Neuroanatomy Ch 10 392-413
Cerebral Hemispheres and Vascular Supply
Review of Main Functional Areas of Cerebral Cortex – face and hands of sensorimotor homunculi are
on lateral convexities, while leg areas are in the interhemispheric fissure
-in the dominant (usually left) hemisphere, Broca’s area is in the inferior frontal gyrus; Wernicke’s area is
in the superior temporal gyrus, next to primary auditory cortex
-Association cortex in the nondominant hemisphere (right) is important for attention to the
contralateral body and space
-primary visual hemifield lies along calcarine fissure of occipital lobe
-optic radiations, white matter pathways carrying visual information from thalamus to visual
cortex pass under parietal and temporal cortex
Circle of Willis: Anterior and Posterior Circulations – supply to cerebral hemispheres derived from:
1. Anterior Circulation: internal carotid arteries arising from common carotid from aorta; at
bifurcation of carotid, the common carotid splits into internal and external carotid
2. Posterior Circulation: vertebral arteries arise from subclavian arteries and ascends through
foramina in the transverse processes of cervical vertebrae before entering foramen magnum
and joining to form the basilar artery
-anterior and posterior circulations meet at the circle of Willis, from which all major cerebral vessels
arise, and provides major collateral flow
-main arteries supplying cerebral hemispheres are anterior cerebral arteries (ACAs), middle cerebral
arteries (MCAs), and posterior cerebral arteries
-the ACAs and MCAs are terminal branches of the internal carotid arteries
-the anterior cerebral arteries anastomose anteriorly at the anterior communicating artery
(Acomm)
-anterior and posterior circulations are linked to each other via posterior communicating
arteries (PComms), which connect internal carotids to the posterior cerebral arteries, joining
the anterior and posterior circulations
-the posterior cerebral arteries (PCAs) arise from top of the basilar artery, formed by
convergence of the two vertebral arteries
-internal carotid artery has several named segments
1. Cervical Segment – is found in the neck
2. Petrous Segment – as cervical segment sharply bends and enters temporal bone
3. Cavernous Segment – as internal carotid begins an S-shaped turn, also known as carotid
siphon within the cavernous sinus
4. Supraclinoid (intracranial Segment) – after cavernous segment, the artery passes anterior
clinoid process to pierce the dura and bends posteriorly to enter subarachnoid space as this
artery. There are several branches of this artery remembered by OPAAM
-Ophthalmic, Posterior communicating, Anterior choroidal, Anterior Cerebral, Middle cerebral
-ophthalmic artery branches just after internal carotid enters the dura
Anatomy of Vascular Territories of the Three Main Cerebral Arteries – the three main arteries ACA,
MCA, PCA give rise to many small branches that travel in subarachnoid space over brain and into sulci
Vascular Territories of Superficial Cerebral Structures –
1. Anterior Cerebral Artery – passes in the interhemispheric fissure as it sweeps around the corpus
callosum and branches into the pericallosal and callosomarginal arteries
2. Middle Cerebral Artery – turns laterally to enter depths of Sylvian fissure, where it bifurcates
into the superior division and the inferior division
a. Superior division supplies the cortex above Sylvian Fissure including lateral frontal lobe
b. Inferior division supplies cortex below Sylvian Fissure including lateral temporal lobe
and part of the parietal lobe
3. Posterior Cerebral Artery – curves back after arising from the top of the basilar and sends
branches over the inferior and medial temporal lobes and over the medial occipital cortex
a. Posterior cerebral artery territory includes inferior and medial temporal/occipital cortex
Vascular Territories of the Deep Cerebral Structures – most important penetrating vessels at the base
of the brain are the lenticulostriate arteries arising from the initial portions of the middle cerebral
artery before it enters the Sylvian fissure
-these arteries supply regions of basal ganglia and internal capsule
Clinical Syndromes of Three Cerebral Arteries: Infarcts
1. Left MCA Superior Division – R face and arm weakness of upper motor neuron type and Broca’s
aphasia
2. Left MCA Inferior Division – Wernicke’s aphasia and R visual field deficit, may seem crazy
3. Left MCA Deep Territory – R pure motor hemiparesis of upper motor neuron type
4. Left MCA stem – combination of above, w/ R hemiplegia, R hemianesthesia, R homonymous
hemianopia, and global aphasia; Often a LEFT GAZE PREFERENCE
5. Right MCA Superior Division – L face and arm weakness, L hemineglect is present
6. Right MCA Inferior Division – profound L hemineglect, L visual field and somatosensory deficits
present, motor neglect on the L side can also occur w/ mild L sided weakness
7. Right MCA Deep Territory – L pure motor hemiparesis of upper motor neuron type
8. Right MCA Stem – combination of above w/ L hemiplegia, L hemianesthesia, L homonymous
hemianopia, and profound L hemineglect; usually RIGHT GAZE PREFERENCE
