3328 PART 13 Neurologic Disorders

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 external carotid branches. Bilateral common carotid artery occlusions at

their origin may occur in Takayasu’s arteritis (Chap. 363).

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. 426-4–426-6). These major arteries

give rise to long and short circumferential branches and to smaller

deep penetrating 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 communicating artery; in 5%, both originate from the respective ipsilateral

internal carotid arteries (Figs. 426-4–426-6). 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 fibromuscular 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 occipital 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 subthalamus and medial thalamus and in the ipsilateral cerebral peduncle

and midbrain (Figs. 426-5 and 426-11). A third nerve palsy with contralateral ataxia (Claude’s syndrome) or with contralateral hemiplegia

(Weber’s syndrome) may result. The ataxia indicates involvement of the

red nucleus or dentatorubrothalamic tract; the hemiplegia is localized

to the cerebral peduncle (Fig. 426-11). 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 thalamogeniculate arteries produces less extensive thalamic and thalamocapsular lacunar syndromes. The thalamic Déjérine-Roussy syndrome

consists of contralateral hemisensory loss followed later by an agonizing, searing, 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. 426-4 and 426-5) Occlusion of the distal PCA

causes infarction of the medial temporal and occipital lobes. Contralateral homonymous hemianopia without macula sparing is the usual

Ant. cerebral a.

Post.

communicating a.

Post. cerebral a.

Medial posterior

choroidal a.

Ant. temporal a.

Hippocampal a.

Post. temporal a.

Post. thalamic a.

Lateral posterior

choroidal a.

Visual

cortex

Internal

carotid a.

Ant.

choroidal a.

Mesencephalic

paramedian As.

Splenial a.

Parietooccipital a.

Calcarine a.

FIGURE 426-5 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. 426-9). 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

hallucinations, 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 subthalamus body or its afferent tracts. Thalamoperforate syndrome:

crossed cerebellar 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.

Basilar a.

Vertebral a.

Posterior Inferior

cerebellar a.

Deep branches

of the basilar a.

Anterior Inferior

cerebellar a.

Posterior cerebral a. Middle cerebral a.

Superior cerebellar a.

FIGURE 426-6 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.

3329 Introduction to Cerebrovascular Diseases CHAPTER 426

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 hemisphere 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. 30), usually resulting from infarctions

secondary to low flow in the “watershed” between the distal PCA and

MCA territories, as occurs after cardiac arrest. Patients may experience persistence 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

12th n.

nucleus

Vestibular

nucleus

Restiform

body

Olivocerebellar

fibers

Medial longitudinal fasciculus

Descending nucleus

and tract - 5th n.

Descending

sympathetic

tract

Dorsal

spinocerebellar tract

10th n.

Ventral

spinocerebellar tract

Spinothalamic tract

Medial lemniscus

Inferior olive

Nucleus ambiguus

– motor 9 +10

Pyramid

12th n.

Medullary syndrome:

Lateral Medial

Tractus solitarius

with nucleus

Medulla

Cerebellum

FIGURE 426-7 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. 426-7 through 426-11, 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

On side opposite lesion

Paralysis of arm and leg, sparing face; impaired tactile and proprioceptive sense over one-half the body: Contralateral pyramidal tract and medial lemniscus

2. Lateral medullary syndrome (occlusion of any of five vessels may be responsible—vertebral, posterior inferior cerebellar, superior, middle, or inferior lateral medullary

arteries)

On side of lesion

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

On side opposite lesion

Impaired pain and thermal sense over half the body, sometimes face: Spinothalamic tract

3. Total unilateral medullary syndrome (occlusion of vertebral artery): Combination of medial and lateral syndromes

4. Lateral pontomedullary syndrome (occlusion of vertebral artery): Combination of lateral medullary and lateral inferior pontine syndrome

 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

3330 PART 13 Neurologic Disorders

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

upward to join the other vertebral artery to form the basilar artery

(Fig. 426-6); 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 segments 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

prevent low-flow TIAs or stroke. When one vertebral artery is atretic

and an atherothrombotic lesion threatens the origin of the other, the

collateral circulation, which may also include retrograde flow down

the basilar artery, is often insufficient (Figs. 426-5 and 426-6). In this

setting, low-flow TIAs may occur, consisting of syncope, vertigo, and

alternating 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

vertebral 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,

Inferior pontine syndrome:

Lateral Medial

Medial longitudinal

fasciculus

Vestibular nucleus

Spinothalamic

tract

7th n.

