Posterior cerebral artery territory infarcts: clinical features, infarct topography, causes and outcome. Multicenter results and a review of the literature.

Only a few large series of posterior cerebral artery (PCA) stroke exist, and clinical features and causes have not been studied as extensively as in other vascular territories. The PCA syndrome includes more clinical signs than the well-known visual field deficits. Concomitant findings are frequently sensory, slight motor and neuropsychological deficits. Unilateral headaches are the common presenting symptom making complicated migraine an important differential diagnosis. Combined deep and superficial PCA territory infarcts involving the lateral thalamus are more frequent than commonly assumed and are mostly associated with sensory and reversible slight motor deficits. Occlusion of the precommunal PCA segment with associated paramedian midbrain infarction causes severe motor deficits, oculomotor signs, and decreased consciousness and has a poorer outcome than other PCA territory infarcts. Embolism from a cardiac or undetermined source is the leading mechanism accounting for up to half of the cases, whereas arterial embolism from significant proximal vertebrobasilar disease is less frequent. Local atherothrombotic stenosis or occlusion of the PCA is uncommon. In spite of thorough diagnostic evaluation, the etiology of PCA territory infarction cannot be determined in at least one quarter of patients. Among the rare causes of PCA territory infarction carotid artery disease is important while the significance of migraine remains controversial.

Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism.

CONTEXT: Intravenous tissue-type plasminogen activator can be beneficial to some patients when given within 3 hours of stroke onset, but many patients present later after stroke onset and alternative treatments are needed. OBJECTIVE: To determine the clinical efficacy and safety of intra-arterial (IA) recombinant prourokinase (r-proUK) in patients with acute stroke of less than 6 hours' duration caused by middle cerebral artery (MCA) occlusion. DESIGN: PROACT II (Prolyse in Acute Cerebral Thromboembolism II), a randomized, controlled, multicenter, open-label clinical trial with blinded follow-up conducted between February 1996 and August 1998. SETTING: Fifty-four centers in the United States and Canada. PATIENTS: A total of 180 patients with acute ischemic stroke of less than 6 hours' duration caused by angiographically proven occlusion of the MCA and without hemorrhage or major early infarction signs on computed tomographic scan. INTERVENTION: Patients were randomized to receive 9 mg of IA r-proUK plus heparin (n = 121) or heparin only (n = 59). MAIN OUTCOME MEASURES: The primary outcome, analyzed by intention-to-treat, was based on the proportion of patients with slight or no neurological disability at 90 days as defined by a modified Rankin score of 2 or less. Secondary outcomes included MCA recanalization, the frequency of intracranial hemorrhage with neurological deterioration, and mortality. RESULTS: For the primary analysis, 40% of r-proUK patients and 25% of control patients had a modified Rankin score of 2 or less (P = .04). Mortality was 25% for the r-proUK group and 27% for the control group. The recanalization rate was 66% for the r-proUK group and 18% for the control group (P<.001). Intracranial hemorrhage with neurological deterioration within 24 hours occurred in 10% of r-proUK patients and 2% of control patients (P = .06). CONCLUSION: Despite an increased frequency of early symptomatic intracranial hemorrhage, treatment with IA r-proUK within 6 hours of the onset of acute ischemic stroke caused by MCA occlusion significantly improved clinical outcome at 90 days.

Mechanisms and clinical features of posterior border-zone infarcts.

BACKGROUND: Previous studies link posterior border-zone cerebral infarcts between the middle cerebral artery (MCA) and the posterior cerebral artery (PCA) to hemodynamic causes, not embolism. OBJECTIVE: To study the cause of these infarcts. METHODS: We studied 21 patients (unilateral = 18, bilateral = 3) with acute, symptomatic posterior border-zone infarcts shown on CT or MRI to clarify stroke mechanisms. Patients were identified by review of CT and MRI logs and medical records during a 35-month period. An embolic mechanism was assigned when a source of embolism from either the heart, aorta, or parent large artery was present in the absence of intrinsic MCA or PCA disease. A hemodynamic mechanism was assigned when systemic hypotension was present. RESULTS: Among patients with unilateral lesions, 10 were embolic (7 cardiac, 3 carotid), 7 were unknown, and one patient had vasospasm from a ruptured aneurysm. Visual field abnormalities predominated over motor, sensory, and language abnormalities. All patients with bilateral posterior border-zone lesions had perioperative hypotension. Prolonged lethargy, bilateral limb weakness, and cortical blindness were common. CONCLUSIONS: Embolism, either cardiac or from the parent carotid artery, is the predominant stroke mechanism in unilateral posterior border-zone infarcts, not distal field perfusion failure. Bilateral posterior border-zone infarcts have a distinctive clinical presentation and are caused by systemic hypotension. Variability of irrigation of the major arteries, passage of emboli to border-zone areas, and decreased clearance of emboli in these areas explain the findings in the patients with unilateral lesions.

