1
Q
What is the definition of stroke?
A
A syndrome of rapid onset of cerebral deficit, usually focal, lasting >24 hours or leading to death, with no cause apparent other than a vascular one.
2
Q
What is the difference between stroke and TIA?
A
TIA (Transient Ischemic Attack): temporary focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction, symptoms resolve within 24 hours (typically <1 hour). Stroke: symptoms last >24 hours or cause death with evidence of infarction or hemorrhage.
3
Q
What is the global burden of stroke?
A
Stroke is the second-leading cause of death worldwide (11.6% of all deaths) and the third-leading cause of disability-adjusted life years (DALYs). Approximately 12.2 million new strokes occur annually.
4
Q
What is the lifetime risk of stroke globally?
A
1 in 4 people over age 25 will have a stroke in their lifetime – approximately 25% lifetime risk.
5
Q
What is the incidence of first-ever stroke in low/middle-income countries?
A
LMICs account for over 80% of all strokes globally, with age-standardized incidence rates up to 3-4 times higher than in high-income countries.
6
Q
List the non-modifiable risk factors for stroke.
A
1) Age (≥65 years), 2) Sex (males have higher risk, though women have worse outcomes), 3) Race (Blacks, Hispanics have higher risk), 4) Family history of stroke or TIA, 5) History of migraine headaches (especially with aura), 6) Spontaneous Coronary Artery Dissection (SCAD).
7
Q
List the modifiable risk factors for stroke.
A
1) Hypertension, 2) Smoking, 3) Diabetes mellitus, 4) Hyperlipidemia, 5) Atrial fibrillation, 6) Severe carotid stenosis, 7) Valvular heart disease, 8) TIA, 9) Hyperhomocysteinemia, 10) Alcohol intake, 11) Obesity, 12) Sleep apnea, 13) Oral contraceptives, 14) Sickle cell disease, 15) Hypercoagulable states, 16) CADASIL, 17) MELAS.
8
Q
What is the most important modifiable risk factor for stroke?
A
Hypertension – it is the single most important modifiable risk factor, accounting for approximately 50% of the population-attributable risk of stroke.
9
Q
What is the target blood pressure for secondary stroke prevention?
A
<130/80 mmHg (AHA/ASA 2025 guidelines).
10
Q
What percentage of strokes are ischemic versus hemorrhagic?
A
Ischemic stroke: approximately 80%. Hemorrhagic stroke: approximately 20% (10-15% intracerebral hemorrhage, 5% subarachnoid hemorrhage).
11
Q
What are the main subtypes of ischemic stroke?
A
1) Large artery occlusion (thrombotic), 2) Cardioembolic stroke, 3) Watershed (border zone) infarct, 4) Lacunar stroke (small vessel disease).
12
Q
What is the most common mechanism of ischemic stroke?
A
Large artery atherosclerosis (thrombotic) – accounts for 20-30% of ischemic strokes. Cardioembolism (e.g., atrial fibrillation) accounts for 20-30% as well.
13
Q
What is the most common cause of cardioembolic stroke?
A
Atrial fibrillation (non-valvular) – responsible for 15-25% of all ischemic strokes. Risk increases with CHA₂DS₂-VASc score.
14
Q
What is the CHA₂DS₂-VASc score?
A
A clinical prediction tool for stroke risk in atrial fibrillation: Congestive heart failure (1), Hypertension (1), Age ≥75 (2), Diabetes (1), Stroke/TIA/TE (2), Vascular disease (1), Age 65-74 (1), Sex category female (1).
15
Q
What is the clinical presentation of right middle cerebral artery (MCA) occlusion?
A
Left-sided weakness (face and limbs, arm > leg), left-sided sensory loss, left homonymous hemianopia, and neglect of the left side of the environment.
16
Q
What is the clinical presentation of left middle cerebral artery (MCA) occlusion?
A
Right-sided weakness (face and limbs, arm > leg), right-sided sensory loss, right homonymous hemianopia, and aphasia.
17
Q
What is the clinical presentation of anterior cerebral artery (ACA) occlusion?
A
Weakness on the contralateral side (leg > arm), reappearance of primitive reflexes (grasp, suck), muteness, perseveration, abulia (lack of initiative), and disinhibition.
18
Q
What is abulia?
