# 07 - 437 Introduction to Cerebrovascular Diseases

### 437 Introduction to Cerebrovascular Diseases

SPECIAL ISSUES RELATED TO EPILEPSY IN 
THE ELDERLY
Epilepsy has a bimodal distribution according to age, with the highest 
incidence in the very young and in the elderly. The increased incidence 
in the elderly may be attributed to age- and aging-related epileptogenic 
factors. The most common cause is stroke, followed by neoplasm, and 
dementia, resulting in a preponderance of extratemporal epilepsy. 
Antiseizure medication selection requires careful consideration of 
medical and psychiatric comorbidities, side effect profiles, effects on 
mood and cognition, and drug-drug interactions.

■
■FURTHER READING
Bui E: Women’s issues in epilepsy. Continuum (Minneap Minn) 
28:399, 2022.
Cornes SB, Shih T: Evaluation of the patient with spells. Continuum 
(Minneap Minn) 17:984, 2011.
Crepeau AZ, Sirven JI: Management of adult onset seizures. Mayo 
Clin Proc 92:306, 2017.
Ellis CA et al: Epilepsy genetics: Clinical impacts and biological 
PART 13
Neurologic Disorders
insights. Lancet Neurol 19:93, 2020.
Fisher RS et al: Operational classification of seizure types by the Inter­
national League Against Epilepsy: Position paper of the ILAE Com­
mission for Classification and Terminology. Epilepsia 58:522, 2017.
Gavvala JR, Schuele SU: New-onset seizure in adults and adoles­
cents: A review. JAMA 316:2657, 2016.
jetté N et al: Surgical treatment for epilepsy: The potential gap 
between evidence and practice. Lancet Neurol 15:982, 2016.
Kanner AM: Management of psychiatric and neurological comorbidi­
ties in epilepsy. Nat Rev Neurol 12:106, 2016.
Krumholz A et al: Evidence-based guideline: Management of an 
unprovoked first seizure in adults: Report of the Guideline Develop­
ment Subcommittee of the American Academy of Neurology and the 
American Epilepsy Society. Neurology 84:1705, 2015.
Kwan P, Brodie MJ: Early identification of refractory epilepsy. N Engl 
J Med 342:314, 2000.
Markert MS, Fisher RS: Neuromodulation: Science and practice in 
epilepsy: Vagus nerve simulation, thalamic deep brain stimulation, 
and responsive neurostimulation. Expert Rev Neurother 19:17, 2019.
Rao VR et al: Cues for seizure timing. Epilepsia 62:S15, 2021.
Sen A et al: Epilepsy in older people. Lancet 395:735, 2020.
Wade S. Smith, J. Claude Hemphill, III

Introduction to 

Cerebrovascular Diseases
Cerebrovascular diseases include some of the most common and devas­
tating disorders: ischemic stroke and hemorrhagic stroke. Stroke is the 
second leading cause of death worldwide, with 7.1 million dying from 
stroke in 2020. Nearly 7 million Americans age 20 or older report having 
had a stroke, and the prevalence is estimated to rise by 3.4 million adults in 
the next decade, representing 4% of the entire adult population. Although 
mortality is increased from 6.2 million in 2010, the age standardized death 
rate has fallen by 15% in this decade, likely due to better prevention and 
treatment. However, overall disease burden will continue to climb as the 
population ages, and stroke is likely to remain the second most common 
disabling condition in individuals aged 50 or older worldwide.
A stroke, or cerebrovascular accident, is defined as an abrupt onset 
of a neurologic deficit that is attributable to a vascular cause. Thus, the 
definition of stroke is clinical, and laboratory studies including brain 
imaging are used to support the diagnosis. The clinical manifestations 
of stroke are highly variable because of the complex anatomy of the 

brain and its vasculature. Cerebral ischemia is caused by a reduction 
in blood flow that lasts longer than several seconds. Neurologic symp­
toms are manifest within seconds because neurons lack glycogen, so 
energy failure is rapid. If the cessation of flow lasts for more than a few 
minutes, infarction or death of brain tissue results. When blood flow is 
quickly restored, brain tissue can recover fully and the patient’s symp­
toms are only transient: this is called a transient ischemic attack (TIA). 
The definition of TIA requires that all neurologic signs and symptoms 
resolve within 24 h without evidence of brain infarction on brain 
imaging. Stroke has occurred if the neurologic signs and symptoms 
last for >24 h or brain infarction is demonstrated. A generalized reduc­
tion in cerebral blood flow due to systemic hypotension (e.g., cardiac 
arrhythmia, sepsis, or hemorrhagic shock) usually produces syncope 
(Chap. 23). If low cerebral blood flow persists for a longer duration, 
then infarction in the border zones between the major cerebral artery 
distributions may develop. In more severe instances as in cardiac arrest, 
global hypoxia-ischemia causes widespread brain injury; the constel­
lation of cognitive sequelae that ensues is called hypoxic-ischemic 
encephalopathy (Chap. 318). Focal ischemia or infarction, conversely, is 
usually caused by thrombosis of the cerebral vessels themselves or by 
emboli from a proximal arterial source or the heart (Chap. 438). Intra­
cranial hemorrhage is caused by bleeding directly into or around the 
brain; it produces neurologic symptoms by producing a mass effect on 
neural structures, from the toxic effects of blood itself, or by increasing 
intracranial pressure (Chap. 439).
APPROACH TO THE PATIENT
Cerebrovascular Disease
Rapid evaluation is essential for use of acute treatments such as 
thrombolysis or thrombectomy. However, patients with acute stroke 
often do not seek medical assistance on their own because they may 
lose the appreciation that something is wrong (anosognosia) or lack 
the knowledge that acute treatment is beneficial; it is often a fam­
ily member or a bystander who calls for help. Therefore, patients 
and their family members should be counseled to call emergency 
medical services immediately if they experience or witness the 
sudden onset of any of the following: loss of sensory and/or motor 
function on one side of the body (nearly 85% of ischemic stroke 
patients have hemiparesis); change in vision, gait, or ability to speak 
or understand; or a sudden, severe headache. The acronym FAST 
(facial weakness, arm weakness, speech abnormality, and time) is 
simple and helpful to teach to the lay public about the common 
physical symptoms of stroke and to underscore that treatments are 
highly time sensitive.
Other causes of sudden-onset neurologic symptoms that may 
mimic stroke include seizure, intracranial tumor, migraine, and 
metabolic encephalopathy. An adequate history from an observer 
that no convulsive activity occurred at the onset usually excludes 
seizure (Chap. 436), although ongoing complex partial seizures 
without tonic-clonic activity can on occasion mimic stroke. Tumors 
(Chap. 95) may present with acute neurologic symptoms due 
to hemorrhage, seizure, or hydrocephalus. Surprisingly, migraine 
(Chap. 441) can mimic stroke, even in patients without a sig­
nificant migraine history. When migraine develops without head 
pain (acephalgic migraine), the diagnosis can be especially dif­
ficult. Patients without any prior history of migraine may develop 
acephalgic migraine even after age 65. A sensory disturbance is 
often prominent, and the sensory deficit, as well as any motor defi­
cits, tends to migrate slowly across a limb, over minutes rather than 
seconds as with stroke. The diagnosis of migraine becomes more 
secure as the cortical disturbance begins to cross vascular bound­
aries or if classic visual symptoms are present such as scintillating 
scotomata. At times, it may be impossible to make the diagnosis of 
migraine until there have been multiple episodes with no residual 
symptoms or signs and no changes on brain magnetic resonance 
imaging (MRI). Metabolic encephalopathies typically produce fluc­
tuating mental status changes without focal neurologic findings. 
However, in the setting of prior stroke or brain injury, a patient with

