Disclosures: Louis R Caplan, MD Nothing to disclose. Jose Biller, MD, FACP, FAAN, FAHA Nothing to disclose. John F Dashe, MD, PhD Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
INTRODUCTION — Twenty percent of ischemic events in the brain involve posterior circulation (vertebrobasilar) structures. This topic will review the major clinical syndromes associated with posterior circulation ischemia related to stenosis or occlusion of the large aortic arch, neck, and intracranial arteries. These arteries are the innominate and subclavian arteries in the chest, the vertebral arteries in the neck, and the intracranial vertebral, basilar, and posterior cerebral arteries.
The evaluation and management of acute ischemic stroke (including stroke involving the posterior circulation) are discussed separately. (See "Initial assessment and management of acute stroke" and "Reperfusion therapy for acute ischemic stroke" and "Neuroimaging of acute ischemic stroke" and "Antithrombotic treatment of acute ischemic stroke and transient ischemic attack".)
SOURCE OF ISCHEMIA — The most common causes of posterior circulation large artery ischemia are atherosclerosis, embolism, and dissection. Dolichoectasia (elongation and tortuosity) of the vertebral and basilar arteries is another occasional cause.
●About one-third of posterior circulation strokes are caused by occlusive disease within the large neck and intracranial arteries, which are the vertebral arteries in the neck and the intracranial vertebral, basilar, and posterior cerebral arteries [1-4].
●The proximal portion of the vertebral artery in the neck is the most common location of atherosclerotic occlusive disease within the posterior circulation [1-5]. Atherosclerosis of the intracranial vertebral arteries and of the basilar artery is also common. (See "Intracranial large artery atherosclerosis".)
●Dissection of the extracranial and intracranial vertebral arteries is another frequent cause of ischemia within the posterior circulation.
●Unlike the vertebral and basilar arteries, atherosclerosis and dissection of the posterior cerebral arteries is not common. Most infarcts in the posterior cerebral artery territory are due to embolism from the heart, aorta, or vertebral arteries.
SUBCLAVIAN AND INNOMINATE ARTERIES — Atherostenotic lesions of the innominate and subclavian arteries do cause arm ischemia and transient ischemic attacks (TIAs) but seldom cause strokes. Because the vertebral arteries in the neck originate from the proximal subclavian arteries, disease of the subclavian or innominate arteries proximal to the vertebral artery origin can cause reduction of vertebral artery flow.
In the subclavian steal syndrome, obstruction of the proximal subclavian artery produces a low-pressure system within the ipsilateral vertebral artery and in blood vessels of the ipsilateral upper extremity. Blood from a higher-pressure system, the contralateral vertebral artery and basilar artery, is diverted and flows retrograde downward into the ipsilateral vertebral artery into the arm. (See "Subclavian steal syndrome", section on 'Clinical features' and "Subclavian steal syndrome", section on 'Symptoms'.)
Most often, subclavian artery disease is detected when patients with coronary or peripheral vascular occlusive disease are referred to ultrasound laboratories for noninvasive testing.
Most patients with subclavian artery disease are asymptomatic. The most frequent symptoms of subclavian artery disease relate to the ipsilateral arm and hand. Coolness, weakness, and pain on use of the arm are common.
Neurologic symptoms are uncommon unless there is accompanying carotid artery disease. Dizziness is by far the most common neurologic symptom of the subclavian steal syndrome, and usually has a spinning or vertiginous character. Diplopia, decreased vision, oscillopsia, and staggering all occur, but less frequently, often accompanying the dizziness. Attacks are brief and occasionally are brought on by exercising the ischemic arm. However, in most patients exercise of the ischemic limb does not provoke neurologic symptoms or signs. (See "Subclavian steal syndrome", section on 'Clinical features' and "Subclavian steal syndrome", section on 'Symptoms'.)
Innominate artery disease is much less common than subclavian artery disease [1,3,6]. When the innominate artery becomes stenotic or occluded, signs and symptoms of decreased carotid artery flow may also develop. Ipsilateral monocular visual loss, ipsilateral cerebral hemisphere ischemia in the territories of the anterior and middle cerebral arteries, ipsilateral arm ischemia, and ischemic symptoms referable to the distal portion of the posterior circulation and/or the cerebellum may be due to innominate artery disease.
Takayasu's disease and giant cell (temporal) arteritis can cause subclavian and innominate artery occlusive disease. Young women who smoke cigarettes and take oral contraceptives may develop occlusive disease of the aortic arch vessels that mimics Takayasu's disease, except that it is not inflammatory. (See "Clinical features and diagnosis of Takayasu arteritis" and "Clinical manifestations of giant cell (temporal) arteritis".)
EXTRACRANIAL VERTEBRAL ARTERIES — The vast majority of occlusive lesions of the proximal vertebral arteries are atherosclerotic. Among a series of 100 patients with angiographically documented vertebral artery lesions, 92 percent were atherosclerotic in origin . The most common location of atherosclerotic occlusive disease within the posterior circulation is the proximal portion of the vertebral artery in the neck [1-5]. Atherosclerotic plaques may begin in the subclavian artery and extend into the ostia of the proximal extracranial vertebral arteries (ECVAs), or begin within the most proximal portion of the ECVAs. Occlusions most often occur within the first inch of the ECVAs. In contrast, atherosclerotic disease rarely involves the more distal ECVAs within the cervical spine or near the penetration of the arteries into the skull (figure 1).
Another common cause of posterior circulation stroke is arterial dissection, which usually involves the ECVA just before it enters the foramen transversarium at C5 or C6, or in the very distal part of the artery in the neck before it penetrates the dura mater to enter the cranial cavity.
CT angiography can show occlusive lesions at the origin of the vertebral arteries from the subclavian arteries as well as dissections. MR angiography often does not show the origins of the vertebral arteries well.
Proximal vertebral artery disease can cause sudden-onset strokes or transient ischemic attacks (TIAs). The most frequently reported symptom during TIAs is dizziness. These vertebral artery TIAs are indistinguishable from those described by patients with subclavian steal, except that vertebral artery TIAs are not precipitated by effort or by arm exertion.
Although dizziness is the most common symptom, it is seldom the only neurologic symptom. Usually, in at least some attacks, dizziness is accompanied by other signs of hindbrain ischemia. Diplopia, oscillopsia, weakness of both legs, hemiparesis, and numbness are often reported.