A
A lack of will or initiative – a reduction in spontaneous speech, movement, and emotional responsiveness. Often associated with frontal lobe lesions, including anterior cerebral artery territory strokes.
19
Q
What is the clinical presentation of posterior cerebral artery (PCA) occlusion?
A
Homonymous hemianopia (contralateral visual field loss), cortical blindness (if bilateral), memory loss (hippocampal involvement), and altered mental status.
20
Q
What is the difference between homonymous hemianopia and quadrantanopia?
A
Homonymous hemianopia: loss of the same half of the visual field in both eyes. Quadrantanopia: loss of one quarter of the visual field (e.g., superior or inferior homonymous quadrantanopia).
21
Q
What is neglect syndrome and which artery occlusion causes it?
A
Neglect syndrome: failure to attend to or respond to stimuli on the contralateral side of space (usually left side). Caused by right middle cerebral artery (MCA) occlusion – particularly right parietal lobe involvement.
22
Q
Define aphasia.
A
A language disorder caused by brain damage (usually left hemisphere) affecting comprehension, production, or repetition of language. Does NOT affect intelligence.
23
Q
What are the three main types of aphasia?
A
1) Wernicke’s aphasia (receptive), 2) Broca’s aphasia (expressive), 3) Conduction aphasia.
24
Q
What brain area is damaged in Wernicke’s aphasia?
A
Superior temporal gyrus (posterior superior temporal lobe) – also called Wernicke’s area.
25
What are the clinical features of Wernicke's aphasia?
Impaired comprehension, fluent but meaningless speech (logorrhea – excessive word output with paraphasic errors), and impaired repetition. Patient is often unaware of the deficit.
26
What brain area is damaged in Broca's aphasia?
Inferior frontal gyrus (Broca's area – pars opercularis and pars triangularis of the frontal lobe).
27
What are the clinical features of Broca's aphasia?
Normal comprehension, non-fluent (halting, effortful, telegraphic) speech, and impaired repetition. Patient is often frustrated and aware of the deficit.
28
What brain area is damaged in conduction aphasia?
Arcuate fasciculus – the white matter tract connecting Wernicke's and Broca's areas (typically left hemisphere).
29
What are the clinical features of conduction aphasia?
Normal comprehension, fluent speech, but impaired repetition – patients can understand but cannot repeat what is said. Often make phonemic paraphasic errors.
30
What is global aphasia?
Combined damage to both Broca's and Wernicke's areas (large left MCA territory stroke) – results in impaired comprehension, non-fluent speech, and impaired repetition. The most severe form of aphasia.
31
What is watershed (border zone) infarction?
Infarction occurring in the cerebral border zones between the territories of major cerebral arteries (ACA/MCA, MCA/PCA). Follows prolonged systemic hypoperfusion (e.g., cardiac arrest, severe hypotension, shock).
32
What are the clinical features of watershed infarction?
Cortical visual loss, memory loss, intellectual impairment, proximal arm and leg weakness (man-in-the-barrel syndrome), and sometimes bilateral deficits.
33
What is 'man-in-the-barrel' syndrome?
A pattern of weakness seen in watershed infarction between ACA and MCA territories – proximal arm weakness with preserved distal strength and leg strength, resembling a person trapped in a barrel.
34
What is a lacunar stroke?
A small, deep infarct (<1.5 cm in diameter) caused by occlusion of a single small penetrating artery (e.g., lenticulostriate arteries, thalamoperforators). Typically associated with chronic hypertension and diabetes.
35
What are the classic lacunar syndromes?
1) Pure motor stroke (most common – internal capsule or pons), 2) Pure sensory stroke (thalamus), 3) Sensorimotor stroke, 4) Ataxic hemiparesis, 5) Clumsy hand-dysarthria syndrome.
36
What is pure motor lacunar syndrome?
Weakness of face, arm, and leg on one side (complete hemiparesis) without sensory loss, visual field defect, aphasia, or neglect. Most common lacunar syndrome – typically involves posterior limb of internal capsule or basis pontis.
37
What is clumsy hand-dysarthria syndrome?
A lacunar syndrome characterized by dysarthria (slurred speech) and clumsiness of the hand on one side, often with mild weakness. Typically involves the basis pontis or genu of internal capsule.
38
What is lateral medullary syndrome (Wallenberg's syndrome)?