Stroke or TIA
ABCs, glucose
Obtain brain
imaging
Ischemic stroke/
TIA, 85%
Hemorrhage
15%
Consider BP
lowering
Consider thrombolysis/
thrombectomy
Establish cause
Establish cause
Atrial
fibrillation,
17%
Carotid
disease,
4%
Aneurysmal
SAH, 4%
Hypertensive
ICH, 7%
Other,
64%
Other,
4%
Consider
oral
anticoagulant
Consider
CEA or
stent
Treat 
specific
cause
Consider
surgery
Clip or coil
(Chap. 440)
Deep venous thrombosis prophylaxis
Physical, occupational, speech therapy
Evaluate for rehab, discharge planning
Secondary prevention based on disease
FIGURE 437-1  Medical management of stroke and TIA. Rounded boxes are diagnoses; 
rectangles are interventions. Numbers are percentages of stroke overall. ABCs, airway, 
breathing, circulation; BP, blood pressure; CEA, carotid endarterectomy; ICH, intracerebral 
hemorrhage; SAH, subarachnoid hemorrhage; TIA, transient ischemic attack.
fever or sepsis may manifest a recurrent hemiparesis, which clears 
rapidly when the infection is treated. The metabolic process serves 
to “unmask” a prior deficit and is termed “stroke recrudescence.”
Once the diagnosis of stroke is made, a brain imaging study is 
necessary to determine if the cause of stroke is ischemia or hemor­
rhage (Fig. 437-1). Computed tomography (CT) imaging of the 
brain is the standard imaging modality to detect the presence or 
absence of intracranial hemorrhage (see “Imaging Studies,” below). 
If the stroke is ischemic, administration of recombinant tissue plas­
minogen activator (rtPA) or endovascular mechanical thrombec­
tomy may be beneficial in restoring cerebral perfusion (Chap. 438). 
Medical management to reduce the risk of complications becomes 
the next priority, followed by plans for secondary prevention. For 
ischemic stroke, several strategies can reduce the risk of subsequent 
stroke in all patients, while other strategies are effective for patients 
with specific causes of stroke such as cardiac embolus and carotid 
atherosclerosis. For hemorrhagic stroke, aneurysmal subarachnoid 
hemorrhage (SAH) and hypertensive intracerebral hemorrhage are 
two important causes. The treatment and prevention of hyperten­
sive intracerebral hemorrhage are discussed in Chap. 439. SAH 
is discussed in Chap. 440.
■
■STROKE SYNDROMES
A careful history and neurologic examination can often localize the 
region of brain dysfunction; if this region corresponds to an arterial 
distribution, the possible causes responsible for the syndrome can be 
narrowed. This is of particular importance when the patient presents 
with a TIA and a normal examination. For example, if a patient devel­
ops language loss and a right homonymous hemianopia, a search for 
causes of left middle cerebral emboli should be performed. A finding 
of an isolated stenosis of the right internal carotid artery in that patient, 
for example, suggests an asymptomatic carotid stenosis, and the search 
for other causes of stroke should continue. The following sections 
describe the clinical findings of cerebral ischemia associated with cere­
bral vascular territories depicted in Figs. 437-2 through 437-11. Stroke 
syndromes are divided into (1) large-vessel stroke within the anterior 

circulation, (2) large-vessel stroke within the posterior circulation, and 
(3) small-vessel disease of either vascular bed.
Stroke within the Anterior Circulation 
The internal carotid 
artery and its branches compose the anterior circulation of the brain. 
These vessels can be occluded by intrinsic disease of the vessel (e.g., 
atherosclerosis or dissection) or by embolic occlusion from a proximal 
source as discussed above. Occlusion of each major intracranial vessel 
has distinct clinical manifestations.

MIDDLE CEREBRAL ARTERY  Occlusion of the proximal middle cere­
bral artery (MCA) or one of its major branches is most often due to an 
embolus (artery-to-artery, cardiac, or of unknown source) rather than 
intracranial atherothrombosis. Atherosclerosis of the proximal MCA 
may cause distal emboli to the middle cerebral territory or, less com­
monly, may produce low-flow TIAs. Collateral formation via leptomen­
ingeal vessels often prevents MCA stenosis from becoming symptomatic.
The cortical branches of the MCA supply the lateral surface of 
the hemisphere except for (1) the frontal pole and a strip along the 
superomedial border of the frontal and parietal lobes supplied by 
the anterior cerebral artery (ACA) and (2) the lower temporal and 
occipital pole convolutions supplied by the posterior cerebral artery 
(PCA) (Figs. 437-2–437-5).
CHAPTER 437
Treat
specific
cause
The proximal MCA (M1 segment) gives rise to penetrating branches 
(termed lenticulostriate arteries) that supply the putamen, outer globus 
pallidus, posterior limb of the internal capsule, adjacent corona radiata, 
and most of the caudate nucleus (Fig. 437-2). In the sylvian fissure, the 
MCA in most patients divides into superior and inferior divisions (M2 
branches). Branches of the inferior division supply the inferior parietal 
and temporal cortex, and those from the superior division supply the 
frontal and superior parietal cortex (Fig. 437-3).
Introduction to Cerebrovascular Diseases 
If the entire MCA is occluded at its origin (blocking both its pen­
etrating and cortical branches) and the distal collaterals are limited, 
the clinical findings are contralateral hemiplegia, hemianesthesia, 
homonymous hemianopia, and a day or two of gaze preference to 
the ipsilateral side. Dysarthria is common because of facial weakness. 
When the dominant hemisphere is involved, global aphasia is present 
also, and when the nondominant hemisphere is affected, anosognosia, 
constructional apraxia, and neglect are found (Chap. 32).
Complete MCA syndromes occur most often when an embolus 
occludes the stem of the artery. Cortical collateral blood flow and differ­
ing arterial configurations are probably responsible for the development 
of many partial syndromes. Partial syndromes may also be due to emboli 
that enter the proximal MCA without complete occlusion, occlude distal 
MCA branches, or fragment and move distally.
Partial syndromes due to embolic occlusion of a single branch include 
hand, or arm and hand, weakness alone (brachial syndrome) or facial 
weakness with nonfluent (Broca) aphasia (Chap. 32), with or without 
arm weakness (frontal opercular syndrome). A combination of sensory 
disturbance, motor weakness, and nonfluent aphasia suggests that an 
embolus has occluded the proximal superior division and infarcted 
large portions of the frontal and parietal cortices (Fig. 437-3). If a fluent 
(Wernicke’s) aphasia occurs without weakness, the inferior division of 
the MCA supplying the posterior part (temporal cortex) of the domi­
nant hemisphere is probably involved. Jargon speech and an inability to 
comprehend written and spoken language are prominent features, often 
accompanied by a contralateral, homonymous superior quadrantanopia. 
Hemineglect or spatial agnosia without weakness indicates that the infe­
rior division of the MCA in the nondominant hemisphere is involved.
Occlusion of a lenticulostriate vessel produces small-vessel (lacu­
nar) stroke within the internal capsule (Fig. 437-2). This produces 
pure motor stroke or sensory-motor stroke contralateral to the lesion. 
Ischemia within the genu of the internal capsule causes primarily facial 
weakness followed by arm and then leg weakness as the ischemia 
moves posterior within the capsule. Alternatively, the contralateral 
hand may become ataxic, and dysarthria will be prominent (clumsy 
hand, dysarthria lacunar syndrome). Lacunar infarction affecting the 
globus pallidus and putamen often has few clinical signs, but parkin­
sonism and hemiballismus have been reported.
ANTERIOR CEREBRAL ARTERY  The ACA is divided into two seg­
ments: the precommunal (A1) circle of Willis, or stem, which connects

