Stroke/TIA Flashcards
What are the important parts of a stroke history?
- focal neurological symptoms of acute onset <– important!
- LOC & Headache <– typical!
- contiguous parts of the body affectged concurrently (no spread - that would be more like seizure)
- negative vs positive symptoms (flashes/prickles/extra movements)
- RF’s (CVS etc)
- FHx, ETOH and rec drugs
what should be looked at on stroke examination?
- Inspection – obvious hemiparesis, facial weakness, neglect of one side.
- Inspection – look for xanthoma, stigmata of endocarditis, marfanoid appearance, skin lesions of Fabry’s.
- Pulse – atrial fibrillation
- BP – hypertension
- CVS – murmurs, carotid and renal bruits, evidence of periph. vasc. disease
- Neuro – Full exam! Or enough to calculate NIH Stroke Scale score!!
What parts of a neuro exam should be done in stroke?
- Cranial nerves – full exam. Check for visual inattention.
- Fundoscopy – hypertensive/diabetic retinopathy.
- PNS – check for drift!
- Gait
- Cerebellar exam.
- Cortical signs – inattention, apraxia, dysphasia
- Speech – dysarthria or dysphasia. Check for fluency, repetition, articulation. Can they follow 1,2 and 3 stage commands?
What is the definition of a stroke
- sudden interruption in vascular supply to the brain
- result in rapidly developing focal neurological deficit; (e.g. acute onset)
- >24hrs
Which strokes are more common out of ischaemic and haemorrhagic?
ischaemic = 85%
haemorrhagic = 15%
out of ischaemic strokes which of thrombotic or embolic is more common? & what are causes of both?
embolic (80%) is more common –>
- cause: left heart AF
- infective endocarditis
- long bone #’s (the haemorrhagic shock and systemic inflammation can precipitate an ischaemic stroke)
- non-thrombotic embolism: fat, air, amniotic fluid
thrombotic (20%)
- rupture of atherosclerotic plaque in an ICA & thrombus –> embolism
- rarely: due to atheromatous rupture of cerebral artery with occlusion at site (less affected by atherosclerosis)
What are the risk factors for ischaemic stroke vs haemorrhagic?
Both RF:
- age,
- HTN
Ischaemic:
- smoking,
- hyperlipidaemia,
- AF
Haemorrhagic:
- ArterioVenous Malformation
- anticoagulation
apart form thrombolic or embolic stroke what else causes ischaemic strokes?
- Systemic hypo-perfusion e.g. cardiac arrest –> watershed infarcts
- Cerebral venous sinus thrombosis - results in venous congestion & hypoxia which damages brain tissue
- Cryptogenic - unknown cause 1/3rd of strokes are these
- Anti-phospholipid syndrome
- Thrombophilia
- Arterial dissection (sudden onset, more common in young on straining)
What are the caues of haemorrhagic strokes?
- HTN
- AVMs
- (Aneurysmal)
- CAA (cerebral amyloid angiopathy e.g. degenerative vasculopathy)
- Anti-coagulation therapy/ haemophilia
- Recreational drugs
Which of white or grey matter dies quicker in ischaemic stroke?
GREY MATTER IS HIGHLY METABOLICALLY ACTIVE, DIES QUICKER
TIME IS BRAIN - each minute stroke is untreated, destroyed is:
- 1.9 million neurons
- 14 billion synapses
- 12 km (7.5 miles) of myelinated fibres
- The ischemic brain ages 3.6 years each hour without treatment
What occurs if you get perfusion failure of the brain?
the ischaemic cascade
- energy failure –> no ATP produced, lactic acid & CO2 build up = acidosis –> ion gradients dissipate from Na/K+ pump failure
- –> mambrane depolarisation and large scale NT release (including toxic-in-high-conc. glutamate!)
- –> excitotoxic injury and oxidaive stress from 10x normal glutamate conc = NMDA receptor overstimulation
- –> large Ca2+ influx = cell apoptosis
point of no return = when membrane integrity is compromised and water leaks into the cell = cytotoxic oedema
What is an ischaemic penumbra?
- an ischaemic penumbra is a poorly perfused area surrounding a necrotic core
- in the necrotic core is <20% normal perfusion
- in the ischaemic penumbra is 20-40% normal flow
- the core will expand if perfusion is not restored
- the neurons in the ischaemic penumbra are viable for ~24hrs and can potentially be salvaged
- they (IP) are a good target for neuroprotective therapies
In strokes you would see UMN lesions & focal neurology based on arterial supply
you would expect to see what else with the signs of UMN lesions of hyperreflexia, spascticity & up going plantars?
Pyramidal weakness
- extensors weak > flexors (flexed position) in UL
- so in LL = extended position as flexors weaker > extensors there
NB: remember upgoing plantars are normal if baby is <6m old
overall: UMN lesion: pyramidal weakness, hyperreflexia, spasticity, up going plantars (normal <6months)
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get leg weakness?
Anterior cerebral
(has inner 1o motor cortex e.g. leg bit supply)
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get face and arm weakness?
middle cerebral artery
(as does the outer segment of 1o motor cortex not the inner bit where legs are thers ACA, the rest is MCA)
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get face, arm and leg weakness?
Lacunae
In stroke depening on the arterial blood supply you get different focal neurology.