A brainstem stroke syndrome caused by occlusion of the vertebral artery or its branch, the posterior inferior cerebellar artery (PICA).
39
What are the clinical features of lateral medullary syndrome?
Loss of pain and temperature sensation on the IPSILATERAL face and CONTRALATERAL limbs (crossed findings), dysphagia, dysarthria, vertigo, nystagmus, Horner syndrome (ptosis, miosis, anhidrosis), and ipsilateral ataxia.
40
Why does lateral medullary syndrome cause 'crossed' sensory findings?
The spinothalamic tract (pain/temperature) decussates in the spinal cord, so limb fibers cross. The spinal trigeminal nucleus (facial pain/temperature) does NOT decussate. Thus: ipsilateral face + contralateral limbs.
41
What is Horner syndrome?
A syndrome caused by disruption of the sympathetic chain: ptosis (drooping eyelid), miosis (constricted pupil), and anhidrosis (lack of sweating) on the ipsilateral side. Seen in lateral medullary syndrome and other brainstem/brain lesions.
42
What is pseudobulbar palsy?
An upper motor neuron (UMN) lesion affecting cranial nerves IX, X, XI (bulbar muscles). Caused by bilateral corticobulbar tract damage (often from multiple lacunar strokes or ALS).
43
What are the clinical features of pseudobulbar palsy?
Dysarthria (spastic speech), dysphagia, spastic facial jerks, and emotional lability (pathological laughing/crying – pseudobulbar affect). Jaw jerk is exaggerated (UMN sign).
44
How does pseudobulbar palsy differ from bulbar palsy?
Pseudobulbar palsy: UMN lesion (bilateral corticobulbar) – spastic dysarthria, exaggerated jaw jerk, emotional lability. Bulbar palsy: LMN lesion (lower cranial nerves) – flaccid dysarthria, wasted tongue with fasciculations, absent jaw jerk.
45
What is locked-in syndrome?
A condition caused by bilateral pontine base (corticospinal and corticobulbar tracts) infarction – typically basilar artery occlusion. Patient is conscious and aware but completely paralyzed except for vertical eye movement and blinking.
46
What is the typical neurological examination finding in locked-in syndrome?
Preserved vertical eye movements and blinking (cranial nerve III and IV are spared) with quadriplegia and anarthria (unable to speak or move limbs). Patient can communicate using eye movements.
47
What is the first-line imaging modality for acute stroke?
Emergency non-contrast CT scan – it is rapid, widely available, and can immediately exclude intracranial hemorrhage. Ischemic changes may not be visible for hours to days.
48
When does cerebral infarction become visible on CT scan?
Subtle signs may appear within 3-6 hours (e.g., hyperdense MCA sign, loss of insular ribbon, loss of grey-white differentiation). Overt hypodensity typically appears after 24-48 hours.
49
What is the hyperdense MCA sign on CT?
A radiological sign of acute ischemic stroke – visible hyperdensity (bright) of the middle cerebral artery due to an intraluminal thrombus or embolus. Highly specific for MCA occlusion.
50
What is the insular ribbon sign on CT?
Loss of the normal grey-white matter distinction in the insular cortex – an early sign of MCA territory ischemia, often visible within 2-6 hours of stroke onset.
51
What is the role of MRI in acute stroke?
MRI with diffusion-weighted imaging (DWI) is more sensitive than CT for early ischemic stroke (visible within minutes). It is the preferred imaging for TIA and posterior circulation strokes but takes longer than CT.
52
What is the time window for intravenous thrombolysis (alteplase) in acute ischemic stroke?
Within 4.5 hours of symptom onset (or last known well for wake-up strokes).
53
What is the dose of alteplase (tPA) for acute ischemic stroke?
0.9 mg/kg (maximum 90 mg) – 10% of total dose given as IV bolus over 1 minute, remaining 90% infused over 60 minutes.
54
What is the absolute blood pressure contraindication to thrombolysis?
Sustained elevated BP >185/110 mmHg despite treatment – thrombolysis should not be given if BP cannot be controlled below this threshold.
55
List the absolute contraindications to IV thrombolysis for stroke.
1) Sustained BP >185/110 mmHg, 2) Platelet count <100,000/mm³, 3) Blood glucose <2.8 mmol/L or >21.2 mmol/L, 4) Major surgery within last 14 days, 5) Heparin use within 48 hours with elevated PTT, 6) Head trauma, stroke, or MI within last 3 months, 7) Active internal bleeding, 8) Intracranial hemorrhage history.