Internal 
capsule
Claustrum
Caudate
Middle cerebral
a. (M2)
Anterior
cerebral a. (A2)
Putamen
Lenticulostriate as.
Anterior
cerebral a. (A1)
Uncus
Internal carotid a.
Middle cerebral a. (M1)
PART 13
Neurologic Disorders
KEY
Ant. cerebral a.
Middle cerebral a.
Deep branches of middle cerebral a.
Post cerebral a.
Deep branches of ant. cerebral a.
FIGURE 437-2  Diagram of a cerebral hemisphere in coronal section showing the 
territories of the major cerebral vessels that branch from the internal carotid arteries.
Ant. parietal a.
Rolandic a.
Prerolandic a.
Lateral 
orbitofrontal a.
Sup. division
middle cerebral a.
Temporopolar a.
Inf. division
middle cerebral a.
Ant. temporal a.
KEY
Broca’s area
Sensory cortex
Auditory area
Contraversive
eye center
Wernicke’s
aphasia area
Visual cortex
FIGURE 437-3  Diagram of a cerebral hemisphere, lateral aspect, showing the branches and distribution of the middle cerebral artery (MCA) and the principal regions of 
cerebral localization. Note the bifurcation of the MCA into a superior and inferior division.
Signs and symptoms: Structures involved 
Paralysis of the contralateral face, arm, and leg; sensory impairment over the same area (pinprick, cotton touch, vibration, position, two-point discrimination, stereog­
nosis, tactile localization, barognosis, cutaneographia): Somatic motor area for face and arm and the fibers descending from the leg area to enter the corona radiata 
and corresponding somatic sensory system 
Motor aphasia: Motor speech area of the dominant hemisphere 
Central aphasia, word deafness, anomia, jargon speech, sensory agraphia, acalculia, alexia, finger agnosia, right-left confusion (the last four comprise the Gerstmann 
syndrome): Central, suprasylvian speech area and parietooccipital cortex of the dominant hemisphere 
Conduction aphasia: Central speech area (parietal operculum) 
Apractagnosia of the nondominant hemisphere, anosognosia, hemiasomatognosia, unilateral neglect, agnosia for the left half of external space, dressing “apraxia,” 
constructional “apraxia,” distortion of visual coordinates, inaccurate localization in the half field, impaired ability to judge distance, upside-down reading, visual illu­
sions (e.g., it may appear that another person walks through a table): Nondominant parietal lobe (area corresponding to speech area in dominant hemisphere); loss of 
topographic memory is usually due to a nondominant lesion, occasionally to a dominant one 
Homonymous hemianopsia (or less frequently a superior quadrantanopsia due to isolated anterior temporal lobe infarction or inferior quadrantanopsia due to isolated 
parietal lobe infarction)
Paralysis of conjugate gaze to the opposite side: Frontal contraversive eye field or projecting fibers.

the internal carotid artery to the anterior communicating artery, and 
the postcommunal (A2) segment distal to the anterior communicating 
artery (Figs. 437-2 and 437-4). The A1 segment gives rise to several 
deep penetrating branches that supply the anterior limb of the internal 
capsule, the anterior perforate substance, amygdala, anterior hypo­
thalamus, and the inferior part of the head of the caudate nucleus.
Occlusion of the proximal ACA is usually well tolerated because of 
collateral flow through the anterior communicating artery and col­
laterals through the MCA and PCA. Occlusion of a single A2 segment 
results in the contralateral symptoms noted in Fig. 437-4. If both A2 
segments arise from a single anterior cerebral stem (contralateral A1 
segment atresia), the occlusion may affect both hemispheres. Profound 
abulia (a delay in verbal and motor response) and bilateral pyramidal 
signs with paraparesis or quadriparesis and urinary incontinence result.
ANTERIOR CHOROIDAL ARTERY  This artery arises from the internal 
carotid artery and supplies the posterior limb of the internal capsule 
and the white matter posterolateral to it, through which pass some of 
the geniculocalcarine fibers (Fig. 437-5). The complete syndrome of 
anterior choroidal artery occlusion consists of contralateral hemiple­
gia, hemianesthesia (hypesthesia), and homonymous hemianopia. 
However, because this territory is also supplied by penetrating vessels 
of the proximal MCA and the posterior communicating and posterior 
choroidal arteries, minimal deficits may occur, and patients frequently 
recover substantially. Anterior choroidal strokes are usually the result 
of in situ thrombosis of the vessel, and the vessel is particularly vul­
nerable to iatrogenic occlusion during surgical clipping of aneurysms 
arising from the internal carotid artery.
Post. parietal a.
Angular a.
Post. temporal a.
Visual radiation
Motor cortex

Pericallosal a.
Post. 
parietal a.
Secondary
motor area
Medial
prerolandic a.
Callosomarginal a.
Frontopolar a.
Ant. cerebral a.
Medial orbitofrontal a.
Post. communicating a.
Penetrating
thalamosubthalamic
paramedian As.
Post. 
cerebral 
stem
FIGURE 437-4  Diagram of a cerebral hemisphere, medial aspect, showing the branches and distribution of the anterior cerebral artery and the principal regions of cerebral 
localization.
Signs and symptoms: Structures involved
Paralysis of opposite foot and leg: Motor leg area
A lesser degree of paresis of opposite arm: Arm area of cortex or fibers descending to corona radiata.
Cortical sensory loss over toes, foot, and leg: Sensory area for foot and leg
Urinary incontinence: Sensorimotor area in paracentral lobule
Contralateral grasp reflex, sucking reflex, gegenhalten (paratonic rigidity): Medial surface of the posterior frontal lobe; likely supplemental motor area
Abulia (akinetic mutism), slowness, delay, intermittent interruption, lack of spontaneity, whispering, reflex distraction to sights and sounds: Uncertain localization—
probably cingulate gyrus and medial inferior portion of frontal, parietal, and temporal lobes
Impairment of gait and stance (gait apraxia): Frontal cortex near leg motor area
Dyspraxia of left limbs, tactile aphasia in left limbs: Corpus callosum
INTERNAL CAROTID ARTERY  The clinical picture of internal carotid 
occlusion varies depending on whether the cause of ischemia is propa­
gated thrombus, embolism, or low flow. The cortex supplied by the MCA 
territory is affected most often. With a competent circle of Willis, occlu­
sion may go unnoticed. If the thrombus propagates up the internal carotid 
artery into the MCA or embolizes it, symptoms are identical to proximal 
MCA occlusion (see above). Sometimes there is massive infarction of the 
entire deep white matter and cortical surface. When the origins of both 
the ACA and MCA are occluded at the top of the carotid artery, abulia or 
stupor occurs with hemiplegia, hemianesthesia, and aphasia or anosogno­
sia. When the PCA arises from the internal carotid artery (a configuration 
called a fetal PCA), it may also become occluded and give rise to symp­
toms referable to its peripheral territory (Figs. 437-4 and 437-5).
In addition to supplying the ipsilateral brain, the internal carotid 
artery perfuses the optic nerve and retina via the ophthalmic artery. 
In ~25% of symptomatic internal carotid disease, recurrent transient 
monocular blindness (amaurosis fugax) warns of the lesion. Patients 
typically describe a horizontal shade that sweeps down or up across the 
field of vision. They may also complain that their vision was blurred in 
that eye or that the upper or lower half of vision disappeared. In most 
cases, these symptoms last only a few minutes. Rarely, ischemia or 
infarction of the ophthalmic artery or central retinal arteries occurs at 
the time of cerebral TIA or infarction.
A high-pitched prolonged carotid bruit fading into diastole is often 
associated with tightly stenotic lesions. As the stenosis grows tighter 
and flow distal to the stenosis becomes reduced, the bruit becomes 
fainter and may disappear when occlusion is imminent.
COMMON CAROTID ARTERY  All symptoms and signs of internal 
carotid occlusion may also be present with occlusion of the common 
carotid artery. Jaw claudication may result from low flow in the exter­
nal carotid branches. Bilateral common carotid artery occlusions at 
their origin may occur in Takayasu’s arteritis (Chap. 375).

