Stroke

Question 1

Define stroke

Answer 1

Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more than 24 hours or leading to death, with no apparent cause other than that of vascular origin

Question 2

TRANSIENT ISCHAEMIC ATTACK

Answer 2

Transient ischemic attacks are episodes of temporary and focal dysfunction of vascular origin, which are variable in duration, commonly lasting from 2 to 15 minutes, but occasionally lasting as long as a day (24 hours). They leave no persistent neurological deficit.

Question 3

What is an Ischaemic stroke?

Answer 3

An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction

Question 4

What is a Stroke caused by ICH (Intracerebral hemorrhage)?

Answer 4

Rapidly developing clinical signs of neurological dysfunction attributable to a focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma

Question 5

What is a Stroke caused by subarachnoid hemorrhage?

Answer 5

Rapidly developing signs of neurological dysfunction and/or headache because of bleeding into the subarachnoid space (the space between the arachnoid membrane and the pia mater of the brain or spinal cord), which is not caused by trauma.

Question 6

What is a Stroke caused by cerebral venous thrombosis?

Answer 6

Infarction or hemorrhage in the brain, spinal cord, or retina because of thrombosis of a cerebral venous structure.

Question 7

What is a Stroke not otherwise specified?

Answer 7

An episode of acute neurological dysfunction presumed to be caused by ischemia or hemorrhage, persisting ≥24 hours or until death, but without sufficient evidence to be classified as one of the above.

Question 8

Classification of Stroke

Answer 8

1. Ischemic stroke (80%)
i) Thrombotic (50%): These are caused by a blood clot (thromus) that develops in the brain’s blood vessels (usually seen in older persons, especially those with high cholesterol and atherosclerosis, or diabetes.

They can be further divided into:
1. Large vessel thrombosis 2. Small vessel thrombosis

ii) Embolic (30%): These are caused by a blood clot or plaque debris that develops elsewhere in the body and then travels to one of the blood vessels in the brain through the bloodstream
Types:
a. Cardioembolic eg. Due to atrial fibrillation
b. Artery- artery embolic

2. Haemorrhagic Stroke (20%): Hemorrhagic strokes occur when an artery supplying the brain ruptures and bleeds. It can be divided into:

i) Intracerebral haemorrhage (15%): Bleeding is from the arteries within the brain.

ii) Subarachnoid haemorrhage (5%): Bleeding is in the subarachnoid space usually due to a ruptured cerebral aneurysm

Question 9

Clinical classification of stroke

Answer 9

1- Completed stroke: Complete focal neurological deficit at onset and lasting > 24hrs.

2- Progressive stroke/Stroke in evolution: symptoms worsening gradually or in stepwise fashion over hrs or days with symptoms lasting >24 hrs

3- Transient ischemic attack (TIA): symptoms lasting < 24hrs

Question 10

Difference between haemorrhagic and ischaemic stroke

Answer 10

In a hemorrhagic stroke, blood leaks into brain tissue
In an ischaemic stroke, the clot stops blood supply to an area of the brain

Question 11

What are 5 Non-modifiable risk factors of stroke?

Answer 11

Age
Race
Male gender
Previous stroke
Family hx

Question 12

What are modifiable risk factors of stroke?

Answer 12

Hypertension
Diabetes mellitus
Alcohol
Cigarette smoking
Dyslipidemia
Physical inactivity
Cardiac risk factors
Hemoglobinopathies
Vasculitis – HIV, syphilis,
Connective tissue diseases

Question 13

Causes of Hemorrhagic Stroke (7 A’s of hemorrhagic stroke)
What is the most common cause?

Answer 13

1. Chronic hypertension (rupture of Charcot-Bouchard aneurysms, Saccular aneurysms)
2. AV malformations
3. Amyloid angiopathy,
4. Anticoagulant therapy (Warfarin, Heparin)
5. Antiplatelets
6. Angioma (Cavernous hemangioma)
7. Amphetamines and other Drugs-cocaine, sympathomimetics

Most common cause is HYPERTENSION

Question 14

What are the areas of infarction in the brain?