Anatomy of sensory findings in patients with posterior cerebral artery territory infarction.

BACKGROUND: Posterior cerebral arteries (PCAs) supply the ventrolateral thalamic sensory nuclei and white matter sensory tracts to the somatosensory parietal cortex. Patients with PCA territory strokes often have visual, memory, cognitive, and sensory signs. Clinicoanatomic correlation of visual, cognitive, and memory functions are well defined but, to our knowledge, no systematic study has analyzed the anatomy of sensory abnormalities. OBJECTIVE: To assess the frequency and anatomic correlation of sensory symptoms and signs in patients with PCA territory infarction. PATIENTS AND METHODS: Sixty patients with hemispheral and hemispheral and deep PCA territory infarcts apparent on computed tomographic and magnetic resonance imaging scans were studied for the presence of sensory findings and location of infarcts. RESULTS: Sensory symptoms or signs were present in 15 (25%) of 60 patients. Among patients with sensory findings, 11 of 15 had infarcts in the ventrolateral thalamus in the territory of the thalamogeniculate or lateral posterior choroidal arteries. The other 4 patients had no ventrolateral thalamic or white matter infarction but had severe proximal vascular occlusive lesions that could have caused temporary thalamic ischemia. One of these 4 patients had a medial thalamic infarct and transient hemisensory symptoms. Twelve patients had thalamic infarcts and no recorded sensory findings. Seven patients with thalamic infarcts (6 medial and 1 ventrolateral) had no sensory findings, and sensory findings could not be accurately assessed in 4 patients with ventrolateral and 1 patient with medial thalamic infarcts. CONCLUSIONS: All patients with PCA territory infarcts and sensory findings either had thalamic infarcts in thalamogeniculate or lateral posterior choroidal artery territory or had thalamic ischemia. Sensory findings in PCA territory infarction indicate ventrolateral thalamic ischemia.

Thrombus in vertebrobasilar dolichoectatic artery treated with intravenous urokinase.

BACKGROUND: Vertebrobasilar dolichoectasia is often found in patients with posterior circulation ischemia. Brain ischemia is caused by abnormal flow in the dilated artery and obstruction of paramedian arteries or intraluminal thrombus with artery-to-artery embolism. We report a patient with vertebrobasilar dolichoectasia and luminal thrombus treated with intravenous urokinase who did well but died 2 months later of subarachnoid hemorrhage. CASE DESCRIPTION: A 60-year-old man developed right-hand clumsiness, dysarthria and ataxia. Computed tomography showed vertebrobasilar dolichoectasia and thrombus in the basilar artery. Symptoms quickly resolved on heparin but recurred on warfarin and again resolved on heparin. Two weeks later, while on warfarin and aspirin 325 mg, he developed hand numbness, oscillopsia and ataxia. Symptoms again resolved on heparin. Angiography showed severe dolichoectasia of the distal right vertebral artery and basilar artery. A large mural thrombus was detected in the ventral part of the distal basilar artery narrowing the lumen by 50%. He was treated with intravenous urokinase 4,400 units/kg as a bolus followed by 4,400 units/kg/h for 12 h. Repeat angiography showed almost complete recanalization and improved filling of basilar artery branches. He was maintained on warfarin and aspirin 81 mg and had no further ischemic episodes. He died 2 months later of rupture of the basilar artery and subarachnoid hemorrhage. CONCLUSION: Some patients with thrombosis of vertebrobasilar dolichoectactic arteries continue to have ischemic symptoms despite adequate anticoagulation. Intravenous thrombolysis may be effective in reducing the risk of stroke, but the risk/benefit ratio needs to be assessed in each patient.

Recovery following lateral medullary infarction.

