Neuro Chapter 10 (392-413)
Review of Main Functional Areas of Cerebral Cortex
Circle of Willis: Anterior and Posterior Circulations
 Arterial supply to cerebral hemispheres derived from anterior circulation (from internal carotid arteries) and
posterior circulation (from vertebral arteries)
o Vertebral arteries arise from subclavian arteries; join after passing through foramen magnum to form
basilar artery
 Complete full-caliber ring of Circle of Willis only present in 34% of people
 Main arteries supplying cerebral hemispheres are anterior, middle, and posterior cerebral arteries
o ACA and MCA are terminal branches of internal carotid
o Anterior communicating artery (AComm) connects anterior cerebral arteries
o Posterior communicating arteries (PComms) connect internal carotids to posterior cerebral arteries,
joining anterior and posterior circulations
o PCAs arise from top of basilar artery
o Several branches to brainstem and cerebellum arise from vertebrobasilar system
 Internal carotid artery has segments
o Relatively vertical cervical segment in neck
o Sharp horizontal bend as internal carotid enters temporal bone as petrous segment
o Cavernous segment as it begins S-shaped turn (carotid siphon) in cavernous sinus
o Enters subarachnoid space as supraclinoid (intracranial) segment
 Main branches of spraclinoid internal carotid artery are OPAAM (ophthalmic, PComm, anterior
choroidal, ACA, and MCA)
 Ophthalmic artery
enters optic
foramen with optic
nerve and provides
blood supply to
retina
Anatomy and Vascular Territories of the
Three Main Cerebral Arteries
 ACA, MCA, and PCA give rise to
branches that travel in
subarachnoid space over surface of
brain into sulci
o Small penetrating branches
arise and supply superficial
portions of brain (cortex
and white matter)


Deep structures of brain (such as basal ganglia, thalamus, and internal capsule) supplied by small, penetrating
branches that arise from initial segments of main cerebral arteries near circle of Willis at base of brain
Lenticulostriate arteries – small penetrating vessels that arise from initial portions of MCA before it enters
Sylvian fissure; penetrate anterior perforated substance to supply basal ganglia and internal capsule
o In hypertension, these arteries particularly prone to narrowing, leading to lacunar infarction as well as
rupture, causing intracerebral hemorrhage
 Anterior choroidal artery arises from internal carotid artery; supplies globus pallidus, putamen, thalamus, and
posterior limb of internal capsule, extending up to
lateral ventricle
o Posterior limb of internal capsule contains
important motor pathways through
corticobulbar and corticospinal tracts
o Lacunar infarction in either lenticulostriate or
anterior choroidal territories often causes
contralateral hemiparesis
 Recurrent artery of Heubner supplies portions of
head of caudate, anterior putamen, globus pallidus,
and internal capsule
 Small, penetrating arteries that arise from proximal
PCAs near top of basilar artery include
thalamoperforator arteries (supply thalamus and
sometimes extend to portion of posterior limb of
internal capsule), thalamogeniculate, and posterior
choroidal arteries; small penetrating vessels from top
of basilar artery supply midbrain
Clinical Syndromes of the Three Cerebral Arteries
 MCA – ischemic events and infarcts more common here than PCA or ACA because of relatively large territory
supplied by MCA; occur in superior division, inferior division, or deep territory
o Proximal MCA occlusions affecting all 3 regions called MCA stem infarcts
o
o
Large MCA territory infarcts often have gaze preference toward side of lesion, especially in acute period
Small deep infarcts involving penetrating branches of MCA or other vessels called lacunes

ACA infarcts typically produce UMN-type weakness and cortical-type sensory loss affecting contralateral leg
more than arm or face
o Larger ACA strokes may cause contralateral hemiplegia
o Dominant ACA strokes sometimes associated with transcortical motor aphasia
o Nondominant ACA strokes can produce contralateral neglect
o May include grasp reflex, impaired judgment, flat affect, apraxia, abulia, and incontinence
o Damage to supplementary motor area and other regions in frontal lobe leads to alien hand syndrome
(semiautomatic movements of contralateral arm that aren’t under voluntary control)
 PCA infarcts typically cause contralateral homonymous hemianopia
o Sometimes small penetrating vessels that come off proximal PCA involved, leading to infarcts in
thalamus or posterior limb of internal capsule