56
What is the number needed to treat (NNT) for IV thrombolysis in acute ischemic stroke?
NNT for one additional patient with excellent functional outcome (modified Rankin score 0-1) is approximately 7-10, depending on time to treatment.
57
What is the risk of symptomatic intracranial hemorrhage after IV thrombolysis?
Approximately 2-7% – highest risk in patients with severe stroke (NIHSS >20), older age, uncontrolled hypertension, and hyperglycemia.
58
What is mechanical thrombectomy?
Endovascular removal of a large vessel occlusion thrombus using a stent retriever or aspiration catheter. It is the standard of care for large artery occlusions (e.g., ICA, M1 MCA, basilar artery).
59
What is the time window for mechanical thrombectomy?
Up to 6 hours from symptom onset (standard window). Extended window up to 24 hours in selected patients with favorable penumbral imaging (CT perfusion or MRI DWI/PWI mismatch).
60
Which patients are eligible for mechanical thrombectomy?
Patients with: 1) Large vessel occlusion (ICA, M1 MCA, basilar artery), 2) Pre-stroke mRS 0-1 (independent), 3) NIHSS ≥6, 4) ASPECTS ≥6 on CT, 5) Time from onset <6 hours (or up to 24 hours with favorable imaging).
61
What is a 'wake-up stroke'?
A stroke that occurs during sleep, so the exact time of symptom onset is unknown. These patients are eligible for thrombectomy (and sometimes thrombolysis using MRI DWI/FLAIR mismatch) if within appropriate imaging windows.
62
What is the ASPECTS score?
Alberta Stroke Program Early CT Score – a 10-point scoring system for early ischemic changes in MCA territory on non-contrast CT. Higher scores = less extensive ischemia. ASPECTS ≥6 is typically required for thrombectomy.
63
What is the management of elevated blood pressure in acute ischemic stroke NOT receiving thrombolysis?
BP should generally NOT be lowered unless >220/120 mmHg or there is evidence of hypertensive emergency (e.g., aortic dissection, acute MI, heart failure). Aggressive lowering may worsen penumbral ischemia.
64
What is the management of elevated blood pressure in acute ischemic stroke patients receiving thrombolysis?
BP must be kept <185/110 mmHg before thrombolysis and <180/105 mmHg for 24 hours after. IV labetalol, nicardipine, or clevidipine are used for control.
65
When should antiplatelet therapy be started in acute ischemic stroke?
Aspirin 300 mg (orally or rectally) should be given within 24-48 hours of ischemic stroke onset (unless contraindicated). Continue for 2 weeks, then switch to long-term antiplatelet (clopidogrel 75 mg daily lifelong).
66
What is the role of dual antiplatelet therapy (DAPT) in minor stroke or high-risk TIA?
Short-term DAPT (aspirin 75 mg + clopidogrel 75 mg) for 21 days followed by clopidogrel monotherapy reduces early recurrent stroke risk (CHANCE and POINT trials).
67
When should anticoagulation be started in ischemic stroke patients with atrial fibrillation?
Not within the first 4-14 days – timing depends on infarct size and severity: small infarct (4-7 days), moderate infarct (7-10 days), large or hemorrhagic infarct (10-14 days or later). Delayed initiation reduces hemorrhagic transformation risk.
68
What is the preferred anticoagulant for secondary prevention in atrial fibrillation?
Direct Oral Anticoagulants (DOACs) – apixaban, dabigatran, edoxaban, rivaroxaban – are preferred over warfarin due to lower risk of intracranial hemorrhage and no need for INR monitoring.
69
When should statin therapy be started after ischemic stroke?
High-intensity statin (atorvastatin 40-80 mg daily or rosuvastatin 20-40 mg daily) should be started as early as possible, regardless of baseline LDL levels (unless contraindicated).
70
What is the target LDL for secondary stroke prevention?
<55 mg/dL (1.4 mmol/L) or at least 50% reduction from baseline – AHA/ASA 2025 guidelines.
71
What is the management of increased intracranial pressure (ICP) in acute stroke?
