climates)
investigations of MS
- lumbar puncture = +ve for oligoclonal bands on CSF
- visual evoked potential = slow signal transmission (due to demyelination)
- MRI = exclude other causes
- examination = UMN signs only
Dx = MRI + clinical features
diagnostic criteria of MS
McDonald Criteria
MRI + clinical features
DDx MS
cauda equina
prolapsed disc
spinal cord infarct
Tx of MS
acute (shorten relapse) = methylprednisolone
chronic (prevent relapse):
- interferon beta-1a
- azathioprine
spasticity = baclofen (GABAb analogue)
pain = carbamazepine
