Stroke

Question 1

Incidence of stroke types: Ischaemic vs Haemorrhagic.

Answer 1

Ischaemic: 85%
Haemorrhagic: 15%

Question 2

Incidence of stroke types: Ischaemic stroke causes as percentage of all strokes

Answer 2

Ischaemic strokes = 85% all strokes:

1. Cryptogenic 30%
2. Lacunar (small vessel) 25%
3. Atherosclerotic large vessel disease 20%
4. Cardiogenic embolism 20%
5. Other 5%

Question 3

Mechanisms of ischaemic stroke:

Answer 3

1. Embolism (50-60%) from heart or carotid arteries
2. Thrombosis (30-40%) - eg. lacunar
3. Hypoperfusion (5-10%) stenosis, hypotension - worst in ‘watershed’ areas

Question 4

Main causes of intracerebral haemorrhage (4):

Answer 4

1. Hypertension (75%)
2. Coagulopathy (5-10%)
   - liver disease, iatrogenic (antithrombotis, thrombolysis)
3. Amyloid angiopathy 5-10%
4. Underlying vascular lesion (AVM, cavernous sinus haemangiomas) 5-10%

Question 5

Risk factors for stroke - modifiable and non-modifiable:

Answer 5

Non- Modifiable:

• AGE
• Gender
• Hx stroke / TIA
• FHx / genetic predisposition

Modifiable:

• HTN
• AF
• Diabetes
• Dyslipidaemia
• Carotid stenosis
• Smoking
• Obesity
• Sedentary lifestyle
• Excess alcohol
• OSA
• Hyperhomocysteinaemia

Question 6

Associations of TIAs:

Answer 6

Further TIAs
Stroke (90-day risk)
Cardiovascular events
Death

Question 7

Do MRI changes rule out TIA?****CHANGED??

Answer 7

CHANGED???*
No, 40-50% have abnormal DWI acutely –> approx. half of these have evidence of infarction on follow up imaging.

DWI +ve TIA patients have higher risk of recurrent TIA or stroke.
They tend to have symptoms >1hr.

Definition of TIA is:

• acute loss of focal cerebral or monocular function
• symptoms last less than 24 hours
• arterial cause

[Attempts to redefine: symptoms <1hr and no evidence of acute infarction].

Question 8

Radiological signs of cerebral infarction on CT:

Answer 8

1. Hypoattenuation
   (in vascular territory)
2. Insular ribbon sign
   - Hypodensity / swelling insular cortex (MCA infarction)
3. Lentiform nucleus obscuration
   (“blurred basal ganglia”) = MCA territory infarct
4. Dense MCA sign
   (due to thrombus or embolus in MCA)
   - Sp but not Sn for MCA occlusion.
5. Haemorrhage: seen as hyperintensity

Question 9

Radiological signs of cerebral infarction on MRI:

Answer 9

T2…
DWI…
MRA….

Question 10

Acute ISCHAEMIC stroke: 4 evidence-based management options:

Answer 10

1. Stroke unit care: decreases death and dependency (46/1000 treated)
2. ASA within 48hours: reduces early stroke recurrence (9/1000 treated)
3. t-PA within 4.5hours of IS (improves odds od good outcome by approx. 30-50%)
4. Decompressive craniectomy for malignant MCA territory infarction (reduces mortality)

Question 11

Evidence for early secondary prevention with Aspirin in acute stroke comes from which trials?

Answer 11

1. IST (International Stroke Trial)
2. Chinese Aspirin Stroke Trial (CAST)
3. Multicentre Acute Stroke Trial - Italy (MAST-I)

• Data approx 15yrs old
• Can prevent 9 recurrent strokes / 1000 pts treated

Question 12

Trials providing evidence for reperfusion (with t-PA) therapy:

Answer 12

1. NINDS Trial (1995): benefit out to 3hrs.
2. ECASS I-III
3. ATLANTIS
4. EPITHET
5. IST-3 (2012): included pts >80yo; showed safety to 3hrs. 3-6hrs no benefit.

Pooled results provide evidence to 3hrs from onset.
Also evidence out to 4.5hrs.
Beyond 4.5hrs: less benefit, more bleeds.

Question 13

Management of ICH - few treatment options (3) - evidence:

Answer 13

1. Surgery: NO benefit early evacuation of haematoma (STICH, Lancet 2005)
2. rFVIIa: reduces haematoma expansion but NO benefit in mortality or functional outcome (still an experimental measure)
3. BP lowering:
   INTERACT II Trial:
   - intensive lowering of blood pressure did not result in a significant reduction in the rate of the primary outcome of death or severe disability.
   - An ordinal analysis of modified Rankin scores indicated improved functional outcomes with intensive lowering of blood pressure.

Question 14

Evidence for decompressive craniectomy:

Answer 14

…….