1) 30-degree head-up positioning, 2) Mannitol 0.25-1 g/kg IV, 3) Hypertonic saline (3% or 23.4%), 4) Short-term hyperventilation (temporizing measure – target PaCO₂ 30-35 mmHg), 5) Decompressive hemicraniectomy for malignant MCA syndrome.
72
What is malignant MCA syndrome?
A life-threatening condition following large MCA territory infarction (typically >50% of MCA territory). Features: declining consciousness, pupillary changes, and brain herniation with mortality up to 80% without surgery. Decompressive hemicraniectomy reduces mortality to 20-30%.
73
List the acute complications (<7 days) of stroke.
1) Hypoxia, 2) Hypertension/hypotension, 3) Hyperglycemia, 4) Aspiration pneumonia, 5) Cardiac arrhythmias (especially atrial fibrillation), 6) SIADH (syndrome of inappropriate antidiuretic hormone).
74
List the chronic complications (>7 days) of stroke.
1) Venous thromboembolism (DVT/PE), 2) Bronchopneumonia, 3) Urinary tract infection, 4) Septicemia, 5) Decubitus ulcers (pressure sores), 6) Joint stiffness and contractures, 7) Post-stroke weight loss, 8) Post-stroke depression (30-50% of survivors).
75
What is SIADH and how does it relate to stroke?
Syndrome of Inappropriate Antidiuretic Hormone – common after subarachnoid hemorrhage and some ischemic strokes. Causes euvolemic hyponatremia (dilutional). Treatment: fluid restriction, demeclocycline, or tolvaptan if severe.
76
What is the recommended rehabilitation after stroke?
Early, multidisciplinary rehabilitation: physiotherapy (mobility and motor recovery), occupational therapy (activities of daily living), speech and language therapy (dysphagia and aphasia), and psychological support (depression).
77
What is the definition of Transient Ischemic Attack (TIA)?
A brief episode of neurological dysfunction due to temporary focal brain, spinal cord, or retinal ischemia WITHOUT acute infarction (by definition, no DWI-positive lesion on MRI).
78
What is the risk of stroke after a TIA?
The 90-day stroke risk after TIA is 10-20%, with the highest risk in the first 48 hours (5-10% within 7 days). The ABCD² score helps stratify risk.
79
What is the ABCD² score for TIA risk stratification?
Age ≥60 (1), BP ≥140/90 (1), Clinical features (unilateral weakness = 2, speech disturbance without weakness = 1), Duration ≥60 min (2), Diabetes (1). Total: 0-7 points. High risk (6-7) = 8% stroke at 7 days.
80
What is the recommended evaluation for suspected TIA?
All patients with suspected TIA should be assessed by a stroke specialist within 24 hours of symptom onset. Imaging: MRI with DWI (preferred) or CT. Carotid imaging (Doppler, CTA, or MRA) if carotid stenosis suspected.
81
What is the immediate management of TIA?
Aspirin 300 mg as soon as possible if TIA is suspected. Short-term dual antiplatelet (aspirin 75 mg + clopidogrel 75 mg) for up to 21 days for high-risk TIA or minor stroke (ABCD² ≥4). Then clopidogrel 75 mg lifelong.
82
What is amaurosis fugax?
Transient monocular vision loss (often described as 'a curtain coming down over one eye') caused by retinal ischemia – usually from ipsilateral carotid artery embolism or hypoperfusion. A form of TIA.
83
What is the indication for carotid endarterectomy (CEA)?
Patients with symptomatic carotid artery stenosis (TIA, minor stroke, or amaurosis fugax) with 50-99% stenosis who are fit for surgery. Timing: within 2 weeks of the event to maximize benefit.
84
What is the number needed to treat (NNT) for carotid endarterectomy?
NNT to prevent one ipsilateral stroke over 5 years: approximately 5-6 for patients with 70-99% stenosis. Benefit is greatest when surgery is performed within 2 weeks of symptoms.
85
What is the alternative to carotid endarterectomy?
Carotid artery stenting (CAS) – may be preferred in patients with high surgical risk (e.g., severe cardiac disease, hostile neck anatomy, or prior neck radiation).
86
What is the definition of intracerebral hemorrhage (ICH)?
Bleeding directly into the brain parenchyma. Accounts for 10-15% of all strokes but causes 30-40% of stroke-related deaths.
87
What is the most common cause of intracerebral hemorrhage?