In patients with proximal ECVA disease, a bruit can often be heard over the supraclavicular region when auscultation is performed by moving the stethoscope bell over the posterior cervical muscles and the mastoid. Sometimes a bruit may be heard over the vertebral artery contralateral to the side of the stenotic vertebral artery because of increased collateral blood flow.
Artery to artery embolism and low flow — Embolization of white platelet-fibrin and red erythrocyte-fibrin thrombi from atherostenotic occlusive lesions is the most common presentation of extracranial vertebral artery (ECVA) origin disease [1-5,8]. The intraarterial emboli travel from the ECVA origin to reach the ipsilateral intracranial vertebral artery (ICVA), and sometimes travel on to block the rostral basilar artery and/or its branches. In support of this observation, patients presenting with ischemia in the distribution of the ICVA (the medulla and posterior inferior cerebellum) or the distal basilar artery (superior cerebellum, occipital and temporal lobes in the territory of the posterior cerebral arteries, or the thalamus or midbrain) show a high frequency of recent ECVA occlusions [1,3-5].
A situation analogous to that of ECVA origin disease is well known in the anterior circulation, where atherosclerotic disease of the internal carotid artery origin can cause distal ischemia by artery to artery embolization. As an example, it is not uncommon that a patient with a small, middle cerebral artery territory infarct is found to have an occlusion at the internal carotid artery origin by ultrasound or angiography. In most of these cases, it is likely that a recently formed occlusive thrombus in the internal carotid artery fragmented and embolized distally, causing the middle cerebral artery territory stroke.
In patients with proximal ECVA stenosis, intraarterial (artery to artery) embolism is a much more frequent cause of ischemia to the intracranial posterior circulation arteries than hemodynamic insufficiency (ie, low flow). This point is illustrated by results from the New England Medical Center Posterior Circulation Registry, which evaluated a series of 407 patients who had posterior circulation TIAs or strokes within the prior six months and included 80 patients with severe stenosis or occlusion of the proximal ECVA . In 45 (56 percent) of these 80 patients, embolization from the vertebral artery lesion was the most likely cause of brain ischemia . Only 13 patients (16 percent) had hemodynamic-related TIAs, and 12 of these 13 had severe bilateral vertebral artery occlusive disease. The only patient with unilateral vertebral artery disease had bilateral internal carotid artery occlusions.
Dissection and other causes — Dissection of the extracranial vertebral artery (ECVA) usually involves the distal portion of the ECVA as it winds around the upper cervical vertebrae . Sometimes dissections involve the proximal ECVA between the origin of the artery and its entry into the vertebral column, usually at C5 or C6. Pain in the neck and/or occiput and TIAs or strokes involving the lateral medulla and cerebellum are the most common findings. (See "Spontaneous cerebral and cervical artery dissection: Clinical features and diagnosis", section on 'Clinical features'.)
Ischemic symptoms due to ECVA dissection are most often vestibulocerebellar and include dizziness, vertigo, veering to one side, and loss of balance. When infarcts develop, they usually involve the inferior portion of the cerebellum, causing gait ataxia. Less common, are emboli to the distal posterior circulation, especially the posterior cerebral artery territories, causing a hemianopia. Occasionally cervical root pain and signs, and spinal cord ischemia can develop.
In older patients, giant cell arteritis is an occasional cause of occlusive disease involving the distal extracranial vertebral artery just before it penetrates the dura to become intracranial. (See "Clinical manifestations of giant cell (temporal) arteritis".)
Rotational vertebral artery occlusion is an uncommon cause of transient posterior circulation ischemic symptoms, mainly paroxysmal vertigo or nonspecific dizziness, which may be accompanied by nystagmus, tinnitus, syncope, blurred vision, nausea, or vomiting [10,11]. The nystagmus typically has a prominent downbeat component, but may also include torsional and horizontal components . The symptoms are due to dynamic compression of one (dominant) vertebral artery by bony elements of the cervical spine, triggered by head turning to one side, or less often by head turning to both sides or head tilting [10,11]. In most reported cases, there is associated hypoplasia or stenosis of the other vertebral artery. The symptoms are relieved by returning the head to the neutral position. Few if any cases result in infarction with permanent neurologic deficits from this mechanism. (See "Pathophysiology, etiology, and differential diagnosis of vertigo", section on 'Rotational vertebral artery syndrome'.)
INTRACRANIAL VERTEBRAL ARTERIES — Atherostenotic disease can involve any portion of the intracranial vertebral arteries (ICVA) (figure 2). The most common location of ICVA stenosis is the distal portion of the artery at or near the vertebral-basilar artery junction. Another common site of ICVA stenosis is the proximal portion of the vertebral artery just after dural penetration and before giving off the posterior inferior cerebellar artery (PICA) branch. Dissection of the ICVA also occurs, and ischemic symptoms are usually accompanied by prominent headache . ICVA dissections often extend into the basilar artery.
Occlusive ICVA disease presents in a variety of different ways [4,14,15]:
●TIAs, usually including vestibulocerebellar symptoms or elements of the lateral medullary syndrome
●Lateral medullary infarcts
●Medial medullary infarction
●Infarction of one-half of the medulla (hemimedullary infarction) including the lateral and medial medulla on one side
●Cerebellar infarction in PICA territory
●Embolization of the ICVA thrombus to the distal basilar artery and its branches causing TIAs and/or strokes
●Propagation of the ICVA thrombus into the basilar artery causing a basilar artery syndrome
Lateral medullary infarction — Lateral medullary infarction (Wallenberg syndrome) is the most common and important syndrome related to intracranial vertebral artery occlusion (figure 3) [4,15]. The diagnosis is often missed by non-neurologists, and so the features are very important to know and understand.
Vestibulocerebellar symptoms and signs — Vestibulocerebellar symptoms and signs are nearly always present in patients with lateral medullary infarcts . These are related to involvement of the vestibular nuclei and their connections, and to involvement of the inferior cerebellar peduncle (restiform body). Common symptoms and signs are as follows:
●Feeling dizzy or off-balance, which may take a number of forms:
•Turning, rotating, whirling or moving in relation to the environment
•Being pulled or falling towards one side, most often ipsilateral to the lesion
•Swaying or rolling as if moving from side to side
•Tilting or leaning
●Difficulty sitting upright without support. Patients topple, lean, or veer to the ipsilateral side when they sit or stand. In many, standing or walking is impossible during the acute period without support. When they regain the ability to walk, patients often feel as if they are being pulled to the side of the lesion. They veer, list, or weave to the side, especially on turns.