Question 15

Components of stroke prevention:

Answer 15

Primary prevention:

• not aspirin (overall risk of stroke neutral, as risk of bleeding)
• anticoagulation in NVAF
• BP control
• cholesterol lowering

Secondary prevention:

• antiplatelet therapy
• BP control
• cholesterol lowering

Question 16

Antiplatelet therapy in secondary prevention of stroke:

Answer 16

1. Aspirin moderately effective
2. Dipyridamole or Clopidogrel - roughly 10% benefit over aspirin
3. Warfarin: no benefit (possibly increased risk) unless non-valvular AF (primary & secondary prevention): warfarin decreases stroke by approx. 65% (aspirin decreases by 20% in NVAF).

MATCH Trial: no benefit with both aspirin and clopidogrel vs aspirin alone (due to bleeding)

PROFESS Trial: Assasantin vs Clopidogrel - equivalent outcomes

Question 17

NOAC Trials, compared with warfarin for stroke prevention in NVAF (?Update………)

Answer 17

1. RE-LY: Dabigatran
   - similar stroke protection
   - less major bleeding and ICH
2. ROCKET: Rivaroxaban
   - similar stroke prevention
   - similar major bleeding
   - less ICH
3. ARISTOTLE: Apixaban
   - better stroke prevention
   - less major bleeding and ICH

Question 18

BP lowering secondary prevention IS - trial……..

Answer 18

PROGRESS Trial…..

BP reduction is more important than agent

Question 19

Statin use acute stroke…..

Answer 19

SPARKLE study……

Question 20

Carotid endarterectomy…..

Answer 20

NASCET……
ACAS….
ACST….

Severe (70-99% stenosis)
NNT = 6
definite benefit within 2 weeks (out to 3 months ok, benefit lost after that)

Mod

Mild

Question 21

BP managment in the acute ischaemic stroke. (discuss both thrombolysis and conservative management)

Answer 21

If patient is candidate for thrombolysis, agents are: labetalol or nicardipine by infusion. Need to get BP less than 185/110 pre-treatment, and post-treatment <220/120, however if concomitant HF or IHD, do not withhold anti-HTN

Question 22

What are Charcot-Bouchard aneurysms?

Answer 22

Small (<1mm) intracerebral aneurysms in small arteries
Particularly common in lenticulostriate vessels of basal ganglia

Due to chronic changes in vessel walls due to HTN

Can lead to lacunar infarct (thrombosis), ICH (rupture), microhaemorrhage (leak)

Microhaemorrhages surrounding basal ganglia suggestive of Charcot-Bouchard aneurysms secondary to chronic hypertension.
Cf. Peripherally-located microhaemorrhages in cerebral amyloid angiopathy (cause of lobar haemorrhage).

Question 23

Important complication of hypertensive intracranial haemorrhages?

Answer 23

Intraventricular extension (as often adjacent to ventricles)
Can --> Hydrocephalus

Question 24

What is Gerstmann syndrome and what is the cause?

Answer 24

Gerstmann syndrome, also known as angular gyrus syndrome, is a dominant hemisphere stroke syndrome consisting of 4 components:

1. agraphia or dysgraphia
2. acalculia or dyscalculia
3. finger agnosia
4. left-right disorientation

Pure Gerstmann syndrome is said to be without aphasia.

Question 25

MCA Stroke Syndromes:

(1) Complete MCA syndromes: clinical features -

Answer 25

Complete MCA syndromes (occlusion of entire MCA at its origin, eg. by thrombus):

• contralateral hemiplegia
• contralateral hemianaesthesia
• homonymous hemianopia
• temporary gaze preference to ipsilateral side ( a few days)
• dysarthria (secondary to facial weakness)
  DOMINANT hemisphere: global aphasia
  NON-DOMINANT hemisphere: anosognosia, constructional apraxia, neglect.

Question 26

Anosognosia

Answer 26

Anosognosia (“without disease knowledge”):

A condition in which an ill patient is unaware of her own illness or the deficits resulting from her illness

Question 27

Location of lesion in quandrantanopia:

Answer 27

Most likely occipital (whether superior or inferior quandrant affected).

If isolated superior quadrantanopia also need to consider temporal lobe lesion.

Parietal lesion can cause INFERIOR quadrantanopia, but usually accompanied by other parietal lobe signs.

Question 28

MCA Stroke Syndromes:

(2) Partial MCA syndromes: clinical features -

Answer 28

Partial MCA syndromes (due to collateral flow / variable arterial configurations, or emboli causing partial MCA occlusion / occlusion of distal branches):

• Brachial syndrome = hand +/- arm weakness alone
• Frontal opercular syndrome = Facial weakness + Broca aphasia (non-fluent) +/- arm weakness
• Superior division occlusion (frontal and parietal infarction): sensory disturbance, motor weakness, non-fluent aphasia.
• Inferior division occlusion (temporal cortex):
  DOMINANT hemisphere: : fluent (Wernicke’s / receptive) aphasia, without weakness. +/- homonymous superior quadrantanopia.
  NON-DOMINANT hemisphere: hemineglect or spatial agnosia (parietal lobe) without weakness

Question 29

MCA Stroke Syndromes:

(3) Lacunar stroke syndromes:

Answer 29

Lacunar stroke syndromes (of MCA):
ie. white matter strokes, no ‘cortical’ signs.

