Stroke pathophysiology, from vessel to deficit

A tumor's edema does not produce a matched core and penumbra pattern around a vascular occlusion.

Bleeding is seen on noncontrast CT as a bright area; perfusion maps show blood flow and volume, not blood products.

The core is the central area where both flow and blood volume have collapsed; the rim with preserved volume is not yet lost.

Reduced flow with preserved blood volume means vessels are still dilating to compensate, so the tissue is at risk but alive and can be saved if the artery reopens.

The right PCA supplies the right occipital cortex, which processes the left visual field of both eyes, so the left half of vision is lost in each eye.

Leg-predominant weakness is the pattern of an anterior cerebral artery stroke, which supplies the medial motor strip.

Loss of both outer fields comes from a lesion at the optic chiasm, typically a pituitary tumor, not a PCA stroke.

This puts the field cut on the side of the lesion; visual pathways behind the chiasm represent the opposite field.

Smooth muscle controls arterioles and larger vessels; true capillaries lack a smooth muscle layer.

Astrocytes support neurons and the blood-brain barrier with their end-feet, but they are not contractile cells inside the capillary basement membrane.

Pericytes wrap capillaries inside the basement membrane and can contract and die in rigor after ischemia, which narrows capillaries and limits reflow even after the large artery is opened.

Endothelial cells line the capillary and form the barrier; the contractile cells sit outside them in the basement membrane.

SAH starts with a sudden, maximal headache, not one that worsens over 4 days, and papilledema is not its usual early sign.

The postpartum state is prothrombotic, and a headache that builds over days with papilledema and a seizure is the classic picture of a clot in the venous sinuses.

IIH also causes headache and papilledema, but it is a diagnosis of exclusion that does not cause seizures, and venous thrombosis must be ruled out first in a postpartum patient.

Migraine does not cause papilledema, and a new seizure after delivery calls for a structural cause to be excluded.

Basilar occlusion brings cranial nerve signs, reduced consciousness or quadriplegia including the hands, not this proximal pattern.

Pontine lacunes cause pure motor weakness of the face, arm and leg together, without sparing of the face and hands.

Prolonged low perfusion pressure injures the areas at the far ends of two arterial territories; the ACA-MCA border zone holds the shoulder and hip representation, giving a man-in-a-barrel pattern.

Emboli lodge in random branches and produce patchy deficits, not a symmetric proximal weakness that follows hypotension.

A left occipital infarct blinds the left visual cortex and the splenial damage cuts the right cortex off from the language areas, so the patient can write but cannot read, even their own writing.

Wernicke aphasia impairs comprehension of speech and produces fluent, empty language; this patient writes meaningful sentences.

This reverses the deficit; the patient here can write but cannot read.

Global aphasia leaves the patient unable to speak, understand, read or write, which does not fit someone who writes normally.

Sudden painless loss in one eye suggests retinal ischemia (amaurosis fugax), a carotid warning sign rather than aura.

Sudden loss of vision, strength or sensation is the signature of ischemia, so this feature argues for a TIA, not migraine.

A deficit that is complete from the first moment points to a vascular event; aura evolves.

Migraine aura usually brings positive phenomena such as flashing or zigzag lights that march across the field over several minutes; ischemia removes function.

Glutamate excitotoxicity is an acute cellular injury mechanism in the ischemic zone, not a rehabilitation concept.

The right hemisphere may support some language recovery, but this model concerns motor inhibition, not transfer of language.

The problem is the reverse: the intact hemisphere sends too much inhibition across the midline, not too little.

In this model the intact hemisphere becomes overactive and sends excess inhibition across the corpus callosum, which suppresses the damaged side; forced use of the weak limb counters it.

Delirium fluctuates and impairs attention and awareness; abulia is a stable lack of initiation in an attentive patient.

Abulia is a loss of will and initiative from frontal (often bilateral ACA) damage; patients can act when prompted but rarely start anything on their own.

In Broca aphasia the patient wants to speak but struggles to form words; abulic patients have intact language but little drive to use it.

Depression includes sad mood, guilt or hopelessness; abulia can look similar but is a lack of initiation without low mood.

A clot at the basilar tip damages the midbrain and thalami, causing somnolence, vertical gaze palsy, pupil changes and visual hallucinations, often with little limb weakness.

Wallenberg syndrome causes vertigo, crossed sensory loss, hoarseness and Horner syndrome with normal alertness.

Bilateral ACA strokes cause leg weakness and urinary incontinence, not gaze palsy and hallucinations.

Locked-in syndrome from a ventral pontine infarct leaves the patient awake but quadriplegic with only vertical eye movement preserved, the opposite of this picture.

A wedge-shaped cortical infarct reflects a branch occlusion, typically embolic, and would usually add cortical signs.

Old white matter change marks chronic small-vessel disease but does not show the new infarct causing the current deficit.

Pure motor hemiparesis is a classic lacunar syndrome, and one small deep infarct in the internal capsule or pons from a penetrating artery confirms it.

Scattered lesions in several territories point to an embolic source such as the heart, not small-vessel disease.

An AVM can bleed into the subarachnoid space, but it more often causes a parenchymal hemorrhage and accounts for a small share of SAH.

Amyloid angiopathy causes lobar hemorrhage in older adults and sometimes small convexity SAH, not the classic aneurysmal pattern.

A thunderclap headache with exertion is typical of nontraumatic subarachnoid hemorrhage, and about 85% of these come from a ruptured saccular (berry) aneurysm.

Lipohyalinosis of penetrating arteries causes deep intracerebral hemorrhage and lacunes, not subarachnoid bleeding.

Bilateral parieto-occipital damage causes the triad of simultanagnosia, optic ataxia and ocular apraxia, which is Balint syndrome.

Gerstmann syndrome from a dominant angular gyrus lesion causes agraphia, acalculia, finger agnosia and left-right confusion.

Weber syndrome is a midbrain stroke with an ipsilateral third-nerve palsy and contralateral hemiparesis.

Anton syndrome is cortical blindness with denial of the blindness, from bilateral occipital infarcts; these patients see but cannot integrate a scene.

Cerebellar hemorrhage causes ataxia, vomiting and headache rather than hemiparesis, and the vermis is a less common hypertensive site.

A lobar cortical bleed in an older adult suggests amyloid angiopathy rather than hypertension.

The right putamen is a typical hypertensive site, but a right-sided bleed would weaken the left side.

Chronic hypertension damages small penetrating arteries, and the putamen is the most common site of hypertensive hemorrhage; a left-sided bleed causes right hemiparesis.

Isolated nonfluent aphasia comes from a cortical branch of the dominant MCA, not a deep artery to the internal capsule.

The anterior choroidal artery supplies the posterior limb of the internal capsule and the optic tract region, so its occlusion causes weakness, sensory loss and a visual field cut on the opposite side.

Leg-predominant weakness with incontinence points to the anterior cerebral artery, which supplies the medial frontal lobe.

Crossed pain loss with the face on the side of the lesion is the lateral medullary pattern of a vertebral or PICA occlusion.