●Hypotonia of the ipsilateral arm. This cerebellar sign can be demonstrated by having the patient quickly lower or raise the outstretched hands together, braking the ascent and descent suddenly. The symptomatic arm on the side ipsilateral to the infarct often overshoots and is not as quickly braked compared with the normal contralateral arm. In some patients, the ipsilateral arm also makes a slower ascent or descent.
●Blurred vision or diplopia. Some also describe oscillopsia, which is the appearance that objects in the visual field are in rhythmic motion or oscillation. Less common is tilting or inversion of the visual environment.
●Nystagmus. This is nearly always present, especially in patients who describe dizziness or vertigo. The nystagmus usually has both horizontal and rotational components. The rapid phase of the rotatory nystagmus usually moves the upper border of the iris towards the side of the lesion. Most often, larger amplitude, slower nystagmus is present on gaze to the side of the lesion, while smaller amplitude, quick nystagmus is found on gaze directed to the contralateral side.
●Ocular torsion. The eye and ear ipsilateral to the lateral medullary infarct may rest in a down position below the contralateral eye and ear . At times, ocular torsion is accompanied by a head tilt and skew deviation with the ipsilateral eye positioned downward. This combination of findings is referred to as the ocular tilt reaction [4,17,18].
●Limb ataxia ipsilateral to the lateral medullary infarct. Some patients cannot feed themselves using the ataxic arm. They overshoot targets and have difficulty pointing accurately to moving targets.
Sensory symptoms and signs — Sensory symptoms and signs are common in patients with lateral medullary infarcts.
●Pain or unpleasant feelings in the face are sometimes the earliest and most prominent feature of the lateral medullary syndrome and are diagnostic of a lateral tegmental brainstem localization. These are related to lesions of the spinal nucleus of V and the descending spinal tract of V. The facial pain is usually described as sharp jolts or stabs of pain most often in the ipsilateral eye or face. Sometimes pain persists and is limited to the forehead and frontal scalp region. At times, the abnormal sensation is described as hot, burning, or scalding.
●Loss of pain and temperature sensation in the contralateral trunk and limbs is related to lesions of the lateral medullary spinothalamic tract.
●The most common pattern of sensory abnormality with lateral medullary infarcts is loss of pain and temperature sensation in the ipsilateral face and the contralateral trunk and limbs. The next most frequent combination is hypalgesia in the ipsilateral face and contralateral face, trunk, and limbs. Less often, the hypalgesia can be solely contralateral, involving the face, arm, and leg, or sometimes only the face and arm [4,19]. The least common pattern of sensory loss is hypalgesia only involving the contralateral trunk, arm, and leg or parts thereof.
●Examination usually shows ipsilateral decreased pain and temperature sensation in the face. The corneal reflex is usually reduced in the ipsilateral eye. Although contralateral loss of pain and thermal sensation involving the body and limbs is usually found on examination, most patients with contralateral hypalgesia are unaware of their sensory loss until they are tested. However, some do notice loss of thermal sensation when they touch hot or cold objects with their contralateral upper and/or lower limbs.
Bulbar muscle weakness — Weakness of bulbar muscles innervated by the lower cranial nerves is a very prominent feature when lateral medullary infarcts extend medially. Usually, the abnormality is unilateral.
●Involvement of the nucleus ambiguus causes paralysis of the ipsilateral palate, pharynx, and larynx, resulting in hoarseness and dysphagia. Oropharyngeal muscle paralysis results in food being trapped in the piriform recess of the pharynx. Food and secretions have relatively free access into the air passages. Patients try to extricate the food with a cough or throat-clearing maneuver, which makes a characteristic crowing-like sound.
●Examination shows paralysis of the ipsilateral vocal cord and a lack of elevation of the ipsilateral palate on phonation. The uvula often deviates to the side contralateral to the lateral medullary infarct. Dysarthria and dysphonia are common. In some patients, dysphagia and aspiration are prominent.
●Aspiration and pneumonia are very important complications of abnormal pharyngeal function. Hiccups are also a relatively common and annoying complaint.
Respiratory dysfunction — Respiratory dysfunction is an important feature of lateral medullary ischemia. Control of inspiration and expiration and their automaticity lies within the ventrolateral medullary tegmentum and the medullary reticular zone.
The most common abnormality described in patients with lateral tegmental caudal brainstem lesions is failure of automatic respirations, a phenomenon especially apparent during sleep. This failure to initiate respiration has been referred to as Ondine's curse. (See "Disorders of ventilatory control", section on 'Ondine's curse'.)
Autonomic dysfunction — Autonomic dysfunction may occur in lateral medullary infarction.
●The ipsilateral eye often shows features of Horner's syndrome due to lesions of the descending sympathetic nervous system. (See "Horner's syndrome".)
●Cardiovascular abnormalities include tachycardia, orthostatic hypotension without cardiac rate acceleration, and intermittent bradycardia . Some patients have labile blood pressures, tachycardia, unusual sweating, and arrhythmias. The anatomic basis is thought to be involvement of the dorsal motor nucleus of the vagus nerve.
Medial medullary infarction — The most consistent finding in patients with medial medullary ischemia is a contralateral hemiparesis [4,20]. Usually the hemiparesis is complete and flaccid at onset. Later, increased tone and spasticity develop. In approximately one-half of patients, the face is also involved. Facial weakness, when it occurs, is usually slight and transient and rarely persists.
Sensory symptoms are related to ischemia of the medial lemniscus. Some patients report paresthesias or, less commonly, dysesthesias in the contralateral lower limb and trunk. Less often, sensory symptoms occur in the arm and hand. In many patients with sensory symptoms there are no objective signs of touch, vibration, or position sense loss. Proprioceptive dysfunction, with slight loss of position and vibration sense in the contralateral foot, is found in some patients.
Ipsilateral tongue paralysis is the least common but most topographically localizing sign of medial medullary infarction, and is due to involvement of the hypoglossal nucleus. Tongue paresis causes slurring of speech, especially of lingual consonants.
Hemimedullary infarction — Occasional patients have infarction that involves both the lateral and medial medullary territories on one side (hemimedullary infarcts). Symptoms are identical to those found in patients with lateral medullary ischemia with the addition of a hemiparesis contralateral to the lesion. The hemiparesis may develop concurrently with lateral medullary symptoms and signs or can occur later. (See 'Lateral medullary infarction' above and 'Medial medullary infarction' above.)