Hypertension – responsible for 60-70% of ICH cases. Chronic hypertension causes lipohyalinosis and microaneurysm formation (Charcot-Bouchard aneurysms) in small deep penetrating arteries.
88
What are the other causes of intracerebral hemorrhage?
1) Coagulopathy (warfarin, DOACs, antiplatelets, thrombocytopenia), 2) Cerebral amyloid angiopathy (CAA – especially in elderly and Alzheimer's patients, lobar hemorrhages), 3) Sympathomimetic drugs (cocaine, methamphetamine), 4) Vascular malformations (AVM, cavernoma), 5) Brain tumor, 6) Venous sinus thrombosis.
89
What are the risk factors for intracerebral hemorrhage?
Advanced age and alcohol abuse (chronic heavy drinking).
90
What are the most common locations for hypertensive intracerebral hemorrhage?
1) Basal ganglia (especially putamen – 35-50%), 2) Thalamus (10-15%), 3) Cerebellum (5-10%), 4) Pons (5-10%). These are deep brain structures supplied by small penetrating arteries.
91
What are the clinical features of putaminal hemorrhage?
Contralateral hemiparesis, contralateral sensory loss, gaze paresis (eyes look toward the side of the lesion – 'wrong-way eyes'), homonymous hemianopia, aphasia (if dominant hemisphere), and apraxia.
92
What are the clinical features of thalamic hemorrhage?
Contralateral sensory loss (prominent – often more than motor), contralateral hemiparesis, gaze paresis (downward and inward deviation), homonymous hemianopia, miosis (small pupil), aphasia (dominant), and apraxia.
93
What are the clinical features of pontine hemorrhage?
Deep coma with quadriplegia, decerebrate rigidity (extensor posturing), pinpoint pupils (1-2 mm but reactive to light), and impaired reflex horizontal eye movement (oculocephalic reflex – 'doll's eyes' – is absent).
94
What are the clinical features of cerebellar hemorrhage?
Ipsilateral ataxia (dysmetria, dysdiadochokinesia), gaze paresis (eyes deviate away from the lesion), skew deviation (vertical misalignment), decreased consciousness, facial weakness, and sensory loss.
95
What is the triad of cerebellar hemorrhage?
Vomiting, headache, and ataxia – followed by rapid deterioration and brainstem compression if not surgically evacuated.
96
What is the first-line imaging for suspected intracerebral hemorrhage?
Emergency non-contrast CT scan – it shows acute hemorrhage as a hyperdense (bright white) lesion within minutes of onset. MRI is more sensitive but takes longer.
97
What is the blood pressure target for intracerebral hemorrhage?
Lower systolic BP to 140-160 mmHg (target typically 160-170 mmHg as per slides). The ATACH-2 and INTERACT2 trials showed intensive BP lowering (target SBP <140) is safe but did not improve functional outcomes.
98
When is surgical evacuation indicated for intracerebral hemorrhage?
1) Cerebellar hemorrhage >3 cm or causing brainstem compression/hydrocephalus – urgent evacuation. 2) Supratentorial lobar hemorrhages >30 mL with deteriorating patient – controversial but may benefit if superficial. 3) Deep hemorrhages (basal ganglia/thalamus) generally NOT operated unless life-threatening.
99
What is the mortality rate of intracerebral hemorrhage?
30-day mortality is 30-50% – significantly higher than ischemic stroke. Early deterioration is common within the first 24 hours due to hematoma expansion.
100
What is the spot sign on CT angiography in ICH?
A contrast extravasation within the hematoma on CTA – predicts ongoing bleeding and hematoma expansion. Associated with worse outcomes and higher mortality.
101
What is subarachnoid hemorrhage (SAH)?
Bleeding into the subarachnoid space – the space between the arachnoid mater and pia mater. Most commonly caused by ruptured saccular (berry) aneurysm (80-85% of non-traumatic SAH).
102
What is the classic presentation of subarachnoid hemorrhage?
'Thunderclap headache' – sudden, severe, worst headache of life, often described as a 'blow to the head.' May be associated with neck stiffness, photophobia, vomiting, and loss of consciousness.
103
What is the first-line imaging for suspected subarachnoid hemorrhage?
Non-contrast CT head – sensitivity is 98-100% within 6 hours of onset. If CT is negative but clinical suspicion is high, lumbar puncture is performed to detect xanthochromia (bilirubin in CSF).