o Result in contralateral sensory loss, contralateral hemiparesis, or thalamic aphasia if infarct is in
dominant hemisphere
o Infarcts involving left occipital cortex and splenium of corpus callosum can produce alexia w/o agraphia
Watershed Infarcts
 When blood supply to 2 adjacent cerebral arteries compromised, regions between the vessels most susceptible
to ischemia and infarction; region between the arteries is watershed zone
 Bilateral watershed infarcts in both ACA-MCA and MCA-PCA watershed zones can occur with severe drops in
systemic BP
 Sudden occlusion of internal carotid artery or drop in BP in patient with carotid stenosis can cause ACA-MCA
watershed infarct since MCA and ACA both fed by carotid
 Watershed infarcts can produce proximal arm and leg weakness (man in barrel syndrome) because regions of
homunculus involved often include trunk and proximal limbs
 In dominant hemisphere, watershed infarcts can cause transcortical aphasia syndromes
 MCA-PCA watershed infarcts can cause disturbances of higher-order visual processing
 Watershed infarcts can occasionally occur between superficial and deep territories of MCA
Transient Ischemic Attack and Other Transient Neurologic Episodes
 Most common causes are transient ischemic attack, migraine, seizures, and other non-neurologic conditions
such as cardiac arrhythmia or hypoglycemia
 Transient ischemic attack (TIA) – neurologic deficit lasting less than 24 hours caused by temporary brain
ischemia; more typical duration of TIA is ~10 minutes
o TIAs lasting more than an hour usually small infarcts
o Complete functional recovery can sometimes occur within a day
o Warning sign for potentially larger ischemic injury to brain
 TIAs are neurologic emergency like acute coronary disease; many patients have stroke in next few days-months
 Episodes of hypoglycemia can sometimes produce transient focal neurologic deficits, especially in elderly
 Transient loss of consciousness w/o other focal features is special case of transient neurologic dysfunction; most
common cause is cardiogenic syncope
Mechanisms of Ischemic Stroke

Stroke refers to both hemorrhagic events and ischemic infarction of brain; sometimes ischemic strokes can
cause blood vessels to become fragile and rupture (hemorrhagic conversion)
 Embolic infarct – piece of material (usually blood clot) formed in one place and travels through bloodstream to
suddenly lodge in and occlude blood vessel supplying brain; occur suddenly with max deficits at onset
 Thrombotic infarct – blood clot formed locally on blood vessel wall, usually at site of underlying atherosclerotic
plaque, causing vessel to occlude; more stuttering course
 Large-vessel infarcts involve major blood vessels on surface of brain (MCA and main branches); most often
caused by emboli; thrombosis can occasionally occur in large proximal vessels (vertebral, basilar, and carotid)
 Small-vessel infarcts involve small, penetrating vessels that supply deep structures (basal ganglia, thalamus, and
internal capsule); affects medial portions of midbrain, pons, and medulla
o Also called lacunar infarcts
 Cardioembolic infarcts – embolus originates in heart; occurs in
o A fib when thrombi form on fibrillating left atrial appendage
o MI have thrombi form on hypokinetic or akinetic regions of infarcted myocardium
o Valvular disease or mechanical prostheses, where thrombi form on valve leaflets or prosthetic parts
 Artery-to-artery emboli can also occur; emboli arising from stenosed segment of internal carotid, vertebral
stenosis, or ectatic dilated basilar artery
 Dissection of carotid or vertebral arteries often results in thrombus formation, which can embolize to brain
 Atherosclerotic disease of aortic arch potential source of artery-to-artery thromboembolus
 Occasionally PFO can allow thromboembolus formed in venous system to bypass lungs and reach brain
 Can occur with air emboli, septic emboli, fat or cholesterol emboli (fracture of long bones), amniotic fluid emboli
 Lacunar infarcts usually associated with small-vessel disease caused by chronic hypertension; small penetrating
vessels can be occluded by atherosclerotic disease, in situ thrombosis, small emboli, or hypertension-related
changes in vessel wall (lipohyalinosis)
o Thalamic lacunes can cause contralateral somatosensory deficits, maybe with thalamic pain syndrome
o Basal ganglia lacunes can cause movement disorders such as hemiballismus
 Cortical vs. subcortical lesions can be differentiated based on cortical signs (aphasia, neglect, homonymous
visual field defects, and cortical sensory loss)
o Deficits can be seen in some cases of subcortical lesions as well