Cerebellar infarction — Cerebellar infarction in posterior inferior cerebellar artery (PICA) distribution can involve just the vermis, or the lateral surface, or the full PICA territory (figure 4). Full PICA territory infarcts are often accompanied by edema formation and mass effect (so-called pseudotumoral cerebellar infarcts). (See 'Pseudotumoral cerebellar infarction' below.)
Approximately one-fifth of PICA territory cerebellar infarcts are accompanied by infarction in the dorsal or dorsolateral medulla [3,4]. The combination of lateral medullary and PICA cerebellar infarction occurs when the intracranial vertebral artery (ICVA) is occluded and blocks the orifice of both PICA and the lateral medullary penetrators. Sometimes medial PICA territory infarcts are accompanied by dorsal medullary infarcts since the medial PICA branch has some supply to the dorsal medulla [4,21,22].
Infarcts limited to the medial vermis in medial PICA territory usually cause a vertiginous labyrinthian syndrome that closely mimics a peripheral vestibulopathy. Severe vertigo and prominent nystagmus are the major findings. Some patients also have truncal lateropulsion characterized by feelings of magnetic pulling of the trunk to the ipsilateral side.
Lateral cerebellar hemisphere PICA territory infarcts are usually characterized by minor degrees of dizziness and gait incoordination with veering to the side of the lesion. Minor limb hypotonia and incoordination are found. A common syndrome is acute unsteadiness with ataxia but without vertigo or dysarthria. Body sway towards the side of the lesion, ipsilateral limb ataxia, and abnormal rapid alternating movements are also common.
When the full PICA cerebellar territory is involved, headache is usually present in the occiput or high neck on the ipsilateral side. The head may also be tilted with the occiput tending to tilt toward the ipsilateral side.
Vomiting, gait ataxia, truncal lateropulsion, and limb incoordination are other common findings. The truncal dysfunction is similar to that found in the lateral medullary syndrome; the body is often tilted or pulled ipsilaterally upon sitting or standing. The limb incoordination consists mostly of hypotonia rather than a rhythmic intention tremor.
Pseudotumoral cerebellar infarction — The syndrome of pseudotumoral cerebellar infarction, with edema formation and mass effect, is most often associated with large full posterior inferior cerebellar artery (PICA) territory infarcts. After the first day or so, patients with this form of cerebellar infarction typically develop increased headache, vomiting, and decreased consciousness, with drowsiness followed by stupor. Bilateral Babinski signs are an early sign of cerebellar mass effect.
Characteristic oculomotor abnormalities of large cerebellar space-taking infarcts can develop and include the following features:
●Most common are a conjugate gaze paresis to the side of the lesion or a paresis of abduction limited to the ipsilateral eye
●Bilateral sixth nerve paresis may occur
●Later bilateral horizontal gaze palsies may develop, often accompanied by ocular bobbing
These signs are due to compression of the pontine tegmentum by the swollen cerebellar infarct. Stupor is followed by deep coma when the oculomotor abnormalities become bilateral.
Dolichoectasia — Dolichoectasia (dilatative arteriopathy) is a term that describes arterial elongation, widening, and tortuosity [23-27]. The intracranial vertebral and basilar arteries are most often affected. Dolichoectatic arteries are characterized by an abnormally large external diameter and a thin arterial wall that shows degeneration of the internal elastic lamina, and multiple gaps in the internal elastica. The media of dilated arteries becomes thin because of reticular fiber deficiency and smooth muscle atrophy.
The most important clinical presentations of dilatative arteriopathy are as follows:
●Acute brain ischemia
●A progressive course related to compression of cranial nerves, the brainstem, or the third ventricle
●A catastrophic outcome caused by vascular rupture
Flow in dilated arteries may become to-and-fro, causing reduced antegrade flow and thrombus formation. Elongation and angulation of arteries can stretch and distort the orifices of arterial branches leading to decreased blood flow, especially in penetrating branches. Dilated intracranial vertebral arteries can compress the medulla leading to the gradual onset of hemiparesis .
Distinguishing vertigo of brainstem and cerebellar ischemia from peripheral causes — A composite three-part test entitled HINTS (Head-Impulse-Nystagmus-Test of Skew) is useful for distinguishing brainstem and cerebellar ischemia from vestibular neuritis or other peripheral causes of vertigo [28-31]. The test is most helpful in patients who have had continuous feelings of vertigo or dizziness. It is not useful in patients with momentary position-related transient vertigo (often benign positional vertigo) or those with TIAs who are not dizzy when examined.
●Head Impulse – For the head impulse test, also called head thrust test (see "Evaluation of the patient with vertigo", section on 'Other vestibular signs'), the patient is instructed to fix their gaze on a distant target while wearing his or her usual prescription eyeglasses. The head is then turned quickly and unpredictably by the examiner, about 15º; the starting position should be about 10º from straight ahead. The normal response is that the eyes remain on the target (figure 5). The abnormal response is that the eyes are dragged off of the target by the head turn (in one direction), followed by a saccade back to the target after the head turn; this response indicates a deficient vestibulo-ocular on the side of the head turn, implying a peripheral vestibular lesion (ie, the inner ear or vestibular nerve) on that side. This reflex is preserved in central lesions, except when cranial nerve (CN) VIII fascicles are affected in the lateral pons.
●Nystagmus – Peripheral vestibular lesions often are accompanied by nystagmus that is always in the same direction (see "Evaluation of the patient with vertigo", section on 'Nystagmus'), while brainstem and cerebellar lesions are typically associated with nystagmus that changes direction with different positions of gaze.
●Test for Skew – The test involves covering one eye and seeing if there is a vertical shift in the eye when uncovered. Brainstem and cerebellar lesions sometimes cause a slight skew deviation.
Any of the following – whether present or untestable – suggest a brainstem or cerebellar lesion [28-31]:
●Normal head impulse test on both sides
The presence of all of the following suggests a peripheral lesion [28-31]:
●An abnormal head impulse test on one side
●Unidirectional horizontal>torsional nystagmus that increases in intensity with gaze toward the fast phase
The importance of these oculomotor tests is that brain imaging with either CT or MRI may be normal during the acute phase of ischemic symptoms. In this regard, the HINTS test appears to be more sensitive for the diagnosis of acute stroke than even brain MRI within the first two days after symptom onset .