Answer 14

Core area: infarct with irreversible damage (dead area) <10% cerebral bloos flow

Penumbra: tissue at risk, sustains reversible damage (dying area) < 20% cerebral blood flow

Oligemia: viable tissue, no infarct or risk

Question 15

PATHOPHYSIOLOGY ISCHAEMIC STROKE

Answer 15

1. Lack of oxygen supply to ischaemic neurones
2. ATP depletion
3. Membrane ions system stops functioning
4. Depolarisation of neurones
5. Influx of calcium
6. Release of neurotransmitters, including glutamate, activation of N-methyl-D-aspartate and other excitatory receptors at the membrane of neurones
7. Further depolarisation of cells
8. Further calcium influx

Question 16

Pathophysiology of Hemorrhagic Stroke

Answer 16

Explosive entry of blood into the brain parenchyma structurally disrupts neuronal activity by:

1. Compression of neurons and vessels leading to additional ischemic damage
2. Cerebral oedema
3. Splitting neuronal planes
4. Vasospasm from Direct neurotoxicity of blood

The above 4 mechanisms leading to severely elevated Intracranial pressure leading to brain herniation and death

Question 17

MCQ What are the Clinical Features of Ischemic stroke & Intracerebral hemorrhage?

(a) General features
(b) MCA distribution
(c) PCA distribution
(d) Internal Capsule

Answer 17

(a) General features – LOC (loss of consciousness), vomiting, seizures, HA (headache)

(b) MCA distribution
– contralateral weakness (face & arm > leg)
+ aphasia (R)(difficulty communicating/speaking) because the left MCA supplies Broca’s areas
+ sensory neglect (L) (they neglect sensations on the opposite side of the body)

(c) PCA distribution – Homonymous hemianopia (loss of vision in the same half of both eyes) + other motor deficits

(d) Internal capsule – sensorimotor loss (face=arm=leg), marked dysarthria (slurred speech), no cortical deficits eg aphasia

ACA distribution
- contractural weakness of lower extremities > face and upper extremities and sensory loss
abulia: decrease motivation or desire to participate in activities, akinetic mutism

Question 17

What are Lacunar Syndromes = Small vessel syndromes?
What’s are they usually associated with?

Answer 17

Lacunar syndromes are clinical manifestations of lacunar infarcts, which are small (<15 mm) subcortical ischemic strokes affecting the deep penetrating arteries of the brain. These infarcts occur due to occlusion of small branches of larger cerebral arteries.

Lacunar strokes do not involve the cerebral cortex, so they lack cortical signs (no aphasia, agnosia, neglect, or visual field deficits).

Indicate occlusion of perforating arteries in the subcortex, brainstem, or cerebellum,
often associated with chronic hypertension and diabetes mellitus

may be clinically silent, (only seen on imaging), or result in stroke syndromes involving densely packed white matter tracts with specific localization patterns.

Question 18

The most commonly described small vessel syndromes include:

Answer 18

1. pure motor: Contralesional hemiparesis
2. pure sensory: Contralesional hemisensory loss
3. sensorimotor: Contralesional
   weakness and numbness
4. ataxic hemiparesis: Contralesional
   (mild to moderate) hemiparesis and limb ataxia out of proportion to the degree of weakness
5. dysarthria-clumsy hand syndrome; Slurred speech and (typically fine motor)
   weakness of contralesional hand

A less common, but striking, small vessel syndrome manifests as hemiballism from infarction in the subthalamic nucleus: Contralesional limb flailing or dyskinesia

Question 18

INVESTIGATIONS for lacunae syndromes

Answer 18

Imaging – non-enhanced CT Brain
Blood workup – FBC, ESR, Glucose, lipid profile, E & U, Cr, (± HIV, VDRL, Clotting profile, autoantibodies for individual cases), lipid profile
ECG, ECHO
± Carotid Doppler (ischaemic stroke)
CXR,

Question 18

Principles of Acute Ischaemic Stroke Care

Answer 18

(1) achieve timely recanalization of the occluded artery and reperfusion of the ischemic tissue
(2) optimize collateral flow
(3) avoid secondary brain injury.