Lateral medullary infarction (LMI) has a well-defined clinical syndrome and vascular pathology. The functional outcome and degree of disability of patients with LMI, however, have not been as well investigated. We followed 18 consecutive patients with LMI during inpatient stroke rehabilitation. Thirteen patients were followed after discharge from the hospital over a mean time of 1 year. The degree of disability on admission and discharge from the hospital, and at follow-up was assessed using the motor component of the Functional Independence Measurement (FIM-motor). All patients were discharged home. During inpatient rehabilitation, the functional performance of all patients improved substantially from FIM-motor 50.9 +/- 13.0 (mean +/- SD) on admission to 76.9 +/- 10.5 at discharge. Patients with lower FIM-motor scores on admission had more functional improvement from admission to discharge than those with higher FIM-motor scores on admission. Patients with disease of the posterior inferior cerebellar artery showed significantly less functional improvement than patients with disease of the vertebral artery or no identified vascular pathology in the posterior circulation. In the follow-up group, the FIM-motor scores further improved to 84.6 +/- 8.4, indicating nearly full functional independence. Eighty-five percent were totally independent with ambulation. Five of seven previously working patients returned to work. Patients with LMI have few functional deficits after completion of inpatient rehabilitation, continue to improve functionally after discharge, and often resume their previous activities.

Proximal extracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry.

OBJECTIVE: To describe the clinical features of patients with occlusive disease of the proximal (V1) segment of the vertebral artery. DESIGN AND PATIENTS: Patients with either occlusion or high-grade stenosis involving the V1 segment were chosen for study from the New England Medical Center Posterior Circulation Registry. The registry is a consecutive series of patients with signs and symptoms of posterior circulation ischemia seen at the New England Medical Center, Boston, Mass, during a 10-year period. Clinical features, radiographic findings, and patient outcome were reviewed. RESULTS: Of the 407 patients in the registry, 80 (20%) had V1 segment lesions. Patients could be classified into 5 groups: (1) V1 disease and coexistent severe intracranial occlusive disease of the posterior circulation (n=22); (2) V1 disease with evidence of artery-to-artery embolism (n=19); (3) suspected V1 disease with artery-to-artery embolism, but with other potential causes of stroke or less certain vascular diagnosis (n=20); (4) V1 disease associated with hemodynamic transient ischemic attacks (n=13); and (5) proximal vertebral arterial dissection (n=6). Hypertension, cigarette smoking, and coronary artery disease were common risk factors. Clinical features, location of infarct, and outcome differed between groups and reflected the presumed mechanisms of stroke. CONCLUSIONS: Occlusive disease involving the V1 segment of the vertebral artery is common in patients with posterior circulation ischemia, but is often associated with other potential mechanisms of stroke. However, in a series of patients seen at a tertiary referral center, occlusive disease of the V1 segment was the primary mechanism of ischemia in 9% of patients.

PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. PROACT Investigators. Prolyse in Acute Cerebral Thromboembolism.

BACKGROUND AND PURPOSE: To test the safety and recanalization efficacy of intra-arterial local delivery of plasminogen activators in acute ischemic stroke, a randomized trial of recombinant pro-urokinase (rpro-UK) versus placebo was undertaken in patients with angiographically documented proximal middle cerebral artery occlusion. METHODS: After exclusion of intracranial hemorrhage by CT scan, patients with abrupt onset of symptoms of focal ischemia likely to receive treatment within 6 hours who satisfied all clinical eligibility criteria underwent carotid angiography. Patients displaying Thrombolysis in Acute Myocardial Infarction grade 0 or 1 occlusion of the M1 or M2 middle cerebral artery were randomized 2:1 to receive rpro-UK (6 mg) or placebo over 120 minutes into the proximal thrombus face. All patients received intravenous heparin. Recanalization efficacy was assessed at the end of the 2-hour infusion, and intracerebral hemorrhage causing neurological deterioration was assessed at 24 hours. RESULTS: Of 105 patients who underwent angiography, 59 were excluded from randomization. Among the 46 patients randomized, 40 were treated with rpro-UK (n=26) or placebo (n=14) a median of 5.5 hours from symptom onset. Recanalization was significantly associated with rpro-UK (2P=.017). Hemorrhagic transformation causing neurological deterioration within 24 hours of treatment occurred in 15.4% of the rpro-UK-treated patients and 7.1% of the placebo-treated patients (2P=.64). Both recanalization and hemorrhage frequencies were influenced by heparin dose. CONCLUSIONS: Intra-arterial local rpro-UK infusion was associated with superior recanalization in acute thrombotic/ thromboembolic stroke compared with placebo. In this regimen, heparin dose influenced hemorrhage frequency and recanalization. Although symptomatic hemorrhage remains a concern, this study suggests that recanalization is enhanced with rpro-UK and heparin.

Intracranial angioplasty: experience and complications.