6th n.

8th n.

Middle cerebellar

peduncle

Restiform body

6th n. nucleus

complex

Corticospinal and

corticobulbar tract

7th n. nucleus

Dorsal

cochlear

nucleus

Descending tract

and nucleus of

5th n.

Medial lemniscus

Inferior pons

Cerebellum

7th and 8th

cranial

nerves

FIGURE 426-8 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

1. Medial inferior pontine syndrome (occlusion of paramedian branch of basilar artery)

On side of lesion

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

On side opposite lesion

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

2. Lateral inferior pontine syndrome (occlusion of anterior inferior cerebellar artery)

On side of lesion

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

On side opposite lesion

Impaired pain and thermal sense over one-half the body (may include face): Spinothalamic tract

3331 Introduction to Cerebrovascular Diseases CHAPTER 426

fibromuscular dysplasia, and, rarely, encroachment by osteophytic

spurs within the vertebral foramina.

Embolic occlusion or thrombosis of a V4 segment causes ischemia

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. 426-7). 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; however, 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 hydrocephalus will exacerbate respiratory and hemodynamic instability.

Drowsiness, Babinski signs, dysarthria, and bifacial weakness may be

absent, or present only briefly, before respiratory arrest ensues. Gait

unsteadiness, 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 viral labyrinthitis can be a challenge, but headache, neck

stiffness, and unilateral dysmetria favor stroke.

BASILAR ARTERY Branches of the basilar artery (Fig. 426-6) 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 segments. 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 communicating 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.

Temporal lobe

Mid-pons

5th cranial

nerve

Cerebellum

Midpontine syndrome:

Lateral Medial

Medial longitudinal

fasciculus

Superior cerebellar

peduncle

5th n. sensory nucleus

5th n. motor nucleus

Middle

cerebellar

peduncle

Lateral

lemniscus

Corticospinal and

corticopontine tracts

Spinothalamic

tract

5th n.

Medial

lemniscus

FIGURE 426-9 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

1. Medial midpontine syndrome (paramedian branch of midbasilar artery)

On side of lesion

Ataxia of limbs and gait (more prominent in bilateral involvement): Pontine nuclei

On side opposite lesion

Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract

Variable impaired touch and proprioception when lesion extends posteriorly: Medial lemniscus

2. Lateral midpontine syndrome (short circumferential artery)

On side of lesion

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

On side opposite lesion

Impaired pain and thermal sense on limbs and trunk: Spinothalamic tract

3332 PART 13 Neurologic Disorders

Although atherothrombosis occasionally occludes the distal portion

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. 426-7–426-11).

The symptoms of transient ischemia or infarction in the territory

of the basilar artery often do not indicate whether the basilar artery

itself or one of its branches is diseased, yet this distinction has important 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

movements 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

quadriplegia 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,”

“unsteadiness,” or “light-headedness”). Other symptoms that warn

of basilar thrombosis include diplopia, dysarthria, facial or circumoral numbness, 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” hemiparesis 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 reduction of flow. Although treatment

with intravenous heparin or various combinations of antiplatelet

agents has been used to prevent clot propagation, there is no specific

Superior pontine syndrome:

Lateral Medial

Medial longitudinal

fasciculus

Lateral

lemniscus

Spinothalamic

tract

Pontine nuclei and

pontocerebellar fibers Corticospinal tract

Medial

lemniscus

Central

tegmental

bundle

Superior cerebellar

peduncle

Basilar artery

Temporal lobe

Superior

pons

FIGURE 426-10 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

1. Medial superior pontine syndrome (paramedian branches of upper basilar artery)

On side of lesion

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

On side opposite lesion

Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract

Rarely touch, vibration, and position are affected: Medial lemniscus

2. Lateral superior pontine syndrome (syndrome of superior cerebellar artery)

On side of lesion

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

On side opposite lesion

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)

3333 Introduction to Cerebrovascular Diseases CHAPTER 426

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 internuclear 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 ipsilateral cerebellar ataxia, nausea and vomiting, dysarthria, and contralateral 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 frequently

(Fig. 426-10). 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 variable

degrees of infarction because the size of this artery and the territory 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. 426-8).