Question 19

Management of stroke; General measures

Answer 19

1. Stabilise; ABCs
2. If applicable care of the unconscious patient (HDU/ICU, careful nursing, attention to airway and vital signs, regular turning & skin care, oral hygiene via suctioning, irrigation of the eyes ± taping, sphincter care, feed – IV, NG, PEG)
3. Monitor blood pressure
4. Assess swallowing (gag reflex ± swallow test); NPO for the 1st 24 hours post stroke
   ISOTONIC IVFs ONLY
5. Early physiotherapy
6. Insulin for elevated blood glucose (Known DM or not)

Question 19

MANAGEMENT; Indications for antihypertensive use in acute ischemic stroke

Answer 19

BP > 220/120mmHg on more than 2 occasions or MAP > 140 (EXCLUDE pain, raised ICP,)
Associated hypertensive emergencies
Acute pulmonary edema
Acute kidney dysfunction
Hypertensive encephalopathy
Aortic dissection
DO NOT CRASH/RAPIDLY LOWER THE BP

Question 19

Which arteries supply the:

1. Lateral potions of the Frontal, Parietal and Temporal lobes
2. Medial portion of the Frontal and Parietal lobes
3. Cerebellum and Brain Stem
4. Occipital lobe

Answer 19

1. Lateral potions of the Frontal, Parietal and Temporal lobes: Middle Cerebral Arteries
2. Medial portion of the Frontal and Parietal lobes: Anterior Cerebral Arteries
3. Cerebellum and Brain Stem:
   branches of the Vertebral (supplies medulla, posterior and inferior cerebellum)
   and Basilar artery (supplies pons, superior, anterior and inferior cerebellum)
4. Occipital lobe: Posterior Cerebral Artery (which also supplies the temporal lobe, thalamus and midbrain)

Question 20

The parts of the primary motor cortex in the frontal lobe that control the legs and arms & face are supplied by which major arteries? Name the parts and the arteries

Answer 20

Primary motor cortex controls voluntary movement of skeletal muscles Legs and personality: controlled by the medial portion of the primary motor cortex and this is supplied by the ACA Arms, face and speech: controlled by the lateral portion of the primary motor cortex and this is supplied by the MCA

Question 21

The parts of the somatosesory cortex in the parietal lobe that control the legs and arms & face are supplied by which major arteries? Name the parts and the arteries

Answer 21

The somatosensory cortex, located in the postcentral gyrus of the parietal lobe, is responsible for processing sensory information from the body. Legs: controlled by the medial portion of the somatosensory cortex and this is supplied by the ACA Arms & face: controlled by the lateral portion of the somatosensory cortex and this is supplied by the MCA

Question 22

Cause of stroke in the young

Answer 22

Congenital heart defect Hypercoaguability

Question 23

Current trends in management of AIS (investigations and treatment) MCQ Timing for medication, when should you bring down the BP?