104
What is xanthochromia?
Yellow discoloration of CSF caused by bilirubin from breakdown of red blood cells. Appears 6-12 hours after subarachnoid hemorrhage and persists for 1-2 weeks. Diagnostic of prior SAH when CT is negative.
105
What is the most common cause of non-traumatic subarachnoid hemorrhage?
Ruptured saccular (berry) aneurysm – most commonly located at the anterior communicating artery, posterior communicating artery, or middle cerebral artery bifurcation.
106
What are the risk factors for cerebral aneurysms?
1) Hypertension, 2) Smoking, 3) Female sex, 4) Autosomal dominant polycystic kidney disease (ADPKD), 5) Ehlers-Danlos syndrome type IV, 6) Marfan syndrome, 7) Family history of aneurysms, 8) Fibromuscular dysplasia.
107
What is the treatment for ruptured cerebral aneurysm?
1) Securing the aneurysm to prevent rebleeding: endovascular coiling (preferred for posterior circulation and many anterior aneurysms) or surgical clipping. 2) Management of complications: vasospasm (nimodipine), hydrocephalus (EVD), hyponatremia (SIADH/cerebral salt wasting).
108
What is nimodipine and why is it used in SAH?
A dihydropyridine calcium channel blocker given orally (60 mg every 4 hours) for 21 days after SAH. It reduces the risk of delayed cerebral ischemia from vasospasm – the only drug proven to improve outcomes in SAH.
109
What is cerebral salt wasting (CSW)?
A complication of SAH and other brain injuries causing hypovolemic hyponatremia due to excessive natriuresis. Differentiates from SIADH by volume status: CSW = hypovolemic (low CVP), SIADH = euvolemic/hypervolemic.
110
How do you distinguish cerebral salt wasting from SIADH?
CSW: low blood volume (hypovolemic), low CVP, high urine sodium, negative fluid balance – treat with IV fluids (normal saline) and fludrocortisone. SIADH: normal/high volume, high urine sodium, positive fluid balance – treat with fluid restriction.
111
What is the prognosis of subarachnoid hemorrhage?
Mortality is 10-15% before hospital arrival and another 25-30% within 30 days. Of survivors, 30-50% have permanent neurological deficits. Rebleeding risk is highest in the first 24 hours (4-5% per hour initially).
112
What is the difference between ischemic and hemorrhagic stroke prognosis?
Hemorrhagic stroke has higher early mortality (30-50% at 30 days vs 10-20% for ischemic) but survivors may have better functional recovery if they survive the acute phase.
113
What are the modifiable lifestyle factors for primary stroke prevention?
1) Smoking cessation, 2) Regular exercise (≥150 min moderate/week), 3) Low-salt, low-fat diet (e.g., DASH or Mediterranean diet), 4) Weight management (BMI <25), 5) Moderate alcohol intake (≤1-2 drinks/day), 6) Treatment of hypertension, diabetes, hyperlipidemia, and atrial fibrillation.
114
What is the role of antiplatelet therapy in primary stroke prevention?
Aspirin is NOT routinely recommended for primary prevention in low-risk individuals due to bleeding risk. It may be considered in high-risk patients (10-year CVD risk >10%) after discussing risks/benefits.
115
What is the role of statins in primary stroke prevention?
Statins reduce stroke risk by approximately 20-25% in patients with cardiovascular risk factors, regardless of baseline LDL levels. Recommended for patients with high CVD risk (ASCVD score ≥7.5-10%).
116
What is the recommended antiplatelet regimen for secondary stroke prevention?
Clopidogrel 75 mg daily lifelong (monotherapy) is preferred over aspirin due to slightly lower risk of recurrent stroke and similar bleeding risk. Aspirin 81-325 mg daily is an alternative if clopidogrel is not tolerated.
117
What is the role of ticagrelor in stroke prevention?
Ticagrelor (with or without aspirin) is NOT superior to clopidogrel for secondary stroke prevention and has higher bleeding rates. Not recommended as first-line.
118
What is the recommended statin regimen for secondary stroke prevention?
High-intensity statin: atorvastatin 40-80 mg daily or rosuvastatin 20-40 mg daily. Target LDL <55 mg/dL (1.4 mmol/L) or ≥50% reduction.
119
What is the role of PCSK9 inhibitors in stroke prevention?
