Neglect is more common and severe at extreme hemoglobin levels in right hemispheric stroke.

BACKGROUND AND PURPOSE: Anemia is 1 potential mechanism by which the brain receives inadequate oxygenation. The purpose of this study was to determine in acute stroke patients whether lower hemoglobin values were associated with worse hemispatial neglect. METHODS: In 203 subjects, neglect testing batteries were administered within 24 hours of admission for acute right hemispheric stroke. We analyzed the error rate on each test as well as "any neglect" (z score >or=2 on any of 3 selected tests compared with normal controls), as predicted by hemoglobin level, with adjustment for infarct size, National Institutes of Health Stroke Scale score, age, and sex. RESULTS: The association between hemoglobin and neglect varied on the basis of hemoglobin level. At lower hemoglobin levels (<12 g/dL), each 1-point higher hemoglobin value was protective (adjusted odds ratio=0.56; 95% CI, 0.35 to 0.89) from having "any neglect." However, for a hemoglobin value >14 g/dL, each 1-point higher hemoglobin value was associated with higher odds of having neglect (adjusted odds ratio=1.67; 95% CI, 1.09 to 2.57). Similar relations were found for predicted error rate on the horizontal line bisection, line cancellation, and copy Ogden scene neglect tests. These relations seemed to be more pronounced in individuals who had a diffusion/perfusion mismatch. CONCLUSIONS: Lower and higher hemoglobin levels were each associated with increased odds of neglect and with worse severity of neglect, independent of stroke size and severity. Higher hemoglobin values may represent dehydration or hyperviscosity. The importance of the extremes of hemoglobin in identifying individuals at risk for worse functional consequences of stroke warrants further study.

Long-term antithrombotic therapy and risk of intracranial haemorrhage from cerebral cavernous malformations: a population-based cohort study, systematic review, and meta-analysis.

BACKGROUND: Antithrombotic (anticoagulant or antiplatelet) therapy is withheld from some patients with cerebral cavernous malformations, because of uncertainty around the safety of these drugs in such patients. We aimed to establish whether antithrombotic therapy is associated with an increased risk of intracranial haemorrhage in adults with cerebral cavernous malformations. METHODS: In this population-based, cohort study, we used data from the Scottish Audit of Intracranial Vascular Malformations, which prospectively identified individuals aged 16 years and older living in Scotland who were first diagnosed with a cerebral cavernous malformation during 1999-2003 or 2006-10. We compared the association between use of antithrombotic therapy after first presentation and the occurrence of intracranial haemorrhage or persistent or progressive focal neurological deficit due to the cerebral cavernous malformations during up to 15 years of prospective follow-up with multivariable Cox proportional hazards regression assessed in all individuals identified in the database. We also did a systematic review and meta-analysis, in which we searched Ovid MEDLINE and Embase from database inception to Feb 1, 2019, to identify comparative studies to calculate the intracranial haemorrhage incidence rate ratio according to antithrombotic therapy use. We then generated a pooled estimate using the inverse variance method and a random effects model. FINDINGS: We assessed 300 of 306 individuals with a cerebral cavernous malformation who were eligible for study. 61 used antithrombotic therapy (ten [16%] of 61 used anticoagulation) for a mean duration of 7·4 years (SD 5·4) during follow-up. Antithrombotic therapy use was associated with a lower risk of subsequent intracranial haemorrhage or focal neurological deficit (one [2%] of 61 vs 29 [12%] of 239, adjusted hazard ratio [HR] 0·12, 95% CI 0·02-0·88; p=0·037). In a meta-analysis of six cohort studies including 1342 patients, antithrombotic therapy use was associated with a lower risk of intracranial haemorrhage (eight [3%] of 253 vs 152 [14%] of 1089; incidence rate ratio 0·25, 95% CI 0·13-0·51; p<0·0001; I2=0%). INTERPRETATION: Antithrombotic therapy use is associated with a lower risk of intracranial haemorrhage or focal neurological deficit from cerebral cavernous malformations than avoidance of antithrombotic therapy. These findings provide reassurance about safety for clinical practice and require further investigation in a randomised controlled trial. FUNDING: UK Medical Research Council, Chief Scientist Office of the Scottish Government, The Stroke Association, Cavernoma Alliance UK, and the Remmert Adriaan Laan Foundation.

Blood pressure management in acute stroke.

