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*Medicine: Neurology > Ischaemic Stroke + TIA > Flashcards

Ischaemic Stroke + TIA Flashcards

1
Q

What is the definition of stroke?

A
  • rapidly developing clinical signs or symptoms
  • of focal neurological deficit
  • lasting more than 24 hours or that lead to death
  • with no apparent cause other than cereberovascular**
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2
Q

What is a TIA and how is it different to stroke?

A
  • temporary (usually embolic from carotid atheroma) occlusion of cerebral circulation, caused by ischaemia but without acute infarction
  • causing focal neurological deficit lasting under 24hrs
  • but actual duration tends to be ~10mins
  • no difference in mechanism between TIA + stroke, only difference is magnitude of presentation
  • TIA is treated like stroke as it’s a neurological emergency (high risk of stroke recurrence)
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3
Q

How common is stroke?

A
  • every 5 mins, someone in England has a stroke
  • 25% of people living to 85 have a stroke
  • 25% of strokes occur in those under 65
  • stroke accounts for 11% of deaths in E+W
  • 20-30% of people who have a stroke die within 1 month
  • 3rd commonest cause of death
  • commonest cause of adult disability
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4
Q

What are the two types of stroke?

A
  • ISCHAEMIC (80%) → due to:
    • arterial embolism
    • thrombosis at site of plaque in major cerebral vessel (ICA)
  • HAEMORRHAGIC (20%) →
    • main cause is rupture of intracranial microaneurysm (Charcot-Bouchard aneurysm) in a hypertensive patient
    • can also be caused by: venous sinus thrombosis, relapse of MS, SOL, thrombophilia, antiphospholipid syndrome
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5
Q

What is the aetiology of stroke?

A
  • Atherosclerosis → causes thrombotic stroke in large extracranial vessels: most commonly carotids or intracranial arteries arising from CoW
  • Cardiac or carotid embolism → embolic stroke from ruptured atherosclerotic plaques or cardiac thrombus lodging in distal narrow sites, bifurcation of common carotid + akinetic segments of myocardium (eg. after MI) are most common sources
  • Arterial dissection → in younger population, dissection either of carotid or vertebral arteries, may be no antecedent history of injury to neck, but sudden twisting movements or flexion/extension injuries
  • Intracerebral haemorrhage → 2o to chronic unrelated HTN but can be caused by other factors eg. trauma, anticoag therapy, neoplasia + coag disorders
  • Lipohyalinosis of small arteries → degenerative process affects small perforating arteries that supply structures deeper to cortex eg. basal ganglia, internal capsule, pons - occlusion of these penetrating arteries causes subcortical infarcts ⇒ ‘lacunes’
  • Disease of vessel wall → rare but should always be considered, esp in young pts who present w/ stroke, causes: rheumatoid vasculitis, SLE, polyarteritis nodosa + temporal arteritis
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6
Q

What are the risk factors for haemorrhagic stroke?

A
  • hypertension
  • advanced age
  • male sex
  • asian, black, hispanic
  • FHx of haemorrhagic stroke
  • haemphilia
  • cerebral amyloid aniopathy
  • autosomal dominant gene mutations
  • hereditary haemorrhagic telangiectasia
  • anticoagulation
  • drugs - cocaine, amfetamine
  • vascular malformations
  • moyamoya disease
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7
Q

What are the risk factors for ischaemic stroke?

A
  • older age
  • FHx of stroke
  • previous ischaemic stroke
  • hypertension
  • smoking
  • diabetes mellitus
  • atrial fibrilation
  • cormorbid cardiac conditions
  • carotid artery stenosis
  • sickle cell disease
  • dyslipidaemia
  • lower socio-economic status
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8
Q

What are differential diagnoses for stroke?

A
  • hypoglycaemia
  • migraine
  • epilepsy
  • multiple sclerosis
  • brain tumours
  • syncope
  • CNS infections - encephalitis, meningitis
  • head injury

In stroke, symptoms are usually negative (losing speech, power), whereas in mimics, positive features (tingling, aura) are more likely

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9
Q

Stroke is a disease of the blood vessels supplying the brain. Commonly (80%) it results as of blockage of large + small arteries, and sometimes (20%) rupture of small arteries w/ bleeding. Rupture of large arteries are usually due to Berry aneurysms, resulting in SAH.

What general points should be asked about in a stroke history?