Answer 23

Emergency triage & initial evaluation; (including immediate stabilization of ABCs). Evaluation also rule out stroke mimics INVESTIGATIONS; ALL patients * non-contrast neuroimaging (CT still standard of care): It rules out hemorrhagic stroke by detecting hyperdense (bright) areas that indicate blood. * RBS: excludes hypoglycemia which can mimic stroke symptoms * SPO2: detects hypoxia which worsens brain injury * serum E, U, Cr (helps check the renal status) * FBC (+ platelets) to check for anemia * ECG: Detect atrial fibrillation (AF), MI, or other cardiac causes of embolism * ECHO: Identify cardiac sources of emboli * Carotid Doppler (to check for occlusion in carotid artery) (not emergent) Selected patients (eg stroke in the young <45years – toxicology screen; CXR; Definitive AIS TREATMENT: * Thrombolysis (rtPa) within a specific time-frame (4.5 hours) * For patients out of therapeutic window & those with contraindications to thrombolysis , commence ASA 300mg (aspirin inhibits platelet aggregation therefore it is CONTRAINDICATED for hemorrhagic stroke). * General measures – adequate positioning, avoid hypoxia, manage fever/hyperthermia * BP management; no intervention in 1st 24 hours unless BP > 220/120mmHg, or presence of medical emergency that warrants antihypertensive Rx (acute kidney injury, myocardial infarction, heart failure, aortic dissection) DO NOT CRASH THE BP!!!! Aim for gradual reduction using titratable parenteral antihypertensives; 15% - 25% reduction in SBP or MAP over 1st 24 hours ***Thrombolysis-eligible patients must have BP < 180/110mmHG*** * Maintain euvolemia using isotonic fluids * Blood glucose management – avoid hypoglycemia. Treat hyperglycemia; Target 140 – 180mg/dl (7.8 – 10mmol/L) * Monitor and manage complications; cerebral edema with ↑ICP, DVT, contractures, pressure ulcers Rehabilitation and secondary prevention

Question 24

MCQ What is the most common location for hypertensive bleeding? Commonest cause of haemorrhagic bleed?

Answer 24

Putamen Putaminal (40-50%)

Question 25

Contradictions to thrombolysis

Answer 25

BP above 180/100mmHg

Question 26

Why shouldn’t you give a stroke patient dextrose-containing fluid?

Answer 26

It can worsen their cerebral oedema

Question 27

What should you give a stroke patient in an acute emergency

Answer 27

Only insulin do not give an oral hypoglycemic agent eg. metformin

Question 28

Cardioembolic strokes are most commonly caused by what?

Answer 28

Atrial fibrillation

Question 29

Difference in onset of embolic and thrombotic stroke

Answer 29

E: maximal in onset T: gradual

Question 30

Management of Ischemic

Answer 30

THROMBOLYSIS; within 3 – 4.5 hours of stroke onset (standard of care) Tab ASA 300mg daily Statin therapy: reduce factor if there is hyperlipidemia Maintain cerebral perfusion (euvolemia) (IVFs 3L/24hours) DVT prophylaxis (SC LMWH/heparin) Anticipate and Rx complications

Question 31

CURRENT TRENDS IN MANAGEMENT OF ICH (investigation

Answer 31

* Rapid triage and ER evaluation * Emergency non-contrast brain imaging (CT scan) * Blood workup - RBS, serum chemistry, clotting profile, PT_INR , platelet count , TT, toxicology * Evaluate for other causes of ICH especially if elderly, atypical location of bleed (lobar), absence of risk factors * Attention to euvolemia, oxygen saturation, euglycemia, treat hyperthermia (>38⁰C) * Monitor for and manage complications – early neurologic deterioration (hematoma expansion, edema), * Treat clinical seizures; no room for prophylactic anticonvulsants

Question 32

MANAGEMENT; INTRACEREBRAL HAEMORRHAGE What time frame should anticoagulants be avoided?

Answer 32

1. Maintain cerebral perfusion 2. Manage raised ICP 3. Treatment of elevated BP to prevent hematoma expansion 4. Intermittent pneumatic compression stockings for DVT prophylaxis 5. NO NSAIDS/ASA 6. Prophylactic anticoagulation in the acute phase (individualized basis) NEUROSURGERY IN SELECTED CASES DVT prophylaxis – Avoid anticoagulants in the 1st 48 – 72 hours post-ICH - Use of anticoagulants in ICH should be on a case by case basis; - also based on availability of non-pharmacologic (mechanical) alternatives (pneumatic compression stockings) Blood pressure management – High BP associated with early neurologic deterioration, hematoma expansion, dependency, death. -For SBP 160 - 220mmHg lowering to 140mmHg considered safe -For SBP > 220mmHg ; aggressive reduction (must be with a titratable agent with facilities for intensive monitoring)

Question 33

What is a CARDIOEMBOLIC STROKE?

