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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.
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 .
As noted above, 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).
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".)
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 [4,11,12]:
Lateral medullary infarction — Lateral medullary infarction (Wallenberg syndrome) is the most common and important syndrome related to intracranial vertebral artery occlusion (figure 3) [4,12]. 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:
Sensory symptoms and signs — Sensory symptoms and signs are common in patients with lateral medullary infarcts.
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.
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.
Medial medullary infarction — The most consistent finding in patients with medial medullary ischemia is a contralateral hemiparesis [4,17]. 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 [4,18,19].
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:
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 [20-24]. 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:
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 .
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 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 [3,4,11,26-29]. 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:
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 ophthalmoplegia".) 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 [3,31,32]. 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 [3,31]. (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 [1-4,33-35]. 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 [3,37-39]. 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 [40-43], anomic aphasia or transcortical sensory aphasia , and Gerstmann syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation) may be found [3,40].
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 [3,40,45,46]. 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) [40,43]. 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 [43,47]. 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.
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