A
  • remember importance of focal neurological symptoms of acute onset
  • contiguous parts of body affected concurrently (no spread)
  • negative vs postive symptoms
  • loss of consciousness + headache are atypical
  • risk factors
  • family history
  • ETOH + rec drugs (eg cocaine)
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10
Q

In a stroke examination we want to look for an early diagnosis and potential causes.

What things are we looking for?

A
  • gen inspection → obvious hemiparesis, facial weakness, neglect of one side
  • inspection → xanthoma, stigmata of endocarditis, marfanoid, Fabry’s
  • pulse → AF
  • BP → hypertension
  • CVS → murmurs, carotid + renal bruits, PVD
  • neuro → full exam!
    • cranial nerves (full) → check for visual inattention
    • fundoscopy → hypertensive/diabetic retinopathy
    • PNS → check for drift
    • gait
    • cerebellar exam
    • cortical signs → inattention, apraxia, dysphasia
    • speech → dysarthria, dysphasia, fluency, repetition, can they follow 1,2,3 stage commands?
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11
Q

What is the difference between cortical and subcortical symptoms?

A
  • Stroke may affect cortex → ie. frontal, parietal, temporal lobes
  • Stroke may affect subcortex → ie. internal capsule, thalamus, basal ganglia, brainstem + cerebellum
  • Cortical strokes may disrupt higher cognitive function, eg. a left MCA stroke to inferior frontal lobe may result in expressive aphasia
  • It is uncommon for subcortical strokes to affect language
  • Motor + sensory impairments can be helpful in differentiating cortical vs subcortical stroke
  • Subcortical brainstem lesions may present with extraocular movement impairments, diplopia, dysphagia, dysarthria, nystagmus
  • A subcortical stroke in the cerebellum may present with nausea, vomiting, vertigo, imbalance. Exam may reveal nystagmus, ataxia and tremor.
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12
Q

What are the major blood vessels that supply the anterior and posterior circulation of the brain?

A
  • Each internal carotid artery bifurcates into middle and anterior cerebral arteries
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13
Q

What is the Circle of Willis?

A
  • anastomosis of anterior and posterior circulations
  • ACA supplies medial frontal + parietal lobes
  • MCA supplies majority of lateral hemisphere
  • PCA supplies medial/inferior temporal + occipital lobes
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14
Q

UMN lesions can result from damage to any nerves within the CNS, before the final common output, eg. the cerebral cortex or internal capsule. UMN lesions commonly occur following stroke or tumours.

What are the key features of an upper motor neuron lesion?

A
  • initial phase → flaccid limbs w/ loss of reflexes
  • long term:
    • spasticity
    • hyperreflexia
    • clonus
    • positive babinski sign
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15
Q

Anterior circulation infarcts are most common (50%). These include the ACA and MCA.

What are features of an ACA infarct?

A
  • contralateral motor / sensory loss (lower limbs > face > upper limbs)
  • apraxia/gait apraxia → individual has difficulty with the motor planning to perform tasks or movements when asked, provided that the request or command is understood and the individual is willing to perform the task
  • frontal release signs - primitive reflexes (grasping)
  • abulia (apathy / loss of motivated behaviour)
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16
Q

The MCA is the largest branch of the ICA and supplies the largest area of the cerebral cortex, it’s the most commonly involved artery in stroke.

What are the features of an MCA infarct?

A
  • Dominant hemisphere ⇒
    • dys/aphasia
    • motor/sensory loss (face/upper limbs > lower limbs)
    • homonymous hemianopia
  • Non-dominant hemisphere ⇒
    • motor/sensory loss (face/upper limbs > lower limbs)
    • homonymous hemianopia
    • hemispatial neglect
    • anosognosia (loss of self-awareness)

In either hemisphere if internal capsule is involved then there will be complete hemiplegia (paralysis) (UL=face=LL)

17
Q

For MCA infarcts, why is dysphasia/aphasia only a problem when the dominant hemisphere is affected?

A
  • MCA supplies motor + sensory cortices
  • also supplies Wernicke’s area (comprehension of speech)
  • and supplies Broca’s area (expression of speech)
  • Wernicke’s and Broca’s are found in dominant hemisphere only
  • thus in majority of right-handed individuals, speech production will be affected only when there is occlusion of left middle cerebral artery (left = dominant hemisphere)
18
Q

The posterior circulation infarcts (25%) include the PCA.

What are the features of a PCA infarct?