The optimal management of arterial blood pressure in the setting of an acute stroke has not been defined. Many articles have been published on this topic in the past few years, but definitive evidence from clinical trials continues to be lacking. This situation is complicated further because stroke is a heterogeneous disease. The best management of arterial blood pressure may differ, depending on the type of stroke (ischemic or hemorrhagic) and the subtype of ischemic or hemorrhagic stroke. This article reviews the relationship between arterial blood pressure and the pathophysiology specific to ischemic stroke, primary intracerebral hemorrhage, and aneurysmal subarachnoid hemorrhage, elaborating on the concept of ischemic penumbra and the role of cerebral autoregulation. The article also examines the impact of blood pressure and its management on outcome. Finally, an agenda for research in this field is outlined.

Transcranial Doppler ultrasound in children with Sturge-Weber syndrome.

Transcranial Doppler ultrasound is a noninvasive vascular assessment technique proved useful in the management of pediatric disorders predisposed to stroke and may have similar utility for Sturge-Weber syndrome. Eight children with Sturge-Weber syndrome had velocities measured in the major cerebral arteries via the Stroke Prevention Trial in Sickle Cell Anemia methodology. Velocities and pulsatility indexes were compared between the unaffected and affected sides. All subjects had reduced velocity on the affected side; the mean middle cerebral artery percentage difference was 20% (95% CI, 15%-25%). Pulsatility index was increased on the affected side; mean middle cerebral artery pulsatility index percentage difference, 34% (95% CI, 15%-53%). Six subjects also had reduced posterior cerebral artery velocity on the affected side. Side-to-side differences in middle cerebral artery and posterior cerebral artery velocities correlated with severity of MRI asymmetry (Spearman rho = 0.88, P = .02). Decreased arterial flow velocity and increased pulsatility index in the middle cerebral artery and posterior cerebral artery suggests a high resistance pattern that may reflect venous stasis and may contribute to chronic hypoperfusion of brain tissue. Further study of Transcranial Doppler in children with Sturge-Weber syndrome is indicated.

Neural regions essential for writing verbs.

Functional imaging data collected during cognitive tasks show which brain regions are active during those tasks, but do not necessarily indicate which regions are essential for those tasks. Here, in a study of two cases of selectively impaired written naming of verbs after focal brain ischemia, we combined imaging and behavioral testing to unambiguously identify brain regions that are crucial for a specific cognitive process. We used magnetic resonance perfusion imaging to show that the selective impairment in each case was due to hypoperfusion (low blood flow) in left posterior inferior frontal gyrus (PIFG) and precentral gyrus (PrG); the impairment was immediately reversed when blood flow was restored to these regions, indicating that parts of the left frontal lobe are crucial for representing and processing verbs.

Blood pressure augmentation in acute ischemic stroke.

Although control of hypertension is established as an important factor in the primary and secondary prevention of stroke, management of blood pressure in the setting of acute ischemic stroke remains controversial. Given limited data, the general consensus is that there is no proven benefit to lowering blood pressure in the first hours to days after acute ischemic stroke. Instead, there is concern that relative hypotension may lead to worsening of cerebral ischemia. For many years, the use of blood pressure augmentation ("induced hypertension") has been studied in animal models and in humans as a means of maintaining or improving perfusion to ischemic brain tissue. This approach is now widely used in neurocritical care units to treat delayed neurological deficits after subarachnoid hemorrhage, but its use in ischemic stroke patients remains anecdotal. This article reviews the cerebral physiology, animal models and human studies of induced hypertension as a treatment for acute ischemic stroke. Although there has not been a large, randomized clinical trial of this treatment, the available clinical data suggests that induced hypertension can result in at least short-term neurological improvement, with an acceptable degree of safety.

The management of blood pressure after stroke.

BACKGROUND: Control of hypertension is a well-established goal of primary prevention of stroke, but management of blood pressure in patients with a previous stroke or in the setting of acute stroke is complicated by the effect blood pressure changes may have on cerebral perfusion. REVIEW SUMMARY: For patients with previous transient ischemic attack or chronic stroke, blood pressure reduction appears to be a safe and important facet of the secondary prevention of recurrent stroke. Less information is available concerning blood pressure management in acute stroke. Current protocols require strict blood pressure control in patients who are treated with thrombolytic therapy, to reduce the risk of hemorrhagic complications. In patients presenting with acute intracerebral hemorrhage, blood pressure reduction does not appear to cause significant reduction of cerebral blood flow, but at this time there are no studies to determine if there is a clinical benefit of acute blood pressure reduction in these patients. Finally, blood pressure reduction is not routinely recommended in patients with acute ischemic stroke, as it may precipitate further cerebral ischemia. Preliminary studies suggest, in fact, that there may be a role in the future for blood pressure elevation in the treatment of patients with acute ischemic stroke. CONCLUSIONS: Current data support the use of blood pressure reduction in the secondary prevention of stroke in patients with cerebrovascular disease. In the setting of acute stroke, however, data are limited and blood pressure management must be tailored to the specific clinical situation.

