normal during the acute phase of ischemic symptoms. In this regard, the HINTS test appears to https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 12/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate be more sensitive for the diagnosis of acute stroke than even brain MRI within the first two days after symptom onset [33]. 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 [32,33]. 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 [34]. Atherostenotic lesions are most common in the proximal and mid basilar artery; emboli have a predilection for stopping at the distal end of the basilar artery. 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. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 13/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 [3,4,14,35-38]. 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 non-hemiparetic 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 of neurologic signs 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 [39]. 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 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 14/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 15/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 [3,40,41]. 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 [17]. 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 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 16/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 [14]. 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 [3,40]. (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. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 17/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 [1-4,42-44]. 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 [45]. 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 [3,46- 48]. 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 [49-52], anomic aphasia or transcortical sensory aphasia [53], and Gerstmann syndrome (acalculia, agraphia, finger agnosia, and right-left disorientation) may be found [3,49]. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 18/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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 [3,49,54,55]. 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) [49,52]. 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 [52,56]. Disorientation to place and an inability to recall routes or to read or visualize the location of places on maps are also common [57]. 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. SUMMARY 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. (See 'Source of ischemia' above.) Subclavian and innominate arteries Atherostenotic lesions of these arteries cause arm ischemia and transient ischemic attacks (TIAs) but seldom cause strokes. (See 'Subclavian and innominate arteries' above.) Extracranial vertebral arteries 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 than hemodynamic insufficiency (ie, low flow). The most frequently reported symptom during TIAs is dizziness. Diplopia, https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 19/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 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.) Intracranial vertebral arteries 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): Asymptomatic occlusion 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 and pontine ischemia Occlusive disease of the basilar artery 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.) https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 20/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Rostral basilar artery 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.) Posterior cerebral artery territory 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.) Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Caplan LR, Wityk RJ, Glass TA, et al. New England Medical Center Posterior Circulation registry. Ann Neurol 2004; 56:389. 2. Savitz SI, Caplan LR. Vertebrobasilar disease. N Engl J Med 2005; 352:2618. 3. Caplan LR. Vertebrobasilar Ischemia and Hemorrhage: Clinical Findings, Diagnosis and Man agement of Posterior Circulation Disease, 2nd edition, Cambridge University Press, Cambrid ge 2015. 4. Caplan L. Posterior circulation ischemia: then, now, and tomorrow. The Thomas Willis Lecture-2000. Stroke 2000; 31:2011. 5. 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. 6. Brewster DC, Moncure AC, Darling RC, et al. Innominate artery lesions: problems encountered and lessons learned. J Vasc Surg 1985; 2:99. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 21/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 7. Labauge R, Boukobza M, Pag s M, et al. [Occlusion of the vertebral artery (100 personal cases)]. Rev Neurol (Paris) 1987; 143:490. 8. Caplan LR, Amarenco P, Rosengart A, et al. Embolism from vertebral artery origin occlusive disease. Neurology 1992; 42:1505. 9. Caplan LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol 2008; 4:34. 10. Rosengart A, Hedges TR 3rd, Teal PA, et al. Intermittent downbeat nystagmus due to vertebral artery compression. Neurology 1993; 43:216. 11. Choi KD, Choi JH, Kim JS, et al. Rotational vertebral artery occlusion: mechanisms and long- term outcome. Stroke 2013; 44:1817. 