A
  • Peripheral branches (hitting occipital cortex) →
    • homonymous hemianopia (w/ macular sparing)
    • visual agnosia (loss of recognition)
    • alexia (loss of ability to read - dominant hemisphere)
    • rarely visual hallucinations
  • Central branches (hitting thalamus, cerebral peduncle or midbrain) →
    • sensory loss
    • central post-stroke pain syndrome (allodynia)
    • hyperkinetic movement disorders (eg. hemiballismus)
    • Weber’s syndrome
19
Q

Another posterior circulation infarct is a brainstem infarct, with lateral medullary syndrome (Wallenberg) being the commonest.

What are features of lateral medullary syndrome?

A
  • ipsilateral horner’s syndrome
  • ipsilateral cerebellar signs (ataxia)
  • ipsilateral facial sensory loss
  • dysphagia, dysarthria, vertigo
  • contralateral limb sensory loss
20
Q

Approx 25% of ischaemic strokes are due to infarction of the internal capsule subsequent to occlusion of small perforating vessels. These originate from the MCA and dive deep within the brain to supply parts of the internal capsule, basal ganglia + thalamus. Lacunes also occur int he brainstem esp the pons.

What are the 5 classic lacunar syndromes?

A
  • Pure motor hemiparesis → occurs w/ infarction of posterior limb of internal capsule, characterised by contralateral hemiparesis (UL = face = LL), ‘pyramidal’ pattern of weakness also present
  • Ataxic Hemiparesis → occurs w/ infarction of posterior limb of internal capsule, basis pontis or corona radiata; displays combo of cerebellar + motor symptoms, incl ‘pyramidal’ weakness on ipsilateral side of body; hence it is known also as homolateral ataxia
  • Pure sensory stroke → infarct of ventral posterolateral (VPL) nucleus of the thalamus, characterised by contralateral numbness of face, arm + leg
  • Sensorimotor stroke → infarction of thalamus + adjacent posterior limb of internal capsule; characterised by contralateral hemiparesis + sensory impairment of face, arm + leg
  • Clumsy-hand dysarthria → infarct of basis pontis or genu of internal capsule; characterised by dysarthria + contralateral weakness of hand, most prominent when writing
21
Q

In a lacunar infarct, what 4 features are usually absent?

A
  • no higher cortical dysfunction as cortex not affected
  • no homonymous hemianopia as lesion away from optic radiation
  • no drowsiness
  • no brainstem signs
22
Q

What investigations are done for stroke?

A
  • IMAGING:
    • CT brain (esp good for blood) → first acute ix, within 1 hr of ED admission
    • MRI brain (gold standard for ischaemic stroke) → used when dx not clear, CT often first-line
    • vascular imaging - carotid doppler → doesn’t visualise posterior circulation, CTA, MRA - can see posterior circulation, formal DSA rarely performed
  • BLOODS:
    • FBC, U+Es, LFTs, CRP, ESR, TFTs, Chol, Glu, HbA1C, sometimes cardiac troponin, sometimes young stroke bloods (HIV, ANA, ANCA, dsDNA, anticardiolipin ab, lupus anticoag)
  • CARDIAC INVESTIGATIONS:
    • ECG
    • Echo
    • 24 hr/ 7day tape
    • in-hospital monitoring (telemetry)

Don’t forget CXR - can identify pneumonia, pulmonary oedema, malignancy

23
Q

Non-contrast CT of brain is mainstay of imaging in setting of acute stroke. It’s fast, inexpensive and readily available. Its main limitation is however the limited sensitivity in acute setting. Detection depends on the territory, the experience of the radiologist and the time of scan from onset.

What are the goals of CT in the acute setting?

A
  • exclude intracranial haemorrhage, which would preclude thrombolysis
  • look for any ‘early’ features of ischaemia
  • exclude other intracranial pathologies that may mimic a stroke, such as tumour
24
Q

What are the early changes that occur on CT for stroke?

A
  • hypo-attenuating brain tissue
  • obscuration of lentiform nucleus
  • dense MCA sign
  • ‘insular ribbon’ sign
  • loss of sulcal effacement

http://radiologyassistant.nl/en/p483910a4b6f14/brain-ischemia-imaging-in-acute-stroke.html

25
Q

When treating a stroke patient, what 5 questions need to be asked/assessed?

A
  • is this a vascular event?
  • which part of the brain is affected?
  • is it haemorrhagic or ischaemic?
  • what caused this stroke?
  • what are this particular patients problems?
26
Q

What is the acute management of ischaemic stroke?