Patients with diffusion-perfusion mismatch on magnetic resonance imaging 48 hours or more after stroke symptom onset: clinical and imaging features.

BACKGROUND: Abnormalities in diffusion-weighted (DWI) and perfusion-weighted (PWI) magnetic resonance imaging (MRI) are thought to reflect the presence of brain tissue at risk for ischemic stroke. Many patients with acute ischemic stroke have a mismatch pattern in which the PWI volume is larger than the DWI lesion. This mismatch typically resolves over 24-48 hours. Little is known about the presence of DWI-PWI mismatch in later stages of stroke. METHODS: This is a retrospective study of 122 patients admitted with a diagnosis of acute ischemic stroke who had DWI and PWI abnormalities on studies performed within 7 days of onset of symptoms. Patients were divided into two groups: those with MRI performed <48 hours and those with MRI performed >or=48 hours from onset of symptoms. RESULTS: Among 42 patients with MRI performed >or=48 hours after onset of stroke symptoms, 15 of 42 (36%) showed a mismatch pattern, compared to 45 of 80 (56%) in the <48 hours group (P < 0.05). Most of the patients in the >or=48 hours group with mismatch had large artery occlusive disease and many had neurological fluctuations. A subset of these patients were treated with induced hypertension and showed clinical improvement. CONCLUSIONS: Some patients have persistent DWI-PWI mismatch up to several days after stroke onset. Further studies are needed to determine if these patients should be candidates for reperfusion therapy.

Blood pressure management in acute stroke.

The optimal management of arterial blood pressure in the setting of acute stroke has not been firmly defined. The different types of stroke--ischemic, intracerebral hemorrhage, and subarachnoid hemorrhage--have different pathophysiologies and require different approaches in terms of blood pressure management in the acute setting. This article reviews the current literature and experience at the authors' institution.

Low-grade carotid stenosis: looking beyond the lumen with MRI.

BACKGROUND AND PURPOSE: The management of carotid atherosclerosis is well-established for symptomatic stenosis above 69%, but the optimal approach for managing lower degrees of narrowing remains uncertain. Because the risk of stroke increases with higher grades of stenosis, we are inclined to consider low-grade disease to be low risk. This approach, however, does not take into account other factors such as plaque size or composition. Plaque may progress to a substantial size before it demonstrates significant stenosis by angiography. We know that low-grade disease can result in cerebrovascular ischemic events, but predicting vulnerable lesions has not been possible by relying on stenosis alone. SUMMARY OF REVIEW: An understanding of the clinical behavior of plaque causing little to no narrowing is now possible with the advent of high-resolution black blood MRI, a modality that does not rely on luminal narrowing for detection. CONCLUSIONS: We present the current understanding of the clinical implications of low-grade carotid stenosis with an example of the MRI assessment of high-risk carotid plaque causing minimal narrowing that highlights the importance of looking beyond the lumen.

Quantitation of contrast TCD in patients with and without atrial septal aneurysm.

BACKGROUND AND PURPOSE: Patients with a combination of atrial septal aneurysm (ASA) and patent foramen ovale (PFO) have a substantially higher rate of recurrent ischemic events as compared to PFO alone. One possible explanation is a greater degree of right-to-left shunting with the combination. METHODS: Retrospective study using contrast transcranial Doppler ultrasonography (c-TCD) to study the degree of shunting in 46 patients with PFO with either transient ischemic attack or cryptogenic ischemic stroke. Eight patients with PFO+ASA identified on transesophageal echocardiogram were compared to 38 patients with PFO but without ASA. RESULTS: The number of embolic counts was no different with or without an ASA. Valsalva maneuver increased number of emboli, especially in patients with large PFOs. CONCLUSIONS: Patients with ASA in addition to PFO do not appear to have an increased risk of right-to-left shunting as measured by c-TCD as compared to PFO alone.

Etiology of perfusion-diffusion magnetic resonance imaging mismatch patterns.