Medial 
rolandic a.
Motor
cortex
Sensory
cortex
Splenial a.
Lateral posterior
choroidal a.
Post. thalamic a.
Parietooccipital a. 
Visual
cortex
Striate area 
along calcarine
sulcus
CHAPTER 437
Calcarine a.
Post. temporal a.
Medial posterior choroidal a.
Introduction to Cerebrovascular Diseases 
Hippocampal As.
Ant.
temporal a.
Stroke within the Posterior Circulation 
The posterior circulation 
is composed of the paired vertebral arteries, the basilar artery, and the 
paired PCAs. The vertebral arteries join to form the basilar artery at the 
pontomedullary junction. The basilar artery divides into two PCAs in 
the interpeduncular fossa (Figs. 437-4–437-6). These major arteries give 
rise to long and short circumferential branches and to smaller deep pen­
etrating branches that supply the cerebellum, medulla, pons, midbrain, 
subthalamus, thalamus, hippocampus, and medial temporal and occipital 
lobes. Occlusion of each vessel produces its own distinctive syndrome.
POSTERIOR CEREBRAL ARTERY  In 75% of cases, both PCAs arise 
from the bifurcation of the basilar artery; in 20%, one has its origin 
from the ipsilateral internal carotid artery via the posterior commu­
nicating artery; in 5%, both originate from the respective ipsilateral 
internal carotid arteries (Figs. 437-4–437-6). The precommunal, or P1, 
segment of the true PCA is atretic in such cases.
PCA syndromes usually result from atheroma formation or emboli 
that lodge at the top of the basilar artery; posterior circulation disease 
may also be caused by dissection of either vertebral artery or fibromus­
cular dysplasia.
Two clinical syndromes are commonly observed with occlusion of 
the PCA: (1) P1 syndrome: midbrain, subthalamic, and thalamic signs, 
which are due to disease of the proximal P1 segment of the PCA or 
its penetrating branches (thalamogeniculate, Percheron, and posterior 
choroidal arteries); and (2) P2 syndrome: cortical temporal and occipi­
tal lobe signs, due to occlusion of the P2 segment distal to the junction 
of the PCA with the posterior communicating artery.
P1 SYNDROMES  Infarction usually occurs in the ipsilateral subthala­
mus and medial thalamus and in the ipsilateral cerebral peduncle and 
midbrain (Figs. 437-5 and 437-11). A third nerve palsy with contra­
lateral ataxia (Claude’s syndrome) or with contralateral hemiplegia 
(Weber’s syndrome) may result. The ataxia indicates involvement of

Ant. cerebral a.
Internal 
carotid a.
Post. 
communicating a.
Post. cerebral a.
Ant. 
choroidal a.
Medial posterior
choroidal a.
Mesencephalic
paramedian As.
Ant. temporal a.
Splenial a.
Parietooccipital a.
Hippocampal a.
PART 13
Neurologic Disorders
Calcarine a.
Post. temporal a.
Post. thalamic a.
Visual
cortex
Lateral posterior 
choroidal a. 
FIGURE 437-5  Inferior aspect of the brain with the branches and distribution of the 
posterior cerebral artery and the principal anatomic structures shown.
Signs and symptoms: Structures involved
Peripheral territory (see also Fig. 437-9). Homonymous hemianopia (often upper 
quadrantic): Calcarine cortex or optic radiation nearby. Bilateral homonymous 
hemianopia, cortical blindness, awareness or denial of blindness; tactile naming, 
achromatopia (color blindness), failure to see to-and-fro movements, inability to 
perceive objects not centrally located, apraxia of ocular movements, inability to 
count or enumerate objects, tendency to run into things that the patient sees and 
tries to avoid: Bilateral occipital lobe with possibly the parietal lobe involved. Verbal 
dyslexia without agraphia, color anomia: Dominant calcarine lesion and posterior 
part of corpus callosum. Memory defect: Hippocampal lesion bilaterally or on the 
dominant side only. Topographic disorientation and prosopagnosia: Usually with 
lesions of nondominant, calcarine, and lingual gyrus. Simultanagnosia, hemivisual 
neglect: Dominant visual cortex, contralateral hemisphere. Unformed visual halluci­
nations, peduncular hallucinosis, metamorphopsia, teleopsia, illusory visual spread, 
palinopsia, distortion of outlines, central photophobia: Calcarine cortex. Complex 
hallucinations: Usually nondominant hemisphere.
Central territory. Thalamic syndrome: sensory loss (all modalities), spontaneous 
pain and dysesthesias, choreoathetosis, intention tremor, spasms of hand, mild 
hemiparesis: Posteroventral nucleus of thalamus; involvement of the adjacent sub­
thalamus body or its afferent tracts. Thalamoperforate syndrome: crossed cerebel­
lar ataxia with ipsilateral third nerve palsy (Claude’s syndrome): Dentatothalamic 
tract and issuing third nerve. Weber’s syndrome: third nerve palsy and contralateral 
hemiplegia: Third nerve and cerebral peduncle. Contralateral hemiplegia: Cerebral 
peduncle. Paralysis or paresis of vertical eye movement, skew deviation, sluggish 
pupillary responses to light, slight miosis and ptosis (retraction nystagmus and 
“tucking” of the eyelids may be associated): Supranuclear fibers to third nerve, 
interstitial nucleus of Cajal, nucleus of Darkschewitsch, and posterior commissure. 
Contralateral rhythmic, ataxic action tremor; rhythmic postural or “holding” tremor 
(rubral tremor): Dentatothalamic tract.
the red nucleus or dentatorubrothalamic tract; the hemiplegia is local­
ized to the cerebral peduncle (Fig. 437-11). If the subthalamic nucleus 
is involved, contralateral hemiballismus may occur. Occlusion of the 
artery of Percheron produces paresis of upward gaze and drowsiness 
and often abulia. Extensive infarction in the midbrain and subthalamus 
occurring with bilateral proximal PCA occlusion presents as coma, 
unreactive pupils, bilateral pyramidal signs, and decerebrate rigidity.
Occlusion of the penetrating branches of thalamic and thalamoge­
niculate arteries produces less extensive thalamic and thalamocapsular 
lacunar syndromes. The thalamic Déjérine-Roussy syndrome consists 
of contralateral hemisensory loss followed later by an agonizing, sear­
ing, or burning pain in the affected areas. It is persistent and responds 
poorly to analgesics. Anticonvulsants (carbamazepine or gabapentin) 
or tricyclic antidepressants may be beneficial.
P2 SYNDROMES  (Figs. 437-4 and 437-5) Occlusion of the distal 
PCA causes infarction of the medial temporal and occipital lobes. 