9. Left ACA – R leg weakness and R leg sensory loss; can cause R hemiplegia if large
10. Right ACA – L leg weakness and L leg sensory loss; can cause L hemiplegia if large
11. Left PCA – R homonymous hemianopia, can cause alexia without agraphia; may cause aphasia
12. Right PCA – L homonymous hemianopia, large infarct in thalamus may cause L hemisensory loss
Watershed Infarcts – when cerebral artery is occluded, ischemia or infarction occurs in the territory
supplied by the vessel, with other regions near vessels spared
-when blood supply to two adjacent cerebral arteries is compromised, regions between the two vessels
are most susceptible to ischemia and infarction
-these regions between cerebral arteries are called watershed zones
-bilateral watershed infarcts can occur in both ACA-MCA and MCA-PCA zones with severe drops in
systemic blood pressure
-a sudden occlusion of internal carotid or a drop in BP in pt w/ carotid stenosis can = ACA-MCA infarct
-watershed infarcts can produce proximal arm/leg weakness because regions of homunculus involved
include trunk and proximal limbs
-in dominant hemisphere, watershed infarcts can cause transcortical aphasia syndromes
-MCA-PCA infarcts can cause disturbances of higher-order visual processing
-they can also occur between superficial and deep territories of MCA
Transient Ischemic Attack (TIA) – typically last for 10 MINUTES, if more than an hour, they are usually
small infarcts. 15% of patients with TIAs will have a stroke causing persistent deficits within 3 months,
and half of them will occur within first 48 hours; they are warning signs of potentially larger ischemic
injury to brain
-can be caused by embolus occluding vessel that dissolves to allow blood to return, in-situ thrombus
formation and/or vasospasm leading to narrowing of blood vessel lumen
Transient Loss of Consciousness – MOST COMMON CAUSE is cardiogenic syncope including vasovagal
transient episodes of hypotension, arrhythmias, and other non-neurological causes
Ischemic Stroke – occurs when inadequate blood supply to a region of the brain lasts long enough to
cause infarction
-in an embolic infarct – piece of material (usually blood clot) is formed in one place and travels through
bloodstream to lodge in and occlude a blood vessel supplying the brain (occur suddenly)
-in a thrombotic infarct – blood clot is formed locally on the blood vessel wall, usually at the site of an
underlying atherosclerotic plaque, causing the vessel to occlude (may have stuttering course)
-Large vessel infarcts – involve major blood vessels on the surface of brain such as the MCA + branches,
often caused by emboli, although thrombosis can occur in proximal vessels such as vertebral, basilar,
and carotid arteries
-Small vessel infarcts – involve small, penetrating vessels supplying deep structures, such as basal
ganglia, thalamus, and internal capsules
-small vessel infarcts are sometimes called lacunar infarcts because they resemble small lakes
Source of Emboli – emboli are most commonly composed of thrombotic (blood clot) material
-Cardioembolic infarcts occur in the heart, in conditions such as atrial fibrillation, MI and
valvular disease
-Artery-to-Artery emboli – arise from a stenosed segment of internal carotid artery, vertebral
stenosis, or an ectatic dilated basilar artery
-Dissection of carotid or vertebral arteries can cause thrombus formation
-emboli can also include air emboli, septic emboli, fat/cholesterol emboli, disc emboli, and amniotic
fluid emboli
Lacunar Syndromes –
Syndrome
Pure Motor Hemiparesis
Ataxic Hemiparesis
Pure Sensory Stroke
(thalamic lacune)
Clinical Features
Unilateral face, arm, and leg
weakness with dysarthria
Same as pure motor
hemiparesis, but with ataxia on
same side as weakness
Sensory loss to all primary
modalities in contralateral face
and body
Sensorimotor Stroke
(thalamocapsular lacune)
Combination of thalamic lacune
and pure motor hemiparesis
Basal Ganglia Lacune
Usually asymptomatic, but may
cause hemiballismus
Locations of Infarct
Posterior limb of internal capsule
Ventral Pons
Posterior limb of internal capsule
Ventral Pons
Ventral posterior lateral nucleus
of thalamus (VPL)
Posterior limb of internal
capsule, and either VPL or
thalamic somatosensory
radiation
Caudate, putamen, globus
pallidus, or subthalamic nucleus
Stroke Risk Factors – hypertension, diabetes, hypercholesterolemia, cigarette smoking, prior history of
vascular disease or stroke
-atrial fibrillation, mechanical valves or other valvular abnormalities, patent foramen ovale, and
decreased ejection fraction
-hypercoagulable states are also risk factors
Treatment and Diagnostic Workup of Ischemic Stroke and TIA
Acute Management – do a CT scan to quickly find an ischemic event; most often not seen in the first few
hours of symptoms, but a hemorrhage will always be visible
-if hemorrhage is ruled out by CT, patients can be treated with the thrombolytic agent tissue
plasminogen activator (tPA) with a good outcome if given within 4.5 hours of stroke onset, earlier the
better; tPA carries risk of intracranial hemorrhage
-if patients are not eligible for tPA or in patients who have had TIA, aspirin can reduce risk of recurrent