One caveat is that there are rare examples of inner ear infarction (usually due to occlusion of the internal auditory artery, an anterior inferior cerebellar artery branch) causing an acute vestibular syndrome. These are typically associated with new hearing loss on the side of the vestibular lesion, which may be the only clue that the mechanism is stroke [30,31]. In such cases, the eye movements elicited on HINTS are indistinguishable from peripheral vestibular causes.
BASILAR ARTERY — The basilar artery begins at the medullopontine junction and ends at the junction of the pons and midbrain. Occlusive lesions may occur anywhere along the basilar artery . In addition, thrombi engrafted upon occlusive lesions within the distal intracranial vertebral artery (ICVA), for example, near or at the ICVA-basilar artery junction, can extend into the proximal basilar artery.
Basilar artery occlusive disease most often presents as ischemia in the pons. The major burden of ischemia is in the middle of the pons, mostly in the paramedian base, and often also in the paramedian tegmentum (picture 1). The reasons for this localization are as follows:
●The largest penetrating arteries supply the paramedian pons (figure 6) and arise directly from the basilar artery.
●The pontine tegmentum is supplied mostly by arteries that arise from the distal basilar artery. When the distal basilar artery remains patent, the tegmentum is relatively spared.
●Collateral circulation comes mainly from the ICVAs through their posterior inferior cerebellar artery (PICA) branches that anastomose with anterior inferior cerebellar artery (AICA) and superior cerebellar artery (SCA) branches; these course around the lateral aspect of the pons, supplying the lateral tegmental and basal structures in the pons (figure 4 and image 1).
The paramedian pontine base contains descending long motor tract and crossing cerebellar fibers. The paramedian tegmentum contains mostly oculomotor fibers. As a result, the predominant symptoms and signs in patients with basilar artery occlusive disease are motor and oculomotor. Sensory and vestibular nuclei and tracts located in the lateral tegmentum are relatively spared.
Alteration in the level of consciousness is an important sign in patients with basilar artery occlusion. They may present with coma when the bilateral medial pontine tegmentum is ischemic.
Motor symptoms and signs — Most patients with symptomatic basilar artery occlusive disease and pontine ischemia have some transient or persistent degree of paresis and corticospinal tract abnormalities [3,4,14,33-36]. The initial motor weakness is often lateralized and has been referred to as the "herald hemiparesis" of basilar artery occlusion.
Hemiparetic patients with basilar artery occlusion almost always show some motor or reflex abnormalities on the nonhemiparetic side. As examples, slight weakness, hyperreflexia, an extensor plantar reflex, or abnormal spontaneous movements such as shivering, twitching, shaking, or jerking may be present on the relatively spared side. Asymmetry but bilaterality is the rule.
Adventitious movements of the arms and/or legs are occasionally seen and can be prominent. These movements are variable and sometimes intermittent. Small movements may resemble fasciculations. Larger movements may resemble shivering, shuddering, or jerking; another variant is that of tremulous shaking. Voluntary or passive limb movements or painful stimuli may precipitate a flurry of abnormal movements. At times there are large repetitive jerking and twitching movements, especially in limbs contralateral to a hemiparesis. These movements are often misdiagnosed as seizures .
Incoordination of limb movements is another common motor finding. Ataxia is invariably combined with some degree of weakness. Incoordination is usually more severe in the legs. Toe-to-object and heel-to-shin testing usually shows clumsiness and diminished coordination due to cerebellar dysfunction. The ataxia is invariably bilateral but may be asymmetric and more severe on the weaker side. Intention tremor is not common.
Bulbar involvement — Weakness of bulbar muscles is very common and is an important cause of morbidity with pontine infarction due to basilar occlusive disease. Bulbar symptoms include facial weakness, dysphonia, dysarthria, dysphagia, and limited jaw movements. The face, pharynx, larynx, and tongue are most often involved. The pattern may be that of crossed motor loss, such as weakness involving one side of the face and the contralateral body, but more often the bulbar muscle weakness is bilateral.
Some patients totally lose the ability to speak, open their mouth, protrude their tongue, swallow, or move their face at will or on command. Secretions pool in the pharynx; and aspiration is an important and serious complication. When all voluntary movements other than the eyes are lost but consciousness is retained, the deficit is referred to as the "locked-in syndrome." (See "Locked-in syndrome".).
Patients with infarction of the pontine base frequently have exaggerated crying and laughing spells and are hypersensitive to emotional stimulus, a condition known as pseudobulbar affect or emotional lability.
Despite the loss of volitional muscle movement, reflexes of the jaw, face, and pharynx may be exaggerated. In addition, clonic jaw movements or clamping down on a tongue blade may occur as a response to attempts to pry the mouth open and to insert a tongue blade.
Some patients with pontine ischemia develop palatal myoclonus (a rhythmic involuntary jerking movement of the soft palate and pharyngopalatine arch) that can involve the diaphragm and larynx. This movement disorder usually begins sometime after the brainstem infarct. The movements of the palate vary in rate between 40 and 200 beats per minute. The movements are readily seen by watching the palate and pharynx when the mouth is open. The movements involve the eustachian tube and make a click that the patient and clinician can hear.
Oculomotor symptoms and signs — Oculomotor symptoms and signs are common with symptomatic basilar artery occlusive disease and pontine ischemia, and few patients with this condition have normal eye movements. Abnormalities include:
●Complete bilateral horizontal gaze palsy
●Unilateral horizontal conjugate gaze palsy
●Unilateral or bilateral internuclear ophthalmoplegia (INO)
●One-and-a-half syndrome (a conjugate gaze palsy combined with an INO)
Skew deviation of the eyes and ocular bobbing may also be present. Horizontal, gaze-paretic nystagmus is common and, when asymmetric, usually is more prominent when gaze is directed to the side of a unilateral pontine tegmental lesion. Dissociated nystagmus, that is nystagmus that is more severe in one eye and not rhythmically concordant in the two eyes, and vertical nystagmus are found in patients with an INO. (See "Internuclear ophthalmoparesis".) Ptosis of the upper eyelids is also very frequent.
The pupils may remain normal or become small. In some patients, the pupils are bilaterally very small ("pinpoint"). Use of a magnifying glass can show that, despite their very small size, the pupillary response to light is preserved, although the amplitude of the response is slight.
Sensory symptoms and signs — Somatosensory abnormalities are generally not prominent in patients with basilar artery occlusions. Paresthesias on one side of the body and limbs reflect involvement of the contralateral medial lemniscus in the paramedian dorsal portion of the basis pontis. Bilateral paramedian lesions that include the medial lemnisci on both sides can cause bilateral paresthesias. Proprioceptive loss is usually minimal or absent despite the paresthesias.