BACKGROUND AND PURPOSE: Diffusion-and perfusion-weighted magnetic resonance imaging (DWI and PWI) are useful tools for the assessment of brain ischemia. Discrepancies between the extent of DWI and PWI abnormalities are thought to depend pre dominantly on time from symptom onset to magnetic resonance imaging (MRI) examination. However, underlying ischemic stroke etiology can also be important. A mismatch may indicate the presence of tissue at risk for infarction, whereas the relevance of other DWI/PWI patterns is uncertain. The authors therefore investigated the etiology of brain ischemia in patients with different DWI/PWI patterns. METHODS: Retrospective study of 130 patients with acute brain ischemia and detailed stroke workup, including MRI within a week after symptom onset (40 +/- 39 hours). Patients were divided into the following groups: mis-match (PWI > DWI), reverse mismatch (DWI > PWI), and match (<25% difference between PWI and DWI). RESULTS: Mismatch occurred in 49% of patients, whereas 22% had reverse mis-match and 29% matched lesions. Time from symptom onset to MRI examination was similar between the 3 groups. Largeartery atherosclerosis increased by almost 4-fold the odds of mismatch (odds ratio: 3.89, 95% confidence interval: 1.72-8.78; P < .001), whereas patients with reverse mismatch were likely to have cryptogenic stroke. Patients with matched lesions were similarly distributed among different stroke subtypes. CONCLUSIONS: Ischemic stroke etiology appears to influence the development of specific DWI/PWI patterns. Prospective studies are needed to confirm these observations.

Neurovascular complications of marfan syndrome: a retrospective, hospital-based study.

BACKGROUND AND PURPOSE: Small case series have associated Marfan syndrome with cerebral and spinal ischemia or hemorrhage. However, there has been no investigation of the frequency and etiology of neurovascular disorders in a large series of Marfan patients. METHODS: We conducted a retrospective, hospital-based study of all Marfan syndrome patients seen in an 8-year period. Records were reviewed in detail, and clinical characteristics of those with and without a neurovascular diagnosis compared. RESULTS: Of 513 patients, 18 (3.5%) had a neurovascular diagnosis, as follows: transient ischemic attack (11), cerebral infarction (2), spinal cord infarction (2), subdural hematoma (2), and spinal subarachnoid hemorrhage (1). A cardioembolic source was identified in 12 of 13 patients with cerebral ischemia, as follows: prosthetic heart valves (9), mitral valve prolapse (2), and atrial fibrillation (1). Chronic anticoagulant therapy was a likely cause in 2 of 3 patients with hemorrhagic events. Compared with other Marfan syndrome patients, those with neurovascular events were older (39.6 versus 31.7 years, P=0.04) and more likely to be in atrial fibrillation (22.2% versus 3.2%, P=<0.01), to have prosthetic heart valves (61.1% versus 7.7%, P=0.001), and to be taking anticoagulant therapy (72.2% versus 16.1%, P<0.001). Aortic disease, a putative factor in the etiology of neurovascular complications, was present in equal measure in Marfan patients with and without neurovascular complications (78% versus 65%, P=NS). CONCLUSIONS: Neurovascular complications of Marfan syndrome are rare during 8 years of follow-up, and generally are ischemic in nature. A high-risk cardiac source was identified in the majority. A significant association with vascular dissection was not established.

Change in perfusion in acute nondominant hemisphere stroke may be better estimated by tests of hemispatial neglect than by the National Institutes of Health Stroke Scale.

BACKGROUND AND PURPOSE: It has been reported that National Institutes of Health Stroke Scale (NIHSS) scores correlate poorly with hypoperfused tissue measured by perfusion-weighted imaging (PWI) in nondominant hemisphere stroke. We conducted 2 studies to determine whether tests of hemispatial neglect provide a better measure of hypoperfusion and reperfusion than NIHSS in nondominant hemisphere stroke. METHODS: In study 1, 74 patients with acute ischemic, supratentorial stroke were administered the NIHSS, tests of neglect or aphasia, and diffusion-weighted imaging (DWI) and PWI on day 1 (<24 hours from onset) of stroke. Pearson correlations between volumes of PWI/DWI abnormality and functional tests were calculated. In study 2, 10 patients with acute, nondominant hemisphere stroke who were candidates for intervention to restore perfusion underwent PWI, DWI, NIHSS, and a line cancellation test on days 1 and 3. Correlations between change in volumes of PWI/DWI abnormality and change in functional tests were calculated. RESULTS: In study 1, in nondominant hemisphere stroke, volume of PWI abnormality correlated significantly with neglect scores (r=0.71; P<0.002) but not with NIHSS scores (r=0.39; P=NS). In dominant hemisphere stroke, volume of PWI abnormality correlated better with aphasia scores (r=0.50; P=0.0001) than with NIHSS scores (r=0.45; P=0.001). In study 2, change in volume of hypoperfused tissue on PWI correlated with change in line cancellation performance (r=0.83; P=0.003) but not with change in NIHSS score (r=0.26; P=NS). CONCLUSIONS: Tests of hemispatial neglect may better reflect dysfunction and reperfusion than NIHSS for patients with nondominant hemisphere stroke.