Evolocumab or alirocumab may be added to high-intensity statins in patients with very high risk (including recurrent stroke) who do not achieve LDL targets. Reduces stroke risk by approximately 20-25%.
120
What is the recommended blood pressure target for secondary stroke prevention?
<130/80 mmHg (AHA/ASA 2025). For patients with lacunar strokes, SBP target <130 mmHg is recommended based on SPS3 trial.
121
What is the role of renal denervation in resistant hypertension for stroke prevention?
Catheter-based renal denervation reduces BP in patients with resistant hypertension (BP uncontrolled on ≥3 medications). May be considered but not yet first-line.
122
What is the relationship between obstructive sleep apnea (OSA) and stroke?
OSA is an independent risk factor for stroke (OR 2-3). Treating OSA with CPAP may reduce stroke risk, though randomized trial data is limited. Screening for OSA is recommended in TIA/stroke patients.
123
What is the role of patent foramen ovale (PFO) closure in stroke prevention?
PFO closure is recommended for patients aged 18-60 with cryptogenic stroke (no other cause identified) and a high-risk PFO (large shunt, associated atrial septal aneurysm). Reduces recurrent stroke risk by approximately 50-60%.
124
What is the recommended workup for cryptogenic stroke (stroke of undetermined etiology)?
1) Prolonged cardiac monitoring (at least 14-30 days) to detect paroxysmal atrial fibrillation, 2) Echocardiography (TTE with bubble study or TEE to detect PFO), 3) Hypercoagulability workup (if age <50 or no vascular risk factors), 4) Aortic arch imaging (if suspected).
125
What is the annual risk of recurrent stroke after a first ischemic stroke?
Approximately 10-15% in the first year, then 3-5% per year thereafter. Optimal secondary prevention reduces this risk by 70-80%.
126
What is the modified Rankin Scale (mRS) used for?
A 7-point disability scale (0-6) used to measure functional outcomes after stroke. 0 = no symptoms, 1 = no significant disability, 2 = slight disability, 3 = moderate disability, 4 = moderately severe disability, 5 = severe disability, 6 = death.
127
What is the NIH Stroke Scale (NIHSS) range and interpretation?
0-42 points. 0 = no stroke, 1-4 = minor, 5-15 = moderate, 16-20 = moderate-severe, 21-42 = severe. Used to quantify stroke severity and predict outcomes.
128
What is the Barthel Index?
A 10-item scale measuring activities of daily living (ADLs) – feeding, bathing, grooming, dressing, bowel/bladder control, toileting, transfers, mobility, stairs. Scores 0-100 (higher = more independent).
129
What is post-stroke depression and how common is it?
Depression affects 30-50% of stroke survivors. It is associated with worse functional outcomes, higher mortality, and increased suicide risk. Screening and treatment (SSRIs) are recommended.
130
What is the role of SSRIs in post-stroke recovery?
SSRIs (especially fluoxetine and escitalopram) may improve motor recovery independent of their antidepressant effect, though recent trials (FOCUS, AFFINITY) showed mixed results. Not routinely recommended for motor recovery.
131
What is the risk of hemorrhagic transformation after ischemic stroke?
Occurs in 10-30% of ischemic strokes, most commonly within 24-48 hours. Higher risk with large infarcts, cardioembolic strokes, thrombolysis, and early anticoagulation. Usually asymptomatic; symptomatic hemorrhage occurs in 2-7%.
132
What is the management of anticoagulation-associated intracerebral hemorrhage?
1) Reverse anticoagulation immediately: warfarin – vitamin K + PCC (prothrombin complex concentrate) or FFP. DOACs – idarucizumab (dabigatran) or andexanet alfa (apixaban, rivaroxaban). 2) BP control. 3) Neurosurgical consultation.
133
What is the role of tranexamic acid in intracerebral hemorrhage?
Tranexamic acid (antifibrinolytic) reduces hematoma expansion but does NOT improve functional outcomes or mortality (TICH-2 trial). Not routinely recommended.
134
What is the future of stroke treatment?
1) Expanding thrombectomy window with advanced imaging (CT perfusion, MRI). 2) New thrombolytics (tenecteplase – easier to administer as single bolus, non-inferior to alteplase). 3) Neuroprotective agents (failed in trials so far). 4) Stem cell therapy and rehabilitation robotics.
Internal Medicine
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