PURPOSE: To review our experience with intracranial angioplasty, including the complications we encountered. METHODS: During a 3-year period, from 1993 to 1996, 10 patients had intracranial percutaneous transluminal angioplasty (PTA). The stenosed vessels included three internal carotid arteries, one middle cerebral artery, one basilar artery, and five vertebral arteries. Stenosis in all patients was 75%, or greater. PTA was technically successful in eight patients; in two patients it could not be performed owing to inability to traverse the stenosed area. RESULTS: Two patients had successful and uneventful PTA. Five patients had vasospasm, which resolved with local vasodilators in two and with repeat PTA in one. Vasospasm led to stroke in two patients. Compromise of perforating vessels and arterial dissection were associated with stroke in two patients. CONCLUSION: Intracranial PTA is technically feasible but associated with risks related to vasospasm, arterial trauma, and compromise of perforating vessels.

Carotid occlusive disease and stroke risk in coronary artery bypass graft surgery.

To clarify the perioperative stroke risk in patients with carotid stenosis or occlusion having coronary artery bypass graft (CABG) surgery, we retrospectively reviewed the records of 1,022 patients who had CABG during a 2-year period (1992, 1993). Of these, 224 had preoperative carotid duplex studies, usually for bruit or remote symptoms. We analyzed clinical and neuroimaging findings for all patients who had strokes to determine infarct topography and presumed mechanism, either low perfusion or embolism. Perioperative stroke was always ipsilateral to severe (> or = 70%) carotid disease, and occurred in 2 (8.0%) of 25 patients with carotid occlusion, 3 (50.0%) of 6 patients with 70 to 99% stenosis, and 9 (4.7%) of 193 patients with less than 70% stenosis. Borderzone infarcts occurred with all degrees of carotid stenosis. Stroke frequency had a positive correlation with the degree of carotid stenosis. Eight (1.0%) of the 798 patients not studied by carotid duplex had stroke in various vascular distributions. Overall, stroke occurred in 22 (2.2%) of the 1,022 patients having CABG surgery. Our results suggest that while the overall risk of perioperative stroke in CABG surgery is low, the risk is increased in patients with severe extracranial carotid stenosis or occlusion. The role of carotid disease and the mechanism of borderzone infarction in CABG surgery remain unsettled.

Intracranial vertebral artery disease in the New England Medical Center Posterior Circulation Registry.

We studied 75 patients with severe intracranial vertebral artery (ICVA) occlusive disease from the New England Medical Center Posterior Circulation Registry to learn the etiologies and locations of the vascular lesions, the location and patterns of related ischemia and infarctions, and the outcomes. All patients had neuroimaging and vascular studies. Thirty-nine percent of patients had bilateral ICVA lesions. Twenty-four percent also had basilar artery disease and 36% had associated extracranial disease. The most common site of lesions was the distal ICVA after the origin of the posterior inferior cerebellar artery (PICA). Twenty-five percent of patients had only proximal intracranial posterior circulation territory infarcts (medullary and PICA cerebellar); 32% had infarcts that involved other intracranial territories in addition to the proximal territory. We found more distal intracranial territory infarcts resulting mainly from embolism from ICVA lesions than reported previously; this occurred in 17% of all patients. The ICVA was a recipient site for emboli in 8% of patients. Thirteen percent of patients died during follow-up. The outcome was favorable in most surviving patients. Three-fourths of them had no deficit or only slight disability. The patients with distal territory infarcts due to emboli from the ICVA had the worst outcome.

Proximal intracranial territory posterior circulation infarcts in the New England Medical Center Posterior Circulation Registry.

We studied 91 patients with proximal intracranial territory posterior circulation ischemia from the New England Medical Center Posterior Circulation Registry to learn their distribution, underlying cardiovascular causes and longterm outcome. All patients had imaging and vascular studies. Six patients had proximal territory TIAs. Among 85 stroke patients, 52% had infarcts limited to the proximal territory, while 48% also had infarcts in other intracranial posterior circulation territories. Eighty-five percent of proximal territory infarcts were posterior inferior cerebellar artery (PICA) territory cerebellar infarcts and 30% were lateral medullary infarcts. One patient had a hemimedullary syndrome. Six patients had PICA territory cerebellar and lateral medullary infarcts. The most common vascular lesion in lateral medullary infarct patients was ipsilateral intracranial vertebral artery (ICVA) disease (38% isolated ICVA disease) and in PICA territory cerebellar infarcts, extracranial vertebral artery (ECVA) disease (29% isolated ECVA disease). Half of all lateral medullary infarcts were due to a hemodynamic mechanism, most often in situ thrombosis of an ICVA occlusive lesion. Half of all PICA territory cerebellar infarcts were due to intra-arterial embolism and one-fifth to cardiac origin embolism. Embolism was a more frequent cause of proximal territory posterior circulation infarcts than intrinsic ICVA disease. The etiological profiles of lateral medullary and PICA cerebellar infarcts were different. Seventeen percent of all patients died during follow-up (41 months) but mortality related to the acute stroke or new strokes was only 6 percent. The outcome was favorable in the surviving patients; 89% had no or only slight disability.