stroke
Diagnostic Evaluation – begins with history/physical exam, including questions about stroke risk factors
and continues with diagnostic tests
-blood flow in major cranial and neck vessels should be assessed with ultrasound or magnetic resonance
angiography or CT angiography; important in suspected internal carotid stenosis
-possibility of cardioembolic source should be investigated with ECG to look for cardiac ischemia or
arrhythmias, and an echocardiogram to look for structural abnormalities or thrombi
-studies have shown that patients with atrial fibrillation are at risk of embolic stroke and the risk is
reduced when treated with warfarin (Coumadin), an oral anticoagulant
Medium-to-Long Term Management – common complications include hemorrhagic conversion,
seizures, and delayed swelling. With large MCA infarcts, substantial edema and mass effect may
develop
-measures for lowering intracranial pressure include hemicraniectomy where a portion of skull is
removed over region of swelling and is later replaced after danger has passed
-Preventive measures are most important in reducing incidence of recurrent stroke
-risk factors such as hypertension, smoking, and hypercholesterolemia should be addressed
-medications such HMG-CoA reductase inhibitors (statins) should be addressed to reduce
cholesterol levels
-antiplatelet drugs like aspirin have been shown to reduce risk of ischemic stroke recurrence
Carotid Stenosis – atherosclerotic disease most commonly leads to stenosis of internal carotid artery
just beyond carotid bifurcation
-thrombi formed on a stenotic internal can embolize to form TIAs, or infarcts of MCA, ACA, or
ophthalmic artery
-can be associated with MCA territory symptoms such as contralateral face-arm, or face-arm-leg
weakness, contralateral sensory changes, contralateral visual field defects, aphasia, or neglect
-ophthalmic artery symptoms such as ipsilateral monocular visual loss is known as amaurosis fugax and
ACA territory symptoms such as contralateral leg weakness
-carotid stenosis can be detected on physical exam as a whooshing sound (bruit) that continues into
diastole and is best hear with the bell at engle of jaw
-symptomatic carotid stenosis – when patients have carotid stenosis along with transient monocular
blindness on same side or TIAs/strokes causing symptoms on contralateral side
-mainstay treatment for symptomatic carotid stenosis is carotid endarterectomy where the carotid is
exposed and clamped temporarily
-incision is made and the atheromatous material is shelled out, eliminating the stenosis
-in less severe carotid stenosis, angioplasty and stenting can be performed if patient is at high surgical
risk for traditional carotid endarterectomy
-if internal carotid becomes 100% occluded, it causes infarcts in the MCA, ACA, or watershed territories;
may be completely asymptomatic if there is adequate collateral flow through anterior/posterior
communicating arteries
-occurs most often just beyond carotid bifurcation
Dissection of the Carotid or Vertebral Arteries – a small tear can form in the intimal surface of carotid
or vertebral arteries, allowing blood to burrow into vessel wall, producing a dissection; a flap protrudes
into the vessel lumen where a thrombus can form and embolize distally
-patients may describe feeling a pop at the onset
-carotid dissection – may hear turbulent sound with each heartbeat and have ipsilateral horner’s
syndrome and pain over the eye
-vertebral dissection – most often posterior neck and occipital pain
-TIAs or infarcts occur in anterior circulation with carotid dissection and in posterior circulation with
vertebral dissection
-diagnosis is with MRI/MRA, or CTA of the neck to show vessel irregularity, narrowing, and sometimes
visualization of a false lumen in the vessel wall adjacent to the true lumen
-primarily treated with intravenous heparin followed by warfarin anticoagulation
Venous Drainage – superficial veins  superior sagittal sinus  cavernous sinus
More specifically:
Superior sagittal sinus  transverse sinuses  sigmoid sinus
Cavernous sinus  superior petrosal sinus  transverse sinus and inferior petrosal sinus  internal
jugular vein
-in the cavernous sinus, the internal carotid, and CN III, IV, V1, V2, and VI pass through
Sagittal Sinus Thrombosis – often associated with a hypercoagulable state and occurs with increased
frequency in pregnant women and within first few weeks post partum
-obstruction of venous drainage can cause elevated intracranial pressure, which can cause parasagittal
hemorrhages and/infarcts
-patients often have headaches and papilledema and a decreased level of consciousness
-Superior sagittal sinus can be seen as a triangular region on axial CT and MRI;
-sinus normally fills with intravenous contrast, but in sagittal sinus thrombosis there may be
central, darker-filled defect, called the empty delta sign
-magnetic resonance venography (MRV) should be performed or a conventional
angiogram
-treatment for sagittal sinus thrombosis can be anticoagulation therapy
-venous thrombosis can occur less commonly leading to infarcts or hemorrhage in territories of deep
cerebral veins or a major cortical vein