1. Pure motor stroke (contralateral) - occlusion of lenticulostriate vessels –> internal capsular infarct
2. Pure sensory stroke (contralateral) - occlusion of lenticulostriate vessels –> internal capsular infarct
3. Ataxic hemiparesis: ipsilateral weakness and limb ataxia that is out of proportion to the motor deficit.
   +/- dysarthria, nystagmus, and gait deviation towards the affected side.
4. Sensorimotor stroke: weakness and numbness of face, UL and LL on one side, but without cortical signs.
5. Dysarthria clumsy-hand syndrome (least common): Facial weakness, dysarthria, dysphagia, and slight weakness and clumsiness of one hand. No sensory deficit.

Question 30

Why is proximal ACA occlusion usually better tolerated than distal ACA (A2 segment) occlusion?

Exception?

Answer 30

Occlusion of the proximal ACA is usually well tolerated due to collateral flow from through the Anterior Communicating Artery and collaterals from the MCA and PCA.

Exception:
Contralateral A1 segment atresia - if both A2 segments arise from a single ACA stem –> occlusion affects both hemispheres.
Results in profound abulia (delay in verbal and motor response), bilateral pyramidal signs, paraparesis or quadriparesis, urinary incontinence.

Question 31

ACA infarct symptoms / signs:

Answer 31

• Frontal lobe behaviours
• Grasp reflex (may also have sucking reflex and paratonia)
• Abulia = akinetic mutism (if complete)
• Contralateral hemiplegia and sensory loss (leg affected > arm if partial)
• Left limb dyspraxia (corpus callosum involvement)
• Urinary incontinence (if complete)

DOMINANT ACA: motor +/- sensory aphasia
NON-DOMINANT ACA: contralateral hemineglect

Question 32

What is praxis and apraxia?
Where is it localised?
When does apraxia occur?

Answer 32

Is the ability to execute learned purposeful tasks.
Eg. ideomotor praxis: ability to perform learned motor movements.
Other forms of praxis: ideational, orofacial, limb-kinetic, dressing, writing, speech, constructional.

Apraxia is the inability to execute purposeful tasks despite having the desire and the physical capacity to perform the movements. It is an acquired disorder of motor planning, but is not caused by incoordination, weakness, sensory loss, or failure to comprehend commands.

Frank problems with ideomotor praxis may be obvious when patient or family member reports difficulty dressing, feeding, and bathing that is not explained by gross motor deficits.

Localisation: Frontal cortex, parietal cortex, basal ganglia, and white matter tracts connecting these areas (ie. corpus callosum).
Often thought to be localised to dominant hemisphere
(ie. left hemisphere controls praxis for both left and right limbs), although probably more complex than this.
Therefore, occurs more often with left-sided lesion.

Unilateral left-limb dyspraxia (callosal apraxia) occurs when there is damage to the anterior corpus callosum and adjacent frontal cortex. The lesion presumably disconnects right hemisphere premotor and motor cortex from left hemisphere praxis input.

May be seen in stroke (ACA, MCA), and disorders of the basal ganglia: corticobasal degeneration (prominent feature), PD, supranuclear palsy, and Huntington’s disease.

Question 33

ACA infarct syndromes:

Answer 33

.

Question 34

What is praxis and apraxia?
Where is it localised?
When does apraxia occur?

Answer 34

Is the ability to execute learned purposeful tasks.
Eg. ideomotor praxis: ability to perform learned motor movements.
Other forms of praxis: ideational, orofacial, limb-kinetic, dressing, writing, speech, constructional.

Apraxia is the inability to execute purposeful tasks despite having the desire and the physical capacity to perform the movements. It is an acquired disorder of motor planning, but is not caused by incoordination, weakness, sensory loss, or failure to comprehend commands.

Frank problems with ideomotor praxis may be obvious when patient or family member reports difficulty dressing, feeding, and bathing that is not explained by gross motor deficits.

Question 35

Definition of abulia (~akinetic mutism):

Answer 35

1. Loss or impairment of the ability to perform voluntary actions or to make decisions.
2. Reduction in speech, movement, thought, and emotional reaction; a common result of bilateral frontal lobe disease.

Seen in:

• Mental illness
• Processes damaging cortical structures, eg. ACA infarct.