o Presence of typical lacunar syndrome, like pure motor hemiparaesis, implies subcortical lesion present
 Ischemic stroke can be associated with headache or less commonly seizures
o When headache unilateral, more commonly on side of infarct
o More common for posterior than anterior circulation infarcts
o Headaches or neck pain often seen in dissection of carotid or vertebral arteries
Stroke Risk Factors
 Hypertension, diabetes, hypercholesterolemia, cigarette smoking, family history, or prior history of stroke or
other vascular disease; A fib, mechanical valves or other valvular abnormalities, PFO, and severely decreased
ejection fraction
 Medical conditions that affect coagulation pathways or work through other mechanisms to increase thrombus
 Relatively uncommon in young individuals because cumulative effects of major stroke risk factors tend to
worsen with age; when stroke occurs in young patient, consider arterial dissection, PFO, or other such
Treatment and Diagnostic Workup of Ischemic Stroke and TIA
 Do a CT if you suspect possible ischemic event; infarct won’t be visible on initial CT, but hemorrhage would be
 Coag studies should be run, especially if young individual with no known vascular risk factors
 Once hemorrhage ruled out, patient might be eligible for tPA (benefit if given within 4.5 hours of onset)
o If they can’t have tPA, go for aspirin (not heparin)
 Patients should be given IV fluids to correct hydration status, maintain cerebral perfusion, and prevent
hypotension; hyperglycemia or hypoglycemia could worsen infarction
 Blood flow in major cranial and neck vessels should be assessed with Doppler ultrasound and/or MRA or CTA
 Possibility of cardioembolic source should be investigated with EKG and echocardiogram
o Patients with A fib at increased risk of embolic stroke; significantly reduced when treated with warfarin
 Check cardiac enzymes for MI

In patients with large MCA infarcts, substantial edema and mass effect may develop over first 3-4 days
o Hemicraniectomy – portion of skull temporarily removed over region of swelling and later replaced after
danger of herniation has passed
Carotid Stenosis
 Atherosclerotic disease commonly leads to stenosis of internal carotid just beyond carotid bifurcation
 Often associated with MCA territory symptoms (contralateral face-arm or face-arm-leg weakness, contralateral
sensory changes, contralateral visual field defects, aphasia, or neglect); may be ACA symptoms
 May be ophthalmic artery symptoms such as ipsilateral monocular visual loss (amaurosis fugax)
 Patients who have carotid stenosis along with transient monocular blindness on same side, or TIAs or strokes
causing symptoms on contralateral side, considered to have symptomatic carotid stenosis
 Carotid endarterectomy – carotid artery temporarily clamped; longitudinal incision made and atheromatous
material removed, eliminating stenosis; reduces rate of stroke on that side
 Carotid occlusion may be asymptomatic if adequate collateral flow via AComm or PComm
Dissection of Carotid or Vertebral Arteries
 Small tear forms on intimal surface of carotid or vertebral arteries; may allow blood to burrow into vessel,
producing dissection; flap protrudes into vessel lumen, under which thrombus forms that can embolize distally
 Carotid dissection – may hear turbulent sound with each heartbeat and have ipsilateral Horner’s syndrome or
pain over the eye
 Vertebral dissection – posterior neck and occipital pain
 Most often treated with IV heparin anticoagulation followed by oral warfarin anticoagulation
Venous Drainage of the Cerebral Hemispheres
 Superficial veins drain mainly into superior sagittal sinus and cavernous sinus
 Deep veins drain into great vein of Galen
 Ultimately nearly all venous drainage for brain reaches internal jugular veins
Sagittal Sinus Thrombosis
 Often associated with hypercoagulable state; occurs with increased frequency in pregnant women and in first
few weeks postpartum
 Obstruction of venous drainage usually causes elevated intracranial pressure; back pressure in cortical veins can
cause parasagittal hemorrhages
 Increased venous pressure can decrease cerebral perfusion, leading to infarcts
 Seizures common; patients have headaches and papilledema, may have depressed LOC
 In sagittal sinus thrombosis, may be central, darker-filling defect (empty delta sign)
 Increased density of sagittal sinus on CT due to coagulated blood or increased T1 signal on MRI
 In suspected sagittal sinus thrombosis, do MRV or conventional angiogram to confirm
 Venous thrombosis can occur less commonly in other intracranial venous sinuses, deep cerebral veins, etc.