Thalamic haemorrhage.

Thalamic haemorrhage is usually considered a single entity although the thalamus is composed of anatomically as well as functionally discrete subregions receiving blood from different arteries. The clinical features vary according to the intrathalamic location of the haematomas and the bleeding artery. We investigated the impact of haematoma location and vascular territory on the clinical symptoms and signs, neuro-imaging findings and clinical courses of patients with thalamic haemorrhages by a retrospective analysis of 175 consecutive patients with thalamic haemorrhage. Based on the neuro-imaging findings we classified thalamic haematomas into four regional types and one global type according to the primary bleeding sites: (i) anterior type occurring in the territory of the tuberothalamic arteries, (ii) posteromedial type occurring in the territory of the thalamic-subthalamic paramedian arteries, (iii) posterolateral type occurring in the territory of the thalamogeniculate arteries. (iv) dorsal type occurring in the territory of the posterior choroidal arteries and (v) global type occupying the entire area of the thalamus. We studied the clinical and neuroimaging characteristics of each type. Eleven patients (7%) had the anterior type: these were the smallest haematomas and often ruptured into the anterior horn of the lateral ventricle. The major clinical signs were acute behavioural abnormalities: the clinical course was usually benign. Twenty-four patients (14%) had the posteromedial type in which haematomas often ruptured into the third ventricle, causing marked hydrocephalus, and often extended mediocaudally, involving the mesencephalon. The prognoses of this type depended on the presence of mesencephalic involvement which was associated with the worst outcome among the types even if the size of the haematoma itself was not large. The posterolateral type was most frequent (77 patients, 44%) and was characterized by large haematomas, rupture into the posterior horn of the lateral ventricle and frequent extension into the posterior limb of the internal capsule. Clinical signs included marked sensory and motor signs, hemineglect in right-side haematomas and language abnormalities with left-side haematomas. The case fatality with this type was relatively high (35%) and permanent neurologic sequelae frequently resulted. In the dorsal type (32 patients, 18%) haematomas were best visualized at the level of the body of the lateral ventricle on CT scans. The size was moderate and haematomas often extended posterolaterally into the adjacent subcortical white matter. Sensory and motor signs were common and about one third of the patients were first misdiagnosed as having lacunar infarcts. The prognoses were excellent. The global type (31 patients, 18%) of thalamic haemorrhage was clinically and radiologically very similar to the posterolateral type except that the haematomas were too large to define the bleeding focus. Severe sensory and motor signs were almost always present. In this type 25 patients died (the case fatality was 81%).

Apolipoprotein E epsilon 4 is associated with the presence and earlier onset of hemorrhage in cerebral amyloid angiopathy.

BACKGROUND AND PURPOSE: Cerebral amyloid angiopathy is an important cause of intracerebral hemorrhage in the elderly. The epsilon 4 allele of the apolipoprotein E gene, recently established as a genetic risk for Alzheimer's disease, has also been suggested as a possible risk factor for cerebral amyloid angiopathy. We sought to determine whether this allele is specifically associated with hemorrhages related to amyloid angiopathy and whether it correlates with the age at which first amyloid angiopathy-related hemorrhage occurs. METHODS: Forty-five consecutive patients presenting with lobar hemorrhage were prospectively classified according to clinical, radiological, and when available, pathological features and evaluated for apolipoprotein E genotype. They were compared with 1899 elderly patients from a population-based sample and with 18 consecutive patients with hemorrhages in deep regions typical of a hypertensive mechanism. RESULTS: Patients with multiple hemorrhages confined to the lobar territory demonstrated a greater than twofold overrepresentation (P < .001) in frequency of the apolipoprotein E epsilon 4 allele compared with the population-based sample. Apolipoprotein E genotypes of patients with hemorrhages in deep territories resembled the population sample. Among patients with strictly lobar hemorrhages, carriers of the epsilon 4 allele had their first hemorrhage more than 5 years earlier than noncarriers (mean age at first hemorrhage, 73.4 +/- 8.0 versus 78.9 +/- 7.4 years; P = .033). These effects were independent of the accompanying presence of Alzheimer's disease. CONCLUSIONS: The data support a specific role for apolipoprotein E epsilon 4 in accelerating the process that leads to amyloid angiopathy-related hemorrhage.