What weakness do you get if the PCA is affected?
none
you get hemianopia
(e.g. PC supplies occipital lobe)
NB: nor do you get any dysphasia, inattention or neglect.
MCA is the only other artery where you get hemianopia - if MC then the eyes look at the lesion e.g. eye deviation towards
In stroke depening on the arterial blood supply you get different focal neurology.
Which artery is affected if you get dysphasia?
Middle cerebral artery only
What artery is affected if a patient has inattention/neglect?
Where is the main language dominant hemisphere in 85% of people and TF what syx would a stroke on this side cause?
>85% of people are left language dominant (e.g. ?RHanded)
TF in assuming a dominant side stoke on LHS you would get
- dysphasia - total/expressive/receptive
- right sided weakness + hemisensory loss
if you were dominant on LHS but had a RHS stroke (non-dominant side). You would get:
- sensory inattention
- hemispatial neglect
- Lef-sided weakness + hemisensory loss
NB: so either side you have a stroke in you get hemisensory loss and weakness. but depending on if its dominant = dysphasia and if non-dom you get sensory inattention and hemispatial neglect.
What are the general symptoms of a LHS stroke (assume dominant) vs a RHS stroke (assume non-dominant)
LHS stroke (dom)
- VERBAL - dysphasia & aphasia
RHS stroke (non-dom)
- VISUO-SPATIAL - sensory inattention & hemisensory neglect
if the brocas area is affected in the LHS/dominant lobe what type of dysphasia so you get?
Non-fluent dysphasia
- cannot EXPRESS what they mean, but can understand you
If Wernickes area on LHS stroke/dominant is affected what type of dyspphasia do you get?
fluent dysphasia also called receptive dysphasia
they talk and can express words
but cannot UNDERSTAND language & self monitor what they are saying
If someone has a non dominant (e.g. RHS stroke) in brocas area what type of problem do they get?
they dont understand: Non-verbal expressive communication
- e.g. gesticulations, facial expressions and subtle intonation, expressing meaning by ‘tone of voice’ (sarcasm?)
if someone has a non dominant lesion in wernickes e.g. RHS stroke. What problems do they get?
AMUSIA a.k.a. Problems understanding speech intonation,
we convey a lot of meaning using tone of voice and this is lost on people with non-dominant Wernicke lesions –> They are blind to the music of speech and misunderstand what is being said, even though their comprehension of grammar and syntax (left hemisphere) is unaffected.
How do you get CONDUCTION APHASIA (a disconnection syndrome)?
e.g. where is the lesion to cause this…
a stroke or lesion on the dominant e.g. LHS, arcuate fasiculus
–> the white matter bundle connecting the anterior (brocas) and posterior (werinickes) language areas
- they cant talk
(no connection between understanding and expressing)
dyslexia is problems reading
–> alexia if the ability is lost completely
How do you get this problem?
a LHS/dominant stroke in the fusiform gyrus
the fusiform gyrus = complex pattern recognition
the fusiform gyrus = complex pattern recognition
a problem/stroke/lesion in the dominant lobe = dyslexia/alexia
What condition do you get if it is in the non-dominant lobe?
problems with facial recognition called
prosopagnosia
A sudden focal neurology and reduced level of consciousness
typically + a known history of HTN
leads you to consider what dx?
Intracranial haemorhage
What is the name of the stroke classification system that considers anatomical location?
Bamford classification (anatomical location)
What scoring system does this show and at what threshold?
this is the ROSIER e.g. recognition of stroke in the ER
used AFTER EXCLUDING HYPOGLYCAEMIA
then any score >0 means its likely to be a stroke
What scoring system is this?
when is it completed?
this is the NIHSS
complete on admission
national institutes of health stroke scale = severity of stroke in the acute setting
Venous stroke/cerebral venous sinus thrombosis symptoms inlcude:
raised ICP (high-pressure headache - sudden onset, double vision, pulsatile tinnitus, papilloedema, visual obscuration, seizures) due to obstruction or
focal neurological deficits and seizures due to venous infarction and venous haemorrhage
how may sagittal sinus thrombosis particularly present with?
- May present with seizures and hemiplegia
- Parasagittal biparietal or bifrontal haemorrhagic infarctions are sometimes seen
- 50% of patients have isolated sagittal sinus thromboses
- the other 50% have coexistent lateral/transverse sinus thromboses and cavernous sinus thromboses
Venous stroke/cerebral venous sinus thrombosis symptoms inlcude:
- raised ICP (high-pressure headache - sudden onset, double vision, pulsatile tinnitus, papilloedema, visual obscuration, seizures) due to obstruction or
- focal neurological deficits and seizures due to venous infarction and venous haemorrhage
how may cavernous sinus thrombosis particularly present with?
cavernous sinus thrombosis = eye stuff (as drains eye veins)
- Periorbital oedema
- Ophthalmoplegia: 6th nerve damage typically occurs before 3rd & 4th
- Trigeminal nerve involvement may lead to hyperaesthesia of upper face and eye pain
- Central retinal vein thrombosis
- Other causes of cavernous sinus syndrome:
- local infection (e.g. sinusitis), neoplasia, trauma
A patient presents with 6th/Abducens and 7th/facial nerve palsy what venous stroke syndrome is likely to give this?
lateral/transverse sinus thrombosis…