Occlusion of one of the short circumferential branches of the basilar

artery affects the lateral two-thirds of the pons and middle or superior cerebellar peduncle, whereas occlusion of one of the paramedian

branches affects a wedge-shaped area on either side of the medial pons

(Figs. 426-8–426-10).

■ IMAGING STUDIES

See also Chap. 423.

CT Scans CT radiographic images identify or exclude hemorrhage

as the cause of stroke, and they identify extraparenchymal hemorrhages, neoplasms, abscesses, and other conditions masquerading

as stroke. Brain CT scans obtained in the first several hours after an

infarction generally show no abnormality, and the infarct may not be

seen reliably for 24–48 h. 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,

aortic arch, and even the coronary arteries in one imaging session.

Carotid disease and intracranial vascular occlusions are readily identified with this method (see Fig. 427-2). After an IV bolus of contrast,

deficits in brain perfusion produced by vascular occlusion can also be

demonstrated (Fig. 426-12) 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 Ischemic Stroke” in Chap. 427).

CT imaging is also sensitive for detecting SAH (although by itself does

Midbrain syndrome:

Lateral Medial

3rd n.

Superior colliculus Cerebral aqueduct

3rd nerve

nucleus

Medial

lemniscus

Spinothalamic

tract

Red nucleus

Substantia

nigra

Crus cerebri

Periaqueductal

gray matter

Basilar artery

Internal

carotid

artery

Midbrain

FIGURE 426-11 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

1. Medial midbrain syndrome (paramedian branches of upper basilar and proximal posterior cerebral arteries)

On side of lesion

Eye “down and out” secondary to unopposed action of fourth and sixth cranial nerves, with dilated and unresponsive pupil: Third nerve fibers

On side opposite lesion

Paralysis of face, arm, and leg: Corticobulbar and corticospinal tract descending in crus cerebri

2. Lateral midbrain syndrome (syndrome of small penetrating arteries arising from posterior cerebral artery)

On side of lesion

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

On side opposite lesion

Hemiataxia, hyperkinesias, tremor: Red nucleus, dentatorubrothalamic pathway

3334 PART 13 Neurologic Disorders

not rule it out), and CTA can readily identify intracranial aneurysms

(Chap. 429). Because of its speed and wide availability, noncontrast

head CT is the imaging modality of choice in patients with acute stroke

(Fig. 426-1), and CTA and CT perfusion 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. It 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 reliable and precise images. Diffusion-weighted imaging

is more sensitive for early brain infarction than standard MR sequences

or CT (Fig. 426-13), as is fluid-attenuated inversion recovery (FLAIR)

imaging (Chap. 423). Using IV administration of gadolinium contrast,

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 penumbra. MR angiography is highly sensitive for stenosis of extracranial

internal carotid arteries and of large intracranial vessels. With higher

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 readily available. Claustrophobia and the logistics of imaging acutely critically 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 identify 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 characterizing other pathologies, including aneurysms, vasospasm, intraluminal

thrombi, fibromuscular dysplasia, arteriovenous fistulae, vasculitis,

and collateral channels of blood flow. Conventional angiography carries risks of arterial damage, groin hemorrhage, embolic stroke, and

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 occlusions and has now part of routine clinical practice at centers that have

this capability (see Chap. 427).

Ultrasound Techniques Stenosis at the origin of the internal

carotid artery can be identified and quantified reliably by ultrasonography that combines a B-mode ultrasound image with a Doppler

ultrasound assessment of flow velocity (“duplex” ultrasound). Transcranial Doppler (TCD) assessment of MCA, ACA, and PCA flow and

of vertebrobasilar flow is also useful. This latter technique can detect

A

C

D E

B

FIGURE 426-12 Acute left middle cerebral artery (MCA) stroke with right hemiplegia but preserved language. A. Computed tomography (CT) perfusion mean-transit time

map showing delayed perfusion of the left MCA distribution (blue). B. Predicted region of infarct (red) and penumbra (green) based on CT perfusion data. C. Conventional

angiogram showing occlusion of the left internal carotid–MCA bifurcation (left panel), and revascularization of the vessels following successful thrombectomy 8 h after

stroke symptom onset (right panel). D. The clot removed with a thrombectomy device (L5, Concentric Medical, Inc.). E. CT scan of the brain 2 days later; note infarction in

the region predicted in B but preservation of the penumbral region by successful revascularization.