A reversible posterior leukoencephalopathy syndrome.

BACKGROUND AND METHODS: In some patients who are hospitalized for acute illness, we have noted a reversible syndrome of headache, altered mental functioning, seizures, and loss of vision associated with findings indicating predominantly posterior leukoencephalopathy on imaging studies. To elucidate this syndrome, we searched the log books listing computed tomographic (CT) and magnetic resonance imaging (MRI) studies performed at the New England Medical Center in Boston and Hôpital Sainte Anne in Paris; we found 15 such patients who were evaluated from 1988 through 1994. RESULTS: Of the 15 patients, 7 were receiving immunosuppressive therapy after transplantation or as treatment for aplastic anemia, 1 was receiving interferon for melanoma, 3 had eclampsia, and 4 had acute hypertensive encephalopathy associated with renal disease (2 with lupus nephritis, 1 with acute glomerulonephritis, and 1 with acetaminophen-induced hepatorenal failure). Altogether, 12 patients had abrupt increases in blood pressure, and 8 had some impairment of renal function. The clinical findings included headaches, vomiting, confusion, seizures, cortical blindness and other visual abnormalities, and motor signs. CT and MRI studies showed extensive bilateral white-matter abnormalities suggestive of edema in the posterior regions of the cerebral hemispheres, but the changes often involved other cerebral areas, the brain stem, or the cerebellum. The patients were treated with antihypertensive medications, and immunosuppressive therapy was withdrawn or the dose was reduced. In all 15 patients, the neurologic deficits resolved within two weeks. CONCLUSIONS: Reversible, predominantly posterior leukoencephalopathy may develop in patients who have renal insufficiency or hypertension or who are immunosuppressed. The findings on neuroimaging are characteristic of subcortical edema without infarction.

Cerebellar hemorrhagic infarction.

We investigated 17 patients with 26 cerebellar hemorrhagic infarcts for their vascular anatomy, stroke mechanisms, and clinical course. Sixteen infarcts involved the superior cerebellar artery, nine the posterior inferior cerebellar artery, and one the anterior inferior cerebellar artery territories. The infarcts involved the full territory of the supplying arteries in 19 of 26 infarcts (73%). Sixteen of 17 patients were stable or improving when the hemorrhagic infarction was detected. All but one patient had an imaging study at the time of presentation that was negative for blood; hemorrhagic infarction was detected on routine serial scans performed during the first 15 days. Nine of the 17 patients were on anticoagulants when the cerebellar hemorrhagic infarct was detected; anticoagulation was maintained in eight of them with no clinical worsening. The stroke mechanism in all patients was considered embolic from cardiac and intra-arterial sources. The causes, imaging findings, and consequences of hemorrhagic infarcts in the posterior circulation are similar to those in the anterior circulation.

Stroke with sensory symptoms mimicking myocardial ischemia.

OBJECTIVE: To report five stroke patients with sensory deficits including prominent chest discomfort mimicking angina. BACKGROUND: Chest wall sensory discomfort, as a part of unilateral sensory dysfunction, has seldom been recognized as a potential imitator of cardiac ischemia. METHODS: A retrospective review of stroke patients with sensory symptoms from the New England Medical Center Stroke Registry. RESULTS: As a part of an acute stroke that included unilateral sensory symptoms and signs, five patients had chest pain or discomfort, which prompted cardiac evaluation for potential coronary artery disease. In two patients, the primary presentation was chest discomfort. In the other three, chest discomfort was part of a more extensive stroke syndrome. The symptoms were described as "burning," "hot feeling," "flashes," "tightness," and "cold." In three patients, an MRI or CT scan showed an infarct in the thalamus, corona radiata, or lateral medulla. Cardiac evaluation was negative in all but one patient who had single vessel percutaneous transluminal coronary angioplasty without resolution of sensory symptoms. Chest discomfort fluctuated but persisted for months or years after presentation. CONCLUSION: Chest discomfort mimicking cardiac ischemia may be a prominent sensory symptom in acute stroke.