Question 36

Anterior choroidal artery infarct:

• area supplied
• mechanism of occlusion
• symptoms / signs

Answer 36

Anterior choroidal artery - arises from ICA and supplies posterior limb of internal capsule.

Usual mechanism of occlusion: in-situ thrombosis, iatrogenic during clipping of ICA aneurysm.

Complete syndrome of occlusion:

• contralateral hemiplegia and hemianaesthesia
• homonymous hemianopia

Complete syndrome uncommon, or may recover substantially. Overlap in supply by: proximal MCA, PCA, posterior choroidal arteries.

Question 37

Carotid artery occlusion - presentations.

• ICA
• CCA

Answer 37

Internal carotid artery ischaemia / infarction:
Presentation varies depends on mechanism (thrombus, embolism, low flow) and competence of Circle of Willis (can vary from relatively asymptomatic to catastrophic).

• MCA territory most commonly affected.
• ACA + MCA may be occluded at top of ICA (–> abulia, stupor, hemiplegia, hemianaesthesia, aphasia, anosognosia).
• PCA can be affected if arises from ICA (‘foetal posterior cerebral artery’).
• Ophthalmic artery. Recurrent transient monocular blindness (amaurosis fugax) may warn of symptomatic ICA lesion. Rarely infarcted at time of TIA / CVA.
• Listen for carotid bruit. Carotid doppler USS.

Common carotid artery:

• symptoms / signs of ICA occlusion
• jaw claudication due to low flow in ECA branches
• Takayasu’s arteritis may be implicated (eg. bilateral CCA stenoses at their origin).

Question 38

Posterior circulation stroke:

Answer 38

.

Question 39

What is cerebral amyloid angiopathy?

With which type of dementia is it associated?

Answer 39

Cerebral amyloid angiopathy:

• amyloid beta peptide deposits
• within small to medium-sized blood vessels
• vessels brain and leptomeninges.

Usually asymptomatic, but an important cause of primary lobar intracerebral haemorrhage in the elderly.

Can occur as:

• a sporadic disorder
• in association with Alzheimer disease
• familial syndrome

Incidence increases with age (onset >50 but usually at least 60-65+yo).

No overlap with non-CNS amyloidosis.

Question 40

What are the main complications of amyloid angiopathy?

Answer 40

Usually asymptomatic, but an important cause of primary lobar intracerebral haemorrhage in the elderly. Lobar haemorrhage is the most common clinical manifestation.

Other complications:

• transient neurological symptoms
• inflammatory leukoencephalopathy
• contributor to cognitive impairment
• incidental microhemorrhages or hemosiderosis on MRI.

Question 41

Where does ICH tend to occur when due to cerebral amyloid angiopathy?

Answer 41

The most common clinical manifestation of cerebral amyloid angiopathy is spontaneous LOBAR haemorrhage.

LOBAR = in the cortex and subcortical white matter.

• as vascular amyloid deposits favour cortical vessels and largely spare white matter, deep gray matter, and the brainstem.
• therefore largely spare the ventricles, but may rupture into SAS.

(cf. deep locations characteristic of hypertensive hemorrhage such as putamen, thalamus, and pons).

More often posterior (temporal & occipital > frontal & parietal) - reason unknown.

Probably underlie substantial proportion of anticoagulant-associated ICH.

Question 42

Diagnosis of cerebral amyloid angiopathy.

Answer 42

Should be suspected in anyone ≥60yo with lobar haemorrhage.

Definitive diagnosis is pathological.

However, a probable diagnosis can be made with MRI:
≥2 haemorrhages or microhaemorrhages
- restricted to regions typical of CAA (cortex or “grey-white” junction)
- entirely sparing regions typical of hypertensive haemorrhage (basal ganglia, thalamus, or pons)

Question 43

Treatment of cerebral amyloid angiopathy:

Answer 43

Symptomatic managment only (eg. in ICH)

Lobar haemorrhages tend to recur. Therefore:

• avoid anticoagulants and antiplatelet agents
• control hypertension

(Some rare inflammatory forms may respond to immunosuppression)

Question 44

What are the clinical features differentiating:

• cerebellar haemorrhage
• pontine haemorrhage
• basal ganglia haemorrhage?

Answer 44

Cerebellar haemorrhage:

The most common symptoms are of severe nausea and vomiting and ataxia. Headache may be severe. Patients with cerebellar haemorrhage can rapidly become comatose within hours after the onset from herniation, because of its limited space in the posterior fossa.

Pontine haemorrhage:

There are numerous nuclei located within the pons. Rapidly deteriorating level of consciousness, impaired extraocular movement and extensive sensorimotor deficits are clinical clues to pontine haemorrhage.

Basal ganglia haemorrhage:

Contralateral hemiparesis, hemisensory loss, or hemi-inattention. Aphasia, especially non-fluency and impaired comprehension, is frequently seen if haemorrhage occurs in the posterior limb of the left internal capsule.