12. Choi KD, Shin HY, Kim JS, et al. Rotational vertebral artery syndrome: oculographic analysis of nystagmus. Neurology 2005; 65:1287. 13. Caplan LR, Baquis GD, Pessin MS, et al. Dissection of the intracranial vertebral artery. Neurology 1988; 38:868. 14. 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. 15. Kim JS. Pure lateral medullary infarction: clinical-radiological correlation of 130 acute, consecutive patients. Brain 2003; 126:1864. 16. Morrow MJ, Sharpe JA. Torsional nystagmus in the lateral medullary syndrome. Ann Neurol 1988; 24:390. 17. Brandt T, Dieterich M. Vestibular syndromes in the roll plane: topographic diagnosis from brainstem to cortex. Ann Neurol 1994; 36:337. 18. Keane JR. Ocular tilt reaction following lateral pontomedullary infarction. Neurology 1992; 42:259. 19. Matsumoto S, Okuda B, Imai T, Kameyama M. A sensory level on the trunk in lower lateral brainstem lesions. Neurology 1988; 38:1515. 20. 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. 21. Amarenco P, Hauw JJ. [Anatomy of the cerebellar arteries]. Rev Neurol (Paris) 1989; 145:267. 22. Amarenco P, Hauw JJ, H nin D, et al. [Cerebellar infarction in the area of the posterior cerebellar artery. Clinicopathology of 28 cases]. Rev Neurol (Paris) 1989; 145:277. 23. Passero S, Filosomi G. Posterior circulation infarcts in patients with vertebrobasilar dolichoectasia. Stroke 1998; 29:653. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 22/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 24. 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. 25. Passero SG, Rossi S. Natural history of vertebrobasilar dolichoectasia. Neurology 2008; 70:66. 26. Savitz SI, Ronthal M, Caplan LR. Vertebral artery compression of the medulla. Arch Neurol 2006; 63:234. 27. Lou M, Caplan LR. Vertebrobasilar dilatative arteriopathy (dolichoectasia). Ann N Y Acad Sci 2010; 1184:121. 28. Pico F, Labreuche J, Amarenco P. Pathophysiology, presentation, prognosis, and management of intracranial arterial dolichoectasia. Lancet Neurol 2015; 14:833. 29. Zhang DP, Peng YF, Ma QK, et al. Why does my patient's basilar artery continue to grow? A four-year case study of a patient with symptoms of vertebrobasilar dolichoectasia. BMC Neurol 2018; 18:45. 30. Newman-Toker DE, Kattah JC, Alvernia JE, Wang DZ. Normal head impulse test differentiates acute cerebellar strokes from vestibular neuritis. Neurology 2008; 70:2378. 31. 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. 32. 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. 33. 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. 34. Pessin MS, Gorelick PB, Kwan ES, Caplan LR. Basilar artery stenosis: middle and distal segments. Neurology 1987; 37:1742. 35. KUBIK CS, ADAMS RD. Occlusion of the basilar artery; a clinical and pathological study. Brain 1946; 69:73. 36. 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. 37. Ferbert A, Br ckmann H, Drummen R. Clinical features of proven basilar artery occlusion. Stroke 1990; 21:1135. 38. 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. 39. Ropper AH. 'Convulsions' in basilar artery occlusion. Neurology 1988; 38:1500. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 23/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate 40. Caplan LR. "Top of the basilar" syndrome. Neurology 1980; 30:72. 41. Mehler MF. The neuro-ophthalmologic spectrum of the rostral basilar artery syndrome. Arch Neurol 1988; 45:966. 42. Pessin MS, Lathi ES, Cohen MB, et al. Clinical features and mechanism of occipital infarction. Ann Neurol 1987; 21:290. 43. Fisher CM. The posterior cerebral artery syndrome. Can J Neurol Sci 1986; 13:232. 44. 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. 45. 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. 46. Hommel M, Besson G, Pollak P, et al. Hemiplegia in posterior cerebral artery occlusion. Neurology 1990; 40:1496. 47. Benson DF, Tomlinson EB. Hemiplegic syndrome of the posterior cerebral artery. Stroke 1971; 2:559. 48. North K, Kan A, de Silva M, Ouvrier R. Hemiplegia due to posterior cerebral artery occlusion. Stroke 1993; 24:1757. 49. Caplan LR, Hedley-Whyte T. Cuing and memory dysfunction in alexia without agraphia. A case report. Brain 1974; 97:251. 50. Geschwind N. Disconnexion syndromes in animals and man. I. Brain 1965; 88:237. 51. Geschwind N, Fusillo M. Color-naming defects in association with alexia. Arch Neurol 1966; 15:137. 52. Barton JS, Caplan LR. Cerebral visual dysfunction. In: Stroke Syndromes, 2nd edition, Bogou sslavsky J, Caplan LR (Eds), Cambridge University Press, Cambridge 2001. p.87. 53. Kertesz A, Sheppard A, MacKenzie R. Localization in transcortical sensory aphasia. Arch Neurol 1982; 39:475. 54. Benson DF, Marsden CD, Meadows JC. The amnesic syndrome of posterior cerebral artery occlusion. Acta Neurol Scand 1974; 50:133. 55. Ott BR, Saver JL. Unilateral amnesic stroke. Six new cases and a review of the literature. Stroke 1993; 24:1033. 56. Damasio AR, Damasio H, Van Hoesen GW. Prosopagnosia: anatomic basis and behavioral mechanisms. Neurology 1982; 32:331. 57. Fisher CM. Disorientation for place. Arch Neurol 1982; 39:33. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 24/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Topic 1102 Version 22.