Superior cerebellar a.
Middle cerebral a.
Posterior cerebral a.
Deep branches
of the basilar a.
Basilar a.
Vertebral a.
Posterior Inferior
cerebellar a.
Anterior Inferior
cerebellar a.
FIGURE 437-6  Diagram of the posterior circulation, showing the intracranial 
vertebral arteries forming the basilar artery that gives off the anterior inferior 
cerebellar, superior cerebellar, and posterior cerebral arteries. The posterior 
inferior cerebellar artery arises from each of the vertebral segments. The majority 
of brainstem blood flow arises from numerous deep branches of the basilar artery 
that penetrate directly into the brainstem.
Contralateral homonymous hemianopia without macula sparing is 
the usual manifestation. (MCA strokes often produce hemianopia 
but typically spare the macula as calcarine cortex is perfused by the 
P2 segment.) Occasionally, only the upper quadrant of visual field is 
involved or the macula vision is spared. If the visual association areas 
are spared and only the calcarine cortex is involved, the patient may 
be aware of visual defects. Medial temporal lobe and hippocampal 
involvement may cause an acute disturbance in memory, particularly 
if it occurs in the dominant hemisphere. The defect usually clears 
because memory has bilateral representation. If the dominant hemi­
sphere is affected and the infarct extends to involve the splenium 
of the corpus callosum, the patient may demonstrate alexia without 
agraphia. Visual agnosia for faces, objects, mathematical symbols, 
and colors and anomia with paraphasic errors (amnestic aphasia) may 
also occur, even without callosal involvement. Occlusion of the PCA 
can produce peduncular hallucinosis (visual hallucinations of brightly 
colored scenes and objects).
Bilateral infarction in the distal PCAs produces cortical blindness 
(blindness with preserved pupillary light reaction). The patient is often 
unaware of the blindness or may even deny it (Anton’s syndrome). Tiny 
islands of vision may persist, and the patient may report that vision 
fluctuates as images are captured in the preserved portions. Rarely, 
only peripheral vision is lost and central vision is spared, resulting in 
“gun-barrel” vision. Bilateral visual association area lesions may result 
in Balint’s syndrome, a disorder of the orderly visual scanning of the 
environment (Chap. 32), usually resulting from infarctions second­
ary to low flow in the “watershed” between the distal PCA and MCA 
territories, as occurs after cardiac arrest. Patients may experience per­
sistence of a visual image for several minutes despite gazing at another 
scene (palinopsia) or an inability to synthesize the whole of an image 
(asimultanagnosia). Embolic occlusion of the top of the basilar artery 
can produce any or all the central or peripheral territory symptoms. 
The hallmark is the sudden onset of bilateral signs, including ptosis, 
pupillary asymmetry or lack of reaction to light, and somnolence. 
Patients will often have posturing and myoclonic jerking that simulates 
seizure. Interrogation of the noncontrast CT scan for a hyperdense 
basilar artery sign (indicating thrombus in the basilar artery) or CT 
angiography (CTA) establishes this diagnosis. Physicians should be 
suspicious of this rare but potentially treatable stroke syndrome in the 
setting of presumed new-onset seizure and cranial nerve deficits.
VERTEBRAL AND POSTERIOR INFERIOR CEREBELLAR ARTERIES  The 
vertebral artery, which arises from the innominate artery on the right 
and the subclavian artery on the left, consists of four segments. The 
first (V1) extends from its origin to its entrance into the sixth or fifth 
transverse vertebral foramen. The second segment (V2) traverses the 
vertebral foramina from C6 to C2. The third (V3) passes through the 
transverse foramen and circles around the arch of the atlas to pierce 
the dura at the foramen magnum. The fourth (V4) segment courses

Pyramid
Medial lemniscus
Spinothalamic tract
Ventral
spinocerebellar tract
Dorsal 
spinocerebellar tract
Nucleus ambiguus
– motor 9 +10
Descending nucleus
and tract - 5th n.
Tractus solitarius
with nucleus
Vestibular
nucleus
12th n. 
nucleus
Medullary syndrome:
Lateral
Medial
FIGURE 437-7  Axial section at the level of the medulla, depicted schematically on the left, with a corresponding magnetic resonance image on the right. Note that in 
Figs. 437-7 through 437-11, all drawings are oriented with the dorsal surface at the bottom, matching the orientation of the brainstem that is commonly seen in all modern 
neuroimaging studies. Approximate regions involved in medial and lateral medullary stroke syndromes are shown.
Signs and symptoms: Structures involved
1. Medial medullary syndrome (occlusion of vertebral artery or of branch of vertebral or lower basilar artery)
On side of lesion
Paralysis with atrophy of one-half half the tongue: Ipsilateral twelfth nerve
Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral pyramidal tract and medial lemniscus
Pain, numbness, impaired sensation over one-half the face: Descending tract and nucleus fifth nerve
Ataxia of limbs, falling to side of lesion: Uncertain—restiform body, cerebellar hemisphere, cerebellar fibers, spinocerebellar tract (?)
Nystagmus, diplopia, oscillopsia, vertigo, nausea, vomiting: Vestibular nucleus
Horner’s syndrome (miosis, ptosis, decreased sweating): Descending sympathetic tract
Dysphagia, hoarseness, paralysis of palate, paralysis of vocal cord, diminished gag reflex: Issuing fibers ninth and tenth nerves
Loss of taste: Nucleus and tractus solitarius
Numbness of ipsilateral arm, trunk, or leg: Cuneate and gracile nuclei
Weakness of lower face: Genuflected upper motor neuron fibers to ipsilateral facial nucleus
Impaired pain and thermal sense over half the body, sometimes face: Spinothalamic tract
5. Basilar artery syndrome (the syndrome of the lone vertebral artery is equivalent): A combination of the various brainstem syndromes plus those arising in the posterior 
cerebral artery distribution.
Bilateral long tract signs (sensory and motor; cerebellar and peripheral cranial nerve abnormalities): Bilateral long tract; cerebellar and peripheral cranial nerves
Paralysis or weakness of all extremities, plus all bulbar musculature: Corticobulbar and corticospinal tracts bilaterally
upward to join the other vertebral artery to form the basilar artery 
(Fig. 437-6); only the fourth segment gives rise to branches that supply 
the brainstem and cerebellum. The posterior inferior cerebellar artery 
(PICA) in its proximal segment supplies the lateral medulla and, in its 
distal branches, the inferior surface of the cerebellum.
Atherothrombotic lesions have a predilection for V1 and V4 seg­
ments of the vertebral artery. The first segment may become diseased at 
the origin of the vessel and may produce posterior circulation emboli; 
collateral flow from the contralateral vertebral artery or the ascending 
cervical, thyrocervical, or occipital arteries is usually sufficient to pre­
vent low-flow TIAs or stroke. When one vertebral artery is atretic and 
an atherothrombotic lesion threatens the origin of the other, the collat­
eral circulation, which may also include retrograde flow down the basi­
lar artery, is often insufficient (Figs. 437-5 and 437-6). In this setting, 
low-flow TIAs may occur, consisting of syncope, vertigo, and alternat­
ing hemiplegia; this state also sets the stage for thrombosis. Disease of 
the distal fourth segment of the vertebral artery can promote thrombus 
formation manifest as embolism or with propagation as basilar artery 
thrombosis. Stenosis proximal to the origin of the PICA can threaten 
the lateral medulla and posterior inferior surface of the cerebellum.
If the subclavian artery is occluded proximal to the origin of the verte­
bral artery, there is a reversal in the direction of blood flow in the ipsilateral 
vertebral artery. Exercise of the ipsilateral arm may increase demand on 
vertebral flow, producing posterior circulation TIAs, or “subclavian steal.”
Although atheromatous disease rarely narrows the second and third 
segments of the vertebral artery, this region is subject to dissection, 
fibromuscular dysplasia, and, rarely, encroachment by osteophytic 
spurs within the vertebral foramina.