Some patients with basilar artery occlusive disease have unusual burning pain in the face usually located in the center of the face near the midline. Tinnitus and hearing loss relate to involvement of the central auditory tracts and nuclei (auditory nuclei, lateral lemnisci, trapezoid bodies, inferior colliculi) or to ischemia of the eighth nerves or the cochlea.
ROSTRAL BRAINSTEM ISCHEMIA AND "TOP OF THE BASILAR" SYNDROME — Occlusion of the rostral portion of the basilar artery (the "top of the basilar") can cause ischemia of the midbrain, thalami, and temporal and occipital lobe hemispheral territories supplied by the posterior cerebral artery branches of the basilar artery.
In most patients, infarction in this region – the top of the basilar – is caused by embolism from a more proximal source such as the heart, the aorta, the vertebral arteries in the neck, or the intracranial vertebral arteries. Less commonly, the syndrome is caused by intrinsic occlusive disease of the rostral portion of the basilar artery. In many patients infarction is limited to the rostral brainstem.
The major abnormalities associated with rostral brainstem infarction involve alertness, behavior, memory, and oculomotor and pupillary functions.
Oculomotor and pupillary abnormalities — The most common abnormalities of eye position and movement involve vertical gaze and convergence [3,38,39]. Some patients lose all voluntary and reflex vertical eye movements. Reflex movements are sometimes preserved despite loss of voluntary vertical eye movements. Either upgaze or downgaze can be selectively involved, but in most patients both directions of vertical gaze are involved. Upgaze and vertical gaze palsies are more common than downgaze palsies.
Asymmetric or unilateral lesions in the midbrain tegmentum and posterior thalami can cause ocular tilt reactions in which the contralateral eye and ear are down. Other abnormalities include skew deviation, ocular torsion, and abnormal estimation of the visual vertical .
Convergence abnormalities are also very common. Usually one or both eyes are hyperconverged. One or both eyes may rest inward or down and in at rest. On attempted upgaze, the eyes may show adductor contractions, causing convergence movements.
A rostral mesencephalic lesion near the level of the posterior commissure can cause pathologic retraction of the upper eyelid with widening of the palpebral fissure (Collier sign). In some patients, both lids are retracted but one eye may have a normal lid position or ptosis.
Lesions in the rostral brainstem also often affect the pupillary light reflex so that the pupils react slowly and incompletely, or not at all, to light. In patients with diencephalic lesions, the pupils are often small at rest, and may be fixed and dilated if the lesions involve the third nerve Edinger-Westphal nuclei. A combination of diencephalic and midbrain lesions may cause mid-position fixed pupils.
The constellation of neuroophthalmologic findings seen with midbrain (pretectal) lesions has been called Parinaud syndrome (table 1).
Altered alertness, behavior, and memory — Abnormalities of alertness and behavior are common in patients with rostral brainstem infarcts . Hypersomnolence and abulia are common. Patients may answer queries with replies that have no relation to reality. The patient may mislocate themselves in place, reporting that they are in a distant geographical location, and in the personal time dimension, saying that they are presently performing activities that they had actually done in childhood, adolescence, or much earlier in adult life.
Thalamic or midbrain injury that "straddles the peduncles" can lead to peduncular hallucinations. These are predominantly visual, but there may be some minor tactile and auditory components. Visual hallucinations are often quite vivid and contain colors, objects, and scenes. The hallucinations occur predominantly after sundown [3,38]. (See "Approach to the patient with visual hallucinations", section on 'Peduncular hallucinosis'.)
Prominent and sometimes persistent memory deficits may develop with rostral brainstem infarcts that include the thalamus. The amnesia involves both anterograde and retrograde memory and usually includes both verbal and nonverbal memory.
Other findings — Sensory and motor abnormalities are usually absent in patients with top of the basilar infarction. Movement disorders, especially hemiballism, have been described in some patients with small infarcts and hemorrhages involving the subthalamic nuclei, but hemiballism is rare in patients with well-documented "top of the basilar" infarcts.
The superior portion of the cerebellum may also be infarcted, since the superior cerebellar arteries branch from the distal end of the basilar artery. Common symptoms are slight dizziness, vomiting, ipsilateral limb dysmetria, gait ataxia, and dysarthria. Vertigo is usually not prominent. Limb incoordination, intention tremor, and dysarthria are more common with superior cerebellar artery territory infarcts than with infarcts involving the territory of other cerebellar arteries.
POSTERIOR CEREBRAL ARTERIES — Most posterior cerebral artery (PCA) territory infarcts are due to embolism from the heart, aorta, or vertebral arteries. Atherosclerosis and dissection of the PCAs is not common.
Visual loss — The most frequent finding in patients with PCA territory infarction is a hemianopia [1-4,40-42]. At times, the central or medial part of the field is spared, so-called macular sparing. A superior quadrant field defect results if the infarct involves just the lower bank of the calcarine fissure (the lingual gyrus). An inferior quadrantanopia results if the lesion affects the cuneus on the upper bank of the calcarine fissure. (See "Homonymous hemianopia".)
When the full PCA territory is involved, visual neglect can accompany the hemianopia. However, patients are aware of the visual defect when infarcts are restricted to the striate cortex and do not extend into the adjacent parietal cortex. The visual defect is often described as a void, blackness, or a limitation of vision to one side, and patients usually recognize that they must focus extra attention to the hemianopic field. When given written material or pictures, patients with hemianopia due to occipital lobe infarction are able to see and interpret stimuli normally, although it may take somewhat longer to explore the hemianopic visual field.
Clinicians can reliably map out the visual fields by confrontation in patients with occipital lobe infarcts. Optokinetic nystagmus is preserved. Some patients, although they accurately report motion or the presence of objects in their hemianopic field, cannot identify the nature, location, or color of those objects.
Sensory and motor abnormalities — In patients with PCA territory ischemia, lateral thalamic infarction is the major reason for somatosensory symptoms and signs . Patients describe paresthesias or numbness in the face, limbs, and trunk. On examination, touch, pinprick, and position sense are reduced.
The combination of hemisensory loss and hemianopia without paralysis is virtually diagnostic of infarction in the PCA territory. The occlusive lesion is within the PCA before the thalamogeniculate branches to the lateral thalamus. Rarely, occlusion of the proximal portion of the PCA causes a hemiplegia, which is probably due to infarction in the lateral midbrain [3,44-46]. Involvement of the corticospinal and/or corticobulbar tracts in the cerebral peduncles is thought to cause hemiplegia in these cases.