A
  • ABCDE
  • Ensure patent airway → avoid hypoxia
  • Monitor BP but do not correct if high unless encephalopathy or aortic dissection as drop in BP → reduced cerebral perfusion
  • Refer to stroke SpR before investigating
  • Monitor blood glucose (keep BM 6-11mmol/l)
  • Urgent CT if indication for thrombolysis, reduced consciousness or suspected bleeding or meningism *
  • Thrombolysis within 4.5hrs of onset w/ tPA (alteplase) if appropriate
  • NBM while assessing swallow + keep hydrated
  • If haemorrhage excluded → anti-platelet (aspirin) + anti-coag (clopidogrel) - this shouldn’t be prescribed until after a 24hr CT
  • If already on anti-hypertensive therapy then continue unless BP low
  • Admit to specialist stroke unit + MDT approach

*A normal CT scan does not rule out stroke

27
Q

Goal time between emergency department arrival and start of CT scan is 25 minutes, and from emergency department arrival to initiation of intravenous r-tPA (if indicated) is 60 minutes.

Who is eligible for thrombolysis?

A
  • anyone <3hrs of known onset
  • <80yo between 3-4.5hrs of known onset
  • >80yo between 3-4.5hrs of known onset (case-by-case basis)
28
Q

What is the typical anti-platelet regime for ischaemic stroke?

A
29
Q

Thrombolysis does not preclude intra-arterial clot extraction/thrombectomy (if available), and those with contraindications to thrombolysis should be considered for intra-arterial clot extraction (if available and NIHSS>5).

What are the contraindications to thrombolysis?

A

“High BROW”

  • High BP eg. diastolic >140
  • B - bleeding tendency
  • R - recent surgery
  • O - over 80 years
  • W - woke wth symptoms
    ______________________________________
  • major infarct or haemorrhage on CT
  • non-disabling deficit
  • seizures at presentation
  • anticoagulated or INR >1.7
  • platelets <100
  • recent surgery/trauma/birth
  • history of CNS haemorrhage
  • history of AVM or aneurysm
  • severe liver disease/varices/portal HTN

Furthermore, consider thrombectomy and decompressive hemicraniectomy (refer to guidelines)

30
Q

What are clinical features of TIA?

A
  • CAROTID SYSTEM:
    • amaurosis fugax → sudden painless loss of vision in 1 eye due to microemboli passing through retinal arteries
    • aphasia, hemiparesis, hemisensory loss, hemianopic visual loss
  • VERTEBROBASILAR SYSTEM:
    • diplopia, vertigo, vomiitng, choking, dysarthria
    • ataxia, hemisensory loss, hemianopic visual loss
    • transient global amnesia
    • loss of consciousness (rare)
31
Q

How do you risk assess and score for a TIA?

A

ABCD2 score

32
Q

What is the management of TIA?

A
  • lifestyle modifications
  • antiplatelet therapy (clopidogrel, aspirin, dual)
  • if cardioembolic → consider warfarin
  • if cardiac artery stenosis >50%, consider carotid endarterectomy or endovascular stenting
  • BP control
  • driving → no driving for 1 month, inform DVLA if multiple or prolonged deficit
33
Q

What is the secondary prevention for stroke?

A
  • lifestyle advice → smoking, ETOH, diet, exercise - applies to all types
  • anitplatelets, warfarin or DOAC for ischaemic stroke
  • if they have risk factors:
    • antihypertensives → BP <130/80
    • cholesterol + statins - chol <4, LDL <2
    • diabetic control
  • carotid endarterectomy + angioplasty
34
Q

What important vascular disease is important to assess for following TIA?

A
  • carotid stenosis
  • rapid assessment post-TIA is essential (TIA clinics)
  • risk of stroke is highest in first few days after TIA
  • urgent assessment should include looking for carotid stenosis:
    • carotid doppler (ultrasound)
    • MRI + CT techniques also valuable + improving
35
Q

Endarterectomy is a surgical procedure to remove the atheromatous plaque material, or blockage, in the lining of an artery constricted by the buildup of deposits. It is carried out by separating the plaque from the arterial wall.

When should endarterectomy be offered?

A
  • greater than 70% stenosis
  • recent symptoms (in last 6 months) in territory supplied by stenosed artery
  • some subgroups benefit more than others
  • stenosis 50-69% management controversial
  • carotid artery stenting also possible
  • timing is important
36
Q

What are the possible complications following an ischaemic stroke?

A

*Medicine: Neurology (21 decks)

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