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 25/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate GRAPHICS Anatomy of extracranial vertebral arteries Graphic 59642 Version 3.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 26/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Posterior circulation to the brain Graphic 66585 Version 3.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 27/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Medulla oblongata The usual location of lateral medullary infarcts is hatch-marked in the upper right of the figure. The anatomical structures are labeled on the diagram. Graphic 62175 Version 1.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 28/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Major cerebellar arterial branches The intracranial vertebral and basilar arteries are depicted with their major cerebellar arterial branches, including PICA (posterior inferior and cerebellar artery), AICA (anterior inferior cerebellar artery), and SCA (superior cerebellar artery). Reproduced with permission from Caplan, LR. Posterior circulation disease. Clinical ndings, diagnosis, and management. Blackwell Science, Boston 1996. Copyright 1996 Blackwell Science. Graphic 73656 Version 1.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 29/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Head impulse test At rest, the patient is asked to fixate on a distant target. The patient's head is rotated rapidly by the examiner, first to the left (A to B), then to the right (C to D). In a normal response, the eyes remain on target (B). In an abnormal response, the eyes are dragged off target (D), followed by a saccade back to the target (E). This response implies a peripheral vestibular lesion on the right. Graphic 52022 Version 5.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 30/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Myelin stain of the pons at necropsy after stroke due to basilar artery occlusive disease A large infarct (shown in white) involves the bilateral basis pontis and extends into the ventral portion of the pontine tegmentum. Reproduced with permission from: Caplan LR. Posterior circulation disease. Clinical ndings, diagnosis, and management. Blackwell Science, Boston 1996. Copyright 1996 Blackwell Science. Graphic 81264 Version 5.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 31/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Vascular supply of the pons The major penetrating arteries from the basilar artery are depicted. A) Large paired median arteries. B) Paramedian arteries lying slightly laterally. C) Arteries that branch at a right angle from the long circumferential artery (the superior cerebellar artery) into the lateral pontine tegmentum. Reproduced with permission from: Caplan LR. Posterior circulation disease. Clinical ndings, diagnosis, and management. Blackwell Science, Boston 1996. Copyright 1996 Blackwell Science. Graphic 69507 Version 3.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 32/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Collateral blood flow in a patient with a proximal basilar artery occlusion Vertebral artery angiogram, lateral view. The proximal portion of the basilar artery is occluded. Blood flow is seen in the intracranial vertebral artery (A), which gives off the posterior inferior cerebellar artery (PICA) (B), which in turn anastamoses with the superior cerebellar artery (SCA) (C). From there, blood flows over the cerebellum to fill the rostral portion of the basilar artery (D). Reproduced with permission from: Caplan LR. Posterior circulation disease. Clinical ndings, diagnosis, and management. Blackwell Science, Boston 1996. Copyright 1996 Blackwell Science. Graphic 61444 Version 4.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 33/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Ophthalmic findings in the Parinaud syndrome Vertical gaze abnormalities, especially upgaze Downward gaze preference or tonic downward deviation of the eyes ("setting-sun sign") Primary position upbeat or downbeat nystagmus Impaired convergence and divergence Excessive convergence tone Convergence-retraction nystagmus Skew deviation, often with the higher eye on the side of the lesion Alternating adduction hypertropia or alternating adduction hypotropia Bilateral upper eyelid retraction (Collier "tucked-lid" sign) Bilateral ptosis Pupillary abnormalities (large with light-near dissociation) Modi ed with permission from: Lee AG, Brazis PW. Clinical Pathways in Neuro-ophthalmology: An Evidence-based Approach, Thieme, New York 1998. Graphic 81227 Version 4.0 https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 34/35 7/5/23, 11:58 AM Posterior circulation cerebrovascular syndromes - UpToDate Contributor Disclosures Louis R Caplan, MD No relevant financial relationship(s) with ineligible companies to disclose. Jos Biller, MD, FACP, FAAN, FAHA No relevant financial relationship(s) with ineligible companies to disclose. John F Dashe, MD, PhD No relevant financial relationship(s) with ineligible companies to disclose. 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. Conflict of interest policy https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes/print 35/35