12th n.
Inferior olive
Medulla
10th n.
Descending 
sympathetic
tract
Restiform
body
Olivocerebellar
fibers
Cerebellum
CHAPTER 437
Medial longitudinal fasciculus
Introduction to Cerebrovascular Diseases 
Embolic occlusion or thrombosis of a V4 segment causes isch­
emia of the lateral medulla. The constellation of vertigo, numbness 
of the ipsilateral face and contralateral limbs, diplopia, hoarseness, 
dysarthria, dysphagia, and ipsilateral Horner’s syndrome is called the 
lateral medullary (or Wallenberg’s) syndrome (Fig. 437-7). Ipsilateral 
upper motor neuron facial weakness can also occur. Most cases result 
from ipsilateral vertebral artery occlusion; in the remainder, PICA 
occlusion is responsible. Occlusion of the medullary penetrating 
branches of the vertebral artery or PICA results in partial syndromes. 
Hemiparesis is not a typical feature of vertebral artery occlusion; how­
ever, quadriparesis may result from occlusion of the anterior spinal 
artery.
Rarely, a medial medullary syndrome occurs with infarction of the 
pyramid and contralateral hemiparesis of the arm and leg, sparing the 
face. If the medial lemniscus and emerging hypoglossal nerve fibers 
are involved, contralateral loss of joint position sense and ipsilateral 
tongue weakness occur.
Cerebellar infarction can lead to respiratory arrest due to brainstem 
herniation from cerebellar swelling, closure of the aqueduct of Silvius 
or fourth ventricle, followed by hydrocephalus and central herniation. 
This added downward displacement of the brainstem from hydroceph­
alus will exacerbate respiratory and hemodynamic instability. Drowsi­
ness, Babinski signs, dysarthria, and bifacial weakness may be absent, 
or present only briefly, before respiratory arrest ensues. Gait unsteadi­
ness, headache, dizziness, nausea, and vomiting may be the only early 
symptoms and signs and should arouse suspicion of this impending 
complication, which may require neurosurgical decompression, often 
with an excellent outcome. Separating these symptoms from those of

Corticospinal and
corticobulbar tract
Spinothalamic
tract
Medial lemniscus
6th n.
Descending tract
and nucleus of
5th n.
7th n.
8th n.
Dorsal
cochlear 
nucleus
7th n. nucleus
Restiform body
PART 13
Neurologic Disorders
Medial longitudinal
fasciculus
Vestibular nucleus
6th n. nucleus
complex
Inferior pontine syndrome:
Lateral
Medial
FIGURE 437-8  Axial section at the level of the inferior pons, depicted schematically on the left, with a corresponding magnetic resonance image on the right. Approximate 
regions involved in medial and lateral inferior pontine stroke syndromes are shown.
Signs and symptoms: Structures involved
Paralysis of conjugate gaze to side of lesion (preservation of convergence): Center for conjugate lateral gaze
Nystagmus: Vestibular nucleus
Ataxia of limbs and gait: Likely middle cerebellar peduncle
Diplopia on lateral gaze: Abducens nerve
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract in lower pons
Impaired tactile and proprioceptive sense over one-half of the body: Medial lemniscus
Horizontal and vertical nystagmus, vertigo, nausea, vomiting, oscillopsia: Vestibular nerve or nucleus
Facial paralysis: Seventh nerve
Paralysis of conjugate gaze to side of lesion: Center for conjugate lateral gaze
Deafness, tinnitus: Auditory nerve or cochlear nucleus
Ataxia: Middle cerebellar peduncle and cerebellar hemisphere
Impaired sensation over face: Descending tract and nucleus fifth nerve
Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract
viral labyrinthitis can be a challenge, but headache, neck stiffness, and 
unilateral dysmetria favor stroke.
BASILAR ARTERY  Branches of the basilar artery (Fig. 437-6) supply 
the base of the pons and superior cerebellum and fall into three groups: 
(1) paramedian, 7–10 in number, which supply a wedge of pons on 
either side of the midline; (2) short circumferential, 5–7 in number, 
that supply the lateral two-thirds of the pons and middle and superior 
cerebellar peduncles; and (3) bilateral long circumferential (superior 
cerebellar and anterior inferior cerebellar arteries), which course 
around the pons to supply the cerebellar hemispheres.
Atheromatous lesions can occur anywhere along the basilar trunk 
but are most frequent in the proximal basilar and distal vertebral seg­
ments. Typically, lesions occlude either the proximal basilar and one 
or both vertebral arteries. The clinical picture varies depending on the 
availability of retrograde collateral flow from the posterior communi­
cating arteries. Rarely, dissection of a vertebral artery may involve the 
basilar artery and, depending on the location of true and false lumen, 
may produce multiple penetrating artery strokes.
Although atherothrombosis occasionally occludes the distal por­
tion of the basilar artery, emboli from the heart or proximal vertebral 
or basilar segments are more commonly responsible for “top of the 
basilar” syndromes.
Because the brainstem contains many structures in close apposition, 
a diversity of clinical syndromes may emerge with ischemia, reflecting 
involvement of the corticospinal and corticobulbar tracts, ascending 
sensory tracts, and cranial nerve nuclei (Figs. 437-7 to 437-11).
The symptoms of transient ischemia or infarction in the territory 
of the basilar artery often do not indicate whether the basilar artery 

Middle cerebellar
peduncle
7th and 8th
cranial
nerves
Inferior pons
Cerebellum
itself or one of its branches is diseased, yet this distinction has impor­
tant implications for therapy. The picture of complete basilar occlusion, 
however, is easy to recognize as a constellation of bilateral long tract 
signs (sensory and motor) with signs of cranial nerve and cerebellar 
dysfunction. Patients may have spontaneous posturing movements that 
are myoclonic in nature and simulate seizure activity. These move­
ments are brief, repetitive, and multifocal and often confused with 
status epilepticus. CT or magnetic resonance angiography can rapidly 
detect basilar thrombosis, and rapid treatment (thrombectomy) can be 
lifesaving. A “locked-in” state of preserved consciousness with quad­
riplegia and cranial nerve signs suggests complete pontine and lower 
midbrain infarction. The therapeutic goal is to identify impending 
basilar occlusion before devastating infarction occurs. A series of TIAs 
and a slowly progressive, fluctuating stroke are extremely significant, 
because they often herald an atherothrombotic occlusion of the distal 
vertebral or proximal basilar artery.
TIAs in the proximal basilar distribution may produce vertigo (often 
described by patients as “swimming,” “swaying,” “moving,” “unsteadi­
ness,” or “light-headedness”). Other symptoms that warn of basilar 
thrombosis include diplopia, dysarthria, facial or circumoral numb­
ness, and hemisensory symptoms. In general, symptoms of basilar 
branch TIAs affect one side of the brainstem, whereas symptoms of 
basilar artery TIAs usually affect both sides, although a “herald” hemi­
paresis has been emphasized as an initial symptom of basilar occlusion. 
Most often, TIAs, whether due to impending occlusion of the basilar 
artery or a basilar branch, are short lived (5–30 min) and repetitive, 
occurring several times a day. The pattern suggests intermittent reduc­
tion of flow. Although treatment with intravenous heparin or various