Answer 33

A cardioembolic stroke is an ischemic stroke caused by a blood clot (embolus) originating from the heart, which travels through the bloodstream and blocks a cerebral artery. * Most commonly caused by atrial fibrillation (responsible for ~50% of all cardioembolic strokes) * Secondary stroke prevention differs in cardioembolic strokes especially that due to atrial fibrillation * Variability in the estimated risk of stroke in Afib depending on presence of other risk factors

Question 34

Presentation Of Cardioembolic Stroke

Answer 34

* Neurologic symptoms that are maximal at onset: Since cardioembolic strokes occur due to sudden arterial occlusion by an embolus, symptoms appear abruptly and at full severity from the beginning (unlike thrombotic strokes, which may progress gradually over hours). * A stroke syndrome that localizes to a large artery territory, particularly when there is clinical evidence of cortical involvement, also suggests a cardioembolic source: Cardioemboli typically lodge in major arteries like the middle cerebral artery (MCA), posterior cerebral artery (PCA), or basilar artery, affecting large areas of the brain. * Evidence of multiple foci of concurrent or sequential ischemia, particularly in multiple cerebrovascular or systemic vascular beds, is also strongly suggestive of cardioembolism: Cardioembolism can result in shower emboli, affecting multiple territories in the brain or other organs. Imaging may show infarcts in different vascular distributions (e.g., MCA + PCA involvement).

Question 35

Use of risk stratification scores IN CARDIOEMBOLIC STROKE

Answer 35

Use of risk stratification scores in Afib CHADS2 - Congestive cardiac failure - 1 - HTN- 1 - Age > 75yrs - 1 - DM -1 - previous stroke/TIA -1 If the Tscore ≥ 2: anticoagulants are recommended CHA2DS2- VASc [CCF – 1, HTN – 1, Age ≥ 75yrs – 2, DM – 1, previous stroke, TIA/ thromboembolism – 2,Vascular Dx (previous M.I., P.A.Dx, aortic plaque – 1, Age 65 – 74yrs - 1 Sex category (female) – 1]. Tscore ≥ 2 (anticoag) CHA₂DS₂-VASc Scoring System: is more refined and includes other risk factors C – Congestive heart failure (CCF) → 1 point H – Hypertension → 1 point A₂ – Age ≥ 75 years → 2 points D – Diabetes mellitus → 1 point S₂ – Previous stroke, TIA, or thromboembolism → 2 points V – Vascular disease (previous MI, PAD, aortic plaque) → 1 point A – Age 65–74 years → 1 point S – Sex category (Female) → 1 point Tscore ≥ 2 (anticoagulant recommended) Target – INR of 2 – 3 Treatment of stroke with Afib includes rate control (eg, beta blockers, ccb, digoxin) +/- rhythm control (antiarrhythmics)

Question 36

RISK OF BLEEDING DURING ANTICOAGULATION IN CARDIOEMBOLIC STROKE

Answer 36

HAS-BLED score (HTN SBP > 160mmHG – 1, Abnormal renal or liver fxn – 1 each, Stroke – 1, History of bleeding predisposition – 1, Labile INR – 1, Elderly Age > 65yrs – 1, Drugs esp NSAIDS +/- antiplatelets, excess alcohol – 1each,). Tscore ≥ 3 (cautious)

Question 37

Complications of stroke

Answer 37

1. CNS – repeat stroke, hematoma growth (ICH), hemorrhagic conversion, cerebral edema, raised ICP (± herniation), hydrocephalus, seizures 2. RS - Aspiration, aspiration pneumonia, hypostatic pneumonia, pulmonary edema, pulmonary embolism 3. CVS - Arrhythmias, cardiogenic shock, 4. Endocrine - ↑RBS, disturbance of salt & water homeostasis 5. UGS – UTI 6. GIT - Stress (Cushing’s) ulcers, GI bleeding, paralytic ileus, malnutrition 7. Limb – DVT, contractures, adhesive capsulitis 8. Skin – decubitus ulcers 9. Psychology – Depression