Left PCA territory symptoms and signs — When the left PCA territory is infarcted, alexia without agraphia [47-50], anomic aphasia or transcortical sensory aphasia , and Gerstmann syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation) may be found [3,47].
Defective acquisition of new memories is common when both medial temporal lobes are damaged but also occurs in lesions limited to the left temporal lobe [3,47,52,53]. The memory deficit in patients with unilateral lesions is usually not permanent but may last up to six months. Patients cannot recall what has happened recently and, when given new information, they do not recall it moments later. They often repeat statements and questions spoken only minutes before.
Some patients with left PCA territory infarction have difficulty in understanding the nature and use of objects presented visually (associative visual agnosia) [47,50]. They can trace with their fingers and copy objects, demonstrating that visual perception is preserved; they can name objects presented in their hand and explored by touch or when verbally described.
Right PCA territory symptoms and signs — Infarcts of the right PCA territory are often accompanied by prosopagnosia, which is difficulty in recognizing familiar faces [50,54]. Disorientation to place and an inability to recall routes or to read or visualize the location of places on maps are also common . Patients with right occipitotemporal infarcts also may have difficulty visualizing what a given object or person look like. Dreams may be devoid of visual imagery.
Visual neglect is much more common after lesions of the right than of the left PCA territory.
●The most common causes of posterior circulation large artery ischemia are atherosclerosis, embolism, and dissection. Dolichoectasia (elongation and tortuosity) of the vertebral and basilar arteries is another occasional cause. (See 'Source of ischemia' above.)
●Atherostenotic lesions of the innominate and subclavian arteries cause arm ischemia and transient ischemic attacks but seldom cause strokes. (See 'Subclavian and innominate arteries' above.)
●The vast majority of occlusive lesions of the proximal vertebral arteries are atherosclerotic. The most common location of atherosclerotic occlusive disease within the posterior circulation is the proximal portion of the vertebral artery in the neck (figure 1). In patients with proximal extracranial vertebral artery (ECVA) stenosis, intraarterial (artery-to-artery) embolism to the intracranial posterior circulation is a much more frequent cause of ischemia arteries than hemodynamic insufficiency (ie, low flow). The most frequently reported symptom during TIAs is dizziness. Diplopia, oscillopsia, bilateral leg weakness, hemiparesis, and numbness are often reported. Patients presenting with ischemia in the distribution of the intracranial vertebral arteries (the medulla and posterior inferior cerebellum) or the distal basilar artery (superior cerebellum, occipital and temporal lobes in the territory of the posterior cerebral arteries, or the thalamus or midbrain) show a high frequency of recent ECVA occlusions. Dissection of the ECVA usually involves the distal portion of the ECVA as it winds around the upper cervical vertebrae. (See 'Extracranial vertebral arteries' above.)
●Atherostenotic disease can involve any portion of the intracranial vertebral arteries (ICVA) (figure 2). Occlusive ICVA disease presents in a variety of different ways (see 'Intracranial vertebral arteries' above):
•TIAs, usually including vestibulocerebellar symptoms or elements of the lateral medullary syndrome
•Lateral medullary infarcts (see 'Lateral medullary infarction' above)
•Medial medullary infarction (see 'Medial medullary infarction' above)
•Infarction of one-half of the medulla including the lateral and medial medulla on one side (see 'Hemimedullary infarction' above)
•Cerebellar infarction in posterior inferior cerebellar artery territory (see 'Cerebellar infarction' above)
•Embolization of the ICVA thrombus to the distal basilar artery and its branches causing TIAs and/or strokes
•Propagation of the ICVA thrombus into the basilar artery causing a basilar artery syndrome
●Basilar artery occlusive disease most often presents as ischemia in the pons. The major burden of ischemia is in the middle of the pons, mostly in the paramedian base, and often also in the paramedian tegmentum (picture 1). Most patients with symptomatic basilar artery occlusive disease and pontine ischemia have some transient or persistent degree of paresis and corticospinal tract abnormalities. Bulbar symptoms include facial weakness, dysphonia, dysarthria, dysphagia, and limited jaw movements. Oculomotor symptoms and signs are common. (See 'Basilar artery' above.)
●Occlusion of the rostral portion of the basilar artery (the "top of the basilar") can cause ischemia of the midbrain, thalami, and temporal and occipital lobe hemispheral territories supplied by the posterior cerebral artery branches of the basilar artery. Infarction in this region is typically caused by embolism from a more proximal source such as the heart, the aorta, the vertebral arteries in the neck, or the intracranial vertebral arteries. Less commonly, the syndrome is caused by intrinsic occlusive disease of the rostral portion of the basilar artery. The major abnormalities associated with rostral brainstem infarction involve alertness, behavior, memory, and oculomotor and pupillary functions. (See 'Rostral brainstem ischemia and "top of the basilar" syndrome' above.)
●Most posterior cerebral artery (PCA) territory infarcts are due to embolism from the heart, aorta, or vertebral arteries. Atherosclerosis and dissection of the PCAs is not common. The most frequent finding in patients with PCA territory infarction is a hemianopia. Lateral thalamic infarction is the major reason for somatosensory symptoms and signs. Additional neurologic syndromes found with infarction of the left PCA territory include alexia without agraphia, anomic aphasia or transcortical sensory aphasia, and Gerstmann syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation). Syndromes observed with right PCA territory infarction include prosopagnosia, which is difficulty in recognizing familiar faces, spatial disorientation, and visual neglect. (See 'Posterior cerebral arteries' above.)
- Caplan LR, Wityk RJ, Glass TA, et al. New England Medical Center Posterior Circulation registry. Ann Neurol 2004; 56:389.
- Savitz SI, Caplan LR. Vertebrobasilar disease. N Engl J Med 2005; 352:2618.
- Caplan LR. Posterior Circulation Disease: clinical findings, diagnosis, and management, Blackwell Science, Boston 1996.
- Caplan L. Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000. Stroke 2000; 31:2011.
- Wityk RJ, Chang HM, Rosengart A, et al. Proximal extracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol 1998; 55:470.
- Brewster DC, Moncure AC, Darling RC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985; 2:99.
- Labauge R, Boukobza M, Pagès M, et al. [Occlusion of the vertebral artery (100 personal cases)]. Rev Neurol (Paris) 1987; 143:490.
- Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology 1992; 42:1505.
- Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol 2008; 4:34.
- Rosengart A, Hedges TR 3rd, Teal PA, et al. Intermittent downbeat nystagmus due to vertebral artery compression. Neurology 1993; 43:216.
- Choi KD, Choi JH, Kim JS, et al. Rotational vertebral artery occlusion: mechanisms and long-term outcome. Stroke 2013; 44:1817.
- Choi KD, Shin HY, Kim JS, et al. Rotational vertebral artery syndrome: oculographic analysis of nystagmus. Neurology 2005; 65:1287.
- Caplan LR, Baquis GD, Pessin MS, et al. Dissection of the intracranial vertebral artery. Neurology 1988; 38:868.
- Searls DE, Pazdera L, Korbel E, et al. Symptoms and signs of posterior circulation ischemia in the new England medical center posterior circulation registry. Arch Neurol 2012; 69:346.
- Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain 2003; 126:1864.
- Morrow MJ, Sharpe JA. Torsional nystagmus in the lateral medullary syndrome. Ann Neurol 1988; 24:390.
- Brandt T, Dieterich M. Vestibular syndromes in the roll plane: topographic diagnosis from brainstem to cortex. Ann Neurol 1994; 36:337.
- Keane JR. Ocular tilt reaction following lateral pontomedullary infarction. Neurology 1992; 42:259.
- Matsumoto S, Okuda B, Imai T, Kameyama M. A sensory level on the trunk in lower lateral brainstem lesions. Neurology 1988; 38:1515.
- Tyler KL, Sandberg E, Baum KF. Medical medullary syndrome and meningovascular syphilis: a case report in an HIV-infected man and a review of the literature. Neurology 1994; 44:2231.
- Amarenco P, Hauw JJ. [Anatomy of the cerebellar arteries]. Rev Neurol (Paris) 1989; 145:267.
- Amarenco P, Hauw JJ, Hénin D, et al. [Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases]. Rev Neurol (Paris) 1989; 145:277.
- Passero S, Filosomi G. Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998; 29:653.
- Pico F, Labreuche J, Seilhean D, et al. Association of small-vessel disease with dilatative arteriopathy of the brain: neuropathologic evidence. Stroke 2007; 38:1197.
- Passero SG, Rossi S. Natural history of vertebrobasilar dolichoectasia. Neurology 2008; 70:66.
- Savitz SI, Ronthal M, Caplan LR. Vertebral artery compression of the medulla. Arch Neurol 2006; 63:234.
- Lou M, Caplan LR. Vertebrobasilar dilatative arteriopathy (dolichoectasia). Ann N Y Acad Sci 2010; 1184:121.
- Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology 2008; 70:2378.
- Kattah JC, Talkad AV, Wang DZ, et al. HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke 2009; 40:3504.
- Tarnutzer AA, Berkowitz AL, Robinson KA, et al. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ 2011; 183:E571.
- Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med 2013; 20:986.
- Pessin MS, Gorelick PB, Kwan ES, Caplan LR. Basilar artery stenosis: middle and distal segments. Neurology 1987; 37:1742.
- KUBIK CS, ADAMS RD. Occlusion of the basilar artery; a clinical and pathological study. Brain 1946; 69:73.
- Labauge R, Pages M, Marty-Double C, et al. [Occlusion of the basilar artery. A review with 17 personal cases (author's transl)]. Rev Neurol (Paris) 1981; 137:545.
- Ferbert A, Brückmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke 1990; 21:1135.
- Voetsch B, DeWitt LD, Pessin MS, Caplan LR. Basilar artery occlusive disease in the New England Medical Center Posterior Circulation Registry. Arch Neurol 2004; 61:496.
- Ropper AH. 'Convulsions' in basilar artery occlusion. Neurology 1988; 38:1500.
- Caplan LR. "Top of the basilar" syndrome. Neurology 1980; 30:72.
- Mehler MF. The neuro-ophthalmologic spectrum of the rostral basilar artery syndrome. Arch Neurol 1988; 45:966.
- Pessin MS, Lathi ES, Cohen MB, et al. Clinical features and mechanism of occipital infarction. Ann Neurol 1987; 21:290.
- Fisher CM. The posterior cerebral artery syndrome. Can J Neurol Sci 1986; 13:232.
- Yamamoto Y, Georgiadis AL, Chang HM, Caplan LR. Posterior cerebral artery territory infarcts in the New England Medical Center Posterior Circulation Registry. Arch Neurol 1999; 56:824.
- Georgiadis AL, Yamamoto Y, Kwan ES, et al. Anatomy of sensory findings in patients with posterior cerebral artery territory infarction. Arch Neurol 1999; 56:835.
- Hommel M, Besson G, Pollak P, et al. Hemiplegia in posterior cerebral artery occlusion. Neurology 1990; 40:1496.
- Benson DF, Tomlinson EB. Hemiplegic syndrome of the posterior cerebral artery. Stroke 1971; 2:559.
- North K, Kan A, de Silva M, Ouvrier R. Hemiplegia due to posterior cerebral artery occlusion. Stroke 1993; 24:1757.
- Caplan LR, Hedley-Whyte T. Cuing and memory dysfunction in alexia without agraphia. A case report. Brain 1974; 97:251.
- Geschwind N. Disconnexion syndromes in animals and man. I. Brain 1965; 88:237.
- Geschwind N, Fusillo M. Color-naming defects in association with alexia. Arch Neurol 1966; 15:137.
- Barton JS, Caplan LR. Cerebral visual dysfunction. In: Stroke Syndromes, 2nd edition, Bogousslavsky J, Caplan LR (Eds), Cambridge University Press, Cambridge 2001. p.87.
- Kertesz A, Sheppard A, MacKenzie R. Localization in transcortical sensory aphasia. Arch Neurol 1982; 39:475.
- Benson DF, Marsden CD, Meadows JC. The amnesic syndrome of posterior cerebral artery occlusion. Acta Neurol Scand 1974; 50:133.
- Ott BR, Saver JL. Unilateral amnesic stroke. Six new cases and a review of the literature. Stroke 1993; 24:1033.
- Damasio AR, Damasio H, Van Hoesen GW. Prosopagnosia: anatomic basis and behavioral mechanisms. Neurology 1982; 32:331.
- Fisher CM. Disorientation for place. Arch Neurol 1982; 39:33.