Medial
lemniscus
5th n. 
Lateral
lemniscus
Middle
cerebellar
peduncle
Spinothalamic
tract
5th n. motor nucleus
5th n. sensory nucleus
Superior cerebellar
peduncle
Medial longitudinal 
fasciculus
Midpontine syndrome:
Lateral
Medial
FIGURE 437-9  Axial section at the level of the midpons, depicted schematically on the left, with a corresponding magnetic resonance image on the right. Approximate 
regions involved in medial and lateral midpontine stroke syndromes are shown.
Signs and symptoms: Structures involved
Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine nuclei
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract
Variable impaired touch and proprioception when lesion extends posteriorly: Medial lemniscus
Ataxia of limbs: Middle cerebellar peduncle
Paralysis of muscles of mastication: Motor fibers or nucleus of fifth nerve
Impaired sensation over side of face: Sensory fibers or nucleus of fifth nerve
Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract
combinations of antiplatelet agents has been used to prevent clot 
propagation, there is no specific evidence to support any one approach, 
and endovascular intervention is also an option.
Atherothrombotic occlusion of the basilar artery with infarction 
usually causes bilateral brainstem signs. A gaze paresis or inter­
nuclear ophthalmoplegia associated with ipsilateral hemiparesis may 
be the only manifestation of bilateral brainstem ischemia. More often, 
unequivocal signs of bilateral pontine disease are present. Complete 
basilar thrombosis carries a high mortality.
Occlusion of a branch of the basilar artery usually causes unilateral 
symptoms and signs involving motor, sensory, and cranial nerves. If 
symptoms remain unilateral, concern over pending basilar occlusion 
should be reduced.
Occlusion of the superior cerebellar artery results in severe ipsi­
lateral cerebellar ataxia, nausea and vomiting, dysarthria, and con­
tralateral loss of pain and temperature sensation over the extremities, 
body, and face (spino- and trigeminothalamic tract). Partial deafness, 
ataxic tremor of the ipsilateral upper extremity, Horner’s syndrome, 
and palatal myoclonus may occur rarely. Partial syndromes occur fre­
quently (Fig. 437-10). With large strokes, swelling and mass effects may 
compress the midbrain or produce hydrocephalus; these symptoms 
may evolve rapidly. Neurosurgical intervention may be lifesaving in 
such cases.
Occlusion of the anterior inferior cerebellar artery produces vari­
able degrees of infarction because the size of this artery and the ter­
ritory it supplies vary inversely with those of the PICA. The principal 
symptoms include (1) ipsilateral deafness, facial weakness, vertigo, 
nausea and vomiting, nystagmus, tinnitus, cerebellar ataxia, Horner’s 
syndrome, and paresis of conjugate lateral gaze; and (2) contralateral 
loss of pain and temperature sensation. An occlusion close to the origin 
of the artery may cause corticospinal tract signs (Fig. 437-8).

Corticospinal and
corticopontine tracts
Temporal lobe
Mid-pons
5th cranial
nerve
CHAPTER 437
Cerebellum
Introduction to Cerebrovascular Diseases 
Occlusion of one of the short circumferential branches of the basilar 
artery affects the lateral two-thirds of the pons and middle or supe­
rior cerebellar peduncle, whereas occlusion of one of the paramedian 
branches affects a wedge-shaped area on either side of the medial pons 
(Figs. 437-8–437-10).
■
■IMAGING STUDIES
See also Chap. 434.
CT Scans 
CT radiographic images identify or exclude hemorrhage 
as the cause of stroke, and they identify extraparenchymal hemor­
rhages, neoplasms, abscesses, and other conditions masquerading 
as stroke. Brain CT scans obtained in the first several hours after an 
infarction generally show no abnormality (Fig. 437-12A), and the 
infarct may not be seen reliably for 24–48 h. The decision to treat 
patients with IV plasminogen activators is based on the clinical diag­
nosis of stroke and a CT scan showing no hemorrhage. CT may fail 
to show small ischemic strokes in the posterior fossa because of bone 
artifact; small infarcts on the cortical surface may also be missed.
Contrast-enhanced CT scans add specificity by showing contrast 
enhancement of subacute infarcts and allow visualization of venous 
structures. Coupled with multidetector scanners, CT angiography can 
be performed with administration of IV iodinated contrast allowing 
visualization of the cervical and intracranial arteries, intracranial veins, 
and aortic arch in one imaging session. Carotid disease and intracranial 
vascular occlusions are readily identified with this method (see Fig. 438-2). 
After an IV bolus of contrast, deficits in brain perfusion produced by 
vascular occlusion can also be demonstrated (Fig. 437-12D) and used 
to predict the region of infarcted brain and the brain at risk of further 
infarction (i.e., the ischemic penumbra, see “Pathophysiology of Isch­
emic Stroke” in Chap. 438). CT imaging is also sensitive for detecting 
SAH (although by itself does not rule it out), and CTA can readily

Pontine nuclei and
pontocerebellar fibers
Corticospinal tract
Spinothalamic 
tract
PART 13
Neurologic Disorders
Superior cerebellar 
peduncle
Medial longitudinal
fasciculus
Superior pontine syndrome:
Lateral
Medial
FIGURE 437-10  Axial section at the level of the superior pons, depicted schematically on the left, with a corresponding magnetic resonance image on the right. Approximate 
regions involved in medial and lateral superior pontine stroke syndromes are shown.
Signs and symptoms: Structures involved
Cerebellar ataxia (probably): Superior and/or middle cerebellar peduncle
Internuclear ophthalmoplegia: Medial longitudinal fasciculus
Myoclonic syndrome, palate, pharynx, vocal cords, respiratory apparatus, face, oculomotor apparatus, etc.: Localization uncertain—central tegmental bundle, dentate 
projection, inferior olivary nucleus
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract
Rarely touch, vibration, and position are affected: Medial lemniscus
Ataxia of limbs and gait, falling to side of lesion: Middle and superior cerebellar peduncles, superior surface of cerebellum, dentate nucleus
Dizziness, nausea, vomiting; horizontal nystagmus: Vestibular nucleus
Paresis of conjugate gaze (ipsilateral): Pontine contralateral gaze
Skew deviation: Uncertain
Miosis, ptosis, decreased sweating over face (Horner’s syndrome): Descending sympathetic fibers
Tremor: Localization unclear—Dentate nucleus, superior cerebellar peduncle
Impaired pain and thermal sense on face, limbs, and trunk: Spinothalamic tract
Impaired touch, vibration, and position sense, more in leg than arm (there is a tendency to incongruity of pain and touch deficits): Medial lemniscus (lateral portion)
3rd n.
Crus cerebri
Substantia
nigra
3rd nerve
nucleus
Superior colliculus
Cerebral aqueduct
Midbrain syndrome:
Lateral
Medial
FIGURE 437-11  Axial section at the level of the midbrain, depicted schematically on the left, with a corresponding magnetic resonance image on the right. Approximate 
regions involved in medial and lateral midbrain stroke syndromes are shown.
Signs and symptoms: Structures involved
Eye “down and out” secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers
Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri
Eye “down and out” secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers and/or third nerve nucleus
Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway

Temporal lobe
Medial
lemniscus
Basilar artery
Central
tegmental
bundle
Lateral
lemniscus
Superior
pons
Basilar artery
Internal
carotid
artery
Red nucleus
Medial
lemniscus
Spinothalamic
tract
Midbrain
Periaqueductal
gray matter

P
A
B
CBF
R
CBF <30%: 112 ml
Mismatch volume: 43 ml
Mismatch ratio: 1.4
D
FIGURE 437-12  (A) Noncontrast head computed tomography (CT) image of an 83-year-old man with sudden onset left hemiplegia, left homonymous hemianopia, rightward 
gaze deviation and left hemineglect showing no clear brain infarction and hyperdensity within the right middle cerebral artery (MCA) suggestive of clot. (B) CT angiography 
performed at the same time as the CT showing absence of the right MCA and anterior cerebral artery (ACA) vessels consistent with occlusion of the bifurcation of the right 
intracranial internal carotid artery. (C) Follow-up head CT 1 day later showing extensive infarction of the right frontal lobe with brain herniation. (D) CT perfusion performed 
with studies shown in A and B. This predicts a large core infarction (pink regions) despite attempts at revascularization with thrombectomy. CBF, cerebral blood flow.
identify intracranial aneurysms (Chap. 440). Because of its speed and 
wide availability, noncontrast head CT is the imaging modality of 
choice in patients with acute stroke (Fig. 437-1), and CTA and CT per­
fusion imaging may also be useful and convenient adjuncts.
■
■MRI
MRI reliably documents the extent and location of infarction in all 
areas of the brain, including the posterior fossa and cortical surface. 
Diffusion-weighted imaging (DWI) identifies regions of brain infarc­
tion within minutes of the stroke onset (Fig. 437-13A, B), while fluidattenuated inversion recovery (FLAIR) imaging reliably reveals areas of 
prior brain infarction from a few days to years later (Fig. 437-13C). CT 
is poorly sensitive to brain infarction in the posterior fossae compared 
to MRI DWI images (Fig. 437-13D, E). MRI also identifies intracranial 
hemorrhage and other abnormalities and, using special sequences, can 
be as sensitive as CT for detecting acute intracerebral hemorrhage. 
MRI scanners with magnets of higher field strength produce more reli­
able and precise images. Using IV administration of gadolinium con­
trast, magnetic resonance (MR) perfusion studies can be performed. 
Brain regions showing poor perfusion but no abnormality on diffusion 
provide, compared to CT, an equivalent measure of the ischemic pen­
umbra. MR angiography is highly sensitive for stenosis of extracranial 
internal carotid arteries and of large intracranial vessels. With higher 

CHAPTER 437
C
P
A
Tmax
Introduction to Cerebrovascular Diseases 
L
Tmax >6.0s: 155 ml
degrees of stenosis, MR angiography tends to overestimate the degree 
of stenosis when compared to conventional x-ray angiography. MRI 
with fat saturation is an imaging sequence used to visualize extra- or 
intracranial arterial dissection. This sensitive technique images clotted 
blood within the dissected vessel wall. Iron-sensitive imaging (ISI) is 
helpful to detect cerebral microbleeds that may be present in cerebral 
amyloid angiopathy and other hemorrhagic disorders.
MRI is more expensive and time consuming than CT and less read­
ily available. Claustrophobia and the logistics of imaging acutely criti­
cally ill patients also limit its application. Most acute stroke protocols 
use CT because of these limitations. However, MRI is useful outside 
the acute period by more clearly defining the extent of tissue injury 
and discriminating new from old regions of brain infarction. MRI may 
have utility in patients with TIA, because it is also more likely to iden­
tify new infarction, which is a strong predictor of subsequent stroke.
Cerebral Angiography 
Conventional x-ray cerebral angiography 
is the gold standard for identifying and quantifying atherosclerotic 
stenoses of the cerebral arteries and for identifying and characteriz­
ing other pathologies, including aneurysms, vasospasm, intraluminal 
thrombi, fibromuscular dysplasia, arteriovenous fistulae, vasculitis, 
and collateral channels of blood flow. Conventional angiography car­
ries risks of arterial damage, groin hemorrhage, embolic stroke, and

PART 13
Neurologic Disorders
A
AHL
D
E
B
C
FIGURE 437-13  Examples of magnetic resonance imaging (MRI) imaging of acute ischemic infarcts. (A) Diffusion-weighted image (DWI) revealing bright region in the left 
pons (arrow), and (B) dark region on apparent diffusion coefficient (ADC) in the same region. Bright regions on DWI and corresponding dark regions on ADC are consistent 
with acute brain ischemia (within minutes to hours of stroke onset). (C) Same region of the brain 2 days later showing bright region in the infarcted tissue on fluid-attenuated 
inversion recovery (FLAIR) images. The DWI and ADC values will return to normal after 10–14 days while the FLAIR abnormality will persist long term. (D) DWI MRI and 
(E) computed tomography (CT) images of a patient with acute-onset vertigo. The DWI image shows an acute ischemic infarction of the right posterior inferior cerebellar 
artery territory within the cerebellum, whereas the CT scan is only subtly hypodense in the same region. MRI is superior to CT imaging for identifying ischemic infarction 
especially within the posterior fossa.
renal failure from contrast nephropathy, so it should be reserved for 
situations where less invasive means are inadequate. Acute stroke 
treatment with endovascular thrombectomy has proven effective in 
ischemic strokes caused by internal carotid terminus or MCA occlu­
sions and is now part of routine clinical practice at centers that have 
this capability (see Chap. 438).
Ultrasound Techniques 
Stenosis at the origin of the internal 
carotid artery can be identified and quantified reliably by ultrasonog­
raphy that combines a B-mode ultrasound image with a Doppler ultra­
sound assessment of flow velocity (“duplex” ultrasound). Transcranial 
Doppler (TCD) assessment of MCA, ACA, and PCA flow and of verte­
brobasilar flow is also useful. This latter technique can detect stenotic 
lesions in the large intracranial arteries because such lesions increase 
systolic flow velocity. TCD can also detect microemboli from other­
wise asymptomatic carotid plaques. In many cases, MR angiography 
combined with carotid and transcranial ultrasound studies eliminates 
the need for conventional x-ray angiography in evaluating vascular 
stenosis. Alternatively, CTA of the entire head and neck can be per­
formed during the initial imaging of acute stroke. Because this images 
the entire arterial system relevant to stroke, with the exception of the 
heart, much of the clinician’s stroke workup can be completed with this 
single imaging study.
Radionuclide Perfusion Techniques 
Both xenon techniques 
(principally xenon-CT) and positron emission tomography (PET) 
can quantify cerebral blood flow. These tools are generally used for 
research (Chap. 434) but can be useful for determining the significance 
of arterial stenosis and planning for revascularization surgery. Singlephoton emission computed tomography (SPECT) and CT or MR per­
fusion techniques report relative cerebral blood flow. As noted above, 
CT imaging is used as the initial imaging modality for acute stroke, and