Question 38

REHABILITATION & SECONDARY PREVENTION of stroke

Answer 38

* Lifestyle modifications * Rx of risk factors (HTN, DM, infections, prophylaxis in Afib), * ASA (or other antiplatelet) for life if ischemic * Statin (regardless of lipid levels) if ischemic * Physiotherapy * Occupational therapy * Speech therapy * Assisted living/ adaptation of home to deficits

Question 39

Risk stratification in TIA

Answer 39

* Historically regarded as benign …no longer so * Decision on evaluation following a TIA - admit or not to admit for evaluation * Neuroimaging for TIA – MRI * Depends on the calculated future risk of stroke The ABCD2: * age ≥ 60 years (1 point) * BP ≥ 140/90 mm Hg at presentation (1 point) * clinical features: unilateral weakness (2 points) or speech/language impairment without weakness (1 point) * duration ≥60 minutes (2 points) or 10 to 59 minutes (1 point) * DM (1 point). ABCD2 score can vary from 0 to 7 < 3 low risk 4-5 moderate risk 6-7 high risk Therefore we aim to reduce risk factors

Question 40

What is a SUBARACHNOID HEMORRHAGE; Nontraumatic/aneurysmal?

Answer 40

Neurologic emergency Accounts for ~5% of all strokes Occurs at a younger age than other types of stroke High mortality Intracranial aneurysms Risk of rupture dependent on other factors

Question 41

Risk factors for SAH

Answer 41

Non-modifiable: Age Female gender Previous hx of SAH FHx of SAH Hx of aneurysm in 1st degree relatives Modifiable; Hypertension Cigarette smoking Heavy alcohol use Sympathomimetic drug ab(use)

Question 42

Clinical features of SAH

Answer 42

1. Sudden severe headache (thunderclap)+/- L.O.C and neck stiffness, nausea and vomiting 2. Focal features may suggest cause or complication 6th cranial nerve palsy – Raised ICP 3rd cranial nerve palsy – posterior communicating /PCA/superior cerebellar artery 3. Paraparesis & abulia (a state of apathy/ diminished motivation); anterior communicating artery 4. Hemiparesis + aphasia/neglect; MCA aneurysm 5. Impaired L.O.C & impaired upgaze; Hydrocephalus 6. Unilateral visual loss & bi-temporal hemianopia (Loss of temporal (outer) vision in both eyes); ICA aneurysm

Question 43

Diagnosis of SAH (investigations)

Answer 43

Non-contrast enhanced CT Lumber puncture (if CT is negative) CT/MR angiography

Question 44

Management of SAH

Answer 44

General measures as for other strokes Prevent rebleeding (Tx aneurysm) Prevent vasospasm; Nimodipine 60mg 4 hourly * 21days Anticipate and Rx complications; hydrocephalus Bedrest (including no bathroom privileges) & supportive management; control HTN, analgesics for headaches, DVT prophylaxis, laxatives

Question 45

Complications of SAH

Answer 45

Rebleed Vasospasm and delayed cerebral infarction Hydrocephalus Cardiopulmonary; arrhythmias, neurogenic pulmonary edema Hyponatremia ; SIADH or cerebral salt wasting DVT Seizures

Question 46

MCQ Antons syndrome is caused by infarct to where?

Answer 46

PCA distribution

Question 47

MCQ imaging of choice for stroke?

Answer 47

Non-enhances/ non-contrast CT scan

Question 48

MCQ all stroke patients require a stroke test T/F

Answer 48

TRUE

Question 49

MCQ The most common cause of SAH

Answer 49

Trauma

Question 50

MCQ The most common cause of non-traumatic SAH

Answer 50

anuerysmal rupture

Question 51

Acute and chronic complications of stroke

Answer 51

Chronic Bladder: UTI Brain: depression Blood: anemia Bedding: bed sores BMR: increase Bones: contracture Acute Cerebral edema Hypoglycemia