Diffusion- and perfusion-weighted magnetic resonance imaging of the brain before and after coronary artery bypass grafting surgery.

BACKGROUND AND PURPOSE: Coronary artery bypass grafting (CABG) is a frequently performed surgical procedure that can be associated with neurological complications. Some studies have demonstrated that new focal brain lesions, detected by MRI, can develop after CABG. Furthermore, it has been suggested that the presence of such new lesions is associated with a decline in neurocognitive test scores. Advanced MRI techniques, including diffusion- (DWI) and perfusion-weighted imaging (PWI), offer important diagnostic advantages over conventional imaging in the assessment of patients undergoing CABG. We sought to determine whether focal PWI and DWI abnormalities could occur after CABG, particularly in patients without any measurable neurological deterioration. METHODS: Thirteen patients prospectively underwent MRI with DWI and PWI before and after CABG. A battery of neurocognitive tests was administered before and after surgery. Demographic, clinical, and radiographic characteristics of the patients were collected and compared. RESULTS: Four patients developed new DWI defects after CABG. The lesions were small, rounded, and multiple (3 of 4 patients). One of these patients was diagnosed with stroke on clinical grounds. The patients with new lesions had a larger neurocognitive decline than their counterparts with stable MRI. Other clinical characteristics of patients with new DWI lesions, including stroke risk factors, were similar to those of patients without MRI changes. No focal perfusion abnormalities were observed on preoperative or postoperative scans. CONCLUSIONS: Postoperative DWI abnormalities can occur after CABG, even in patients without overt neurological defects. The PWI scans remained unchanged. Larger prospective studies are required to determine whether the new lesions are clearly associated with neurocognitive decline or with specific perioperative stroke risk factors.

Cryptogenic stroke in relation to genetic variation in clotting factors and other genetic polymorphisms among young men and women.

BACKGROUND AND PURPOSE: The purpose of the present study was to compare the prevalences of genetic polymorphisms in persons with cryptogenic stroke with those among stroke patients with evidence of large-artery occlusive disease or an unequivocal cardioembolic source (noncryptogenic stroke). METHODS: We compared the prevalences of genetic polymorphisms thought to be related to thrombi formation in young stroke patients with evidence of large-artery occlusive disease or an unequivocal cardioembolic source (noncryptogenic stroke; controls; n=79) with those in young stroke patients without such sources (cryptogenic stroke; cases; n=67). Common variations in the genes encoding factor V, prothrombin, angiotensin I-converting enzyme, 5,10-methylenetetrahydrofolate reductase, endothelial cell nitric oxide synthase, tissue plasminogen activator, plasminogen activator inhibitor-1, and fibrinogen were evaluated. We also compared the allele prevalence of these genes among all stroke patients with those among a large pool of historical controls assayed for these genes. RESULTS: None of these genetic polymorphisms was statistically significantly related to cryptogenic stroke. With respect to a comparison of all ischemic stroke with historical controls, only the prevalence of tissue plasminogen activator D allele among stroke subjects was statistically significantly higher than that of the historical controls (P=0.0014). CONCLUSIONS: These findings generally do not support the hypothesis that genes associated with a prothrombotic state are risk factors among a subgroup of young people with stroke of undetermined cause. Except for the D tissue plasminogen activator allele, the findings also indicated that these genetic factors are unrelated, or only weakly related, to all ischemic stroke.

Acquired immunodeficiency syndrome and the risk of stroke.

BACKGROUND AND PURPOSE: Although acquired immunodeficiency syndrome (AIDS) is thought to increase the risk of stroke, few data exist to quantify this risk. This is the first population-based study to quantify the AIDS-associated risk of stroke. METHODS: We identified all incident ischemic stroke (IS) and intracerebral hemorrhage (ICH) cases among young adults 15 to 44 years of age in central Maryland and Washington, DC, who were discharged from any of the 46 hospitals in the study area in 1988 and 1991. Using data from the medical records, 2 neurologists reviewed each case to confirm the diagnosis. Cases of AIDS among these patients with stroke were defined using Centers for Disease Control and Prevention criteria (1987). The number of cases of AIDS in the central Maryland and Washington population during 1988 and 1991 was determined from regional health departments working with the Centers for Disease Control and Prevention. Poisson regression was used to estimate the age-, race-, and sex-adjusted relative risk of stroke associated with AIDS. RESULTS: There were 385 IS cases (6 with AIDS) and 171 ICH cases (6 with AIDS). The incidences of IS and ICH among persons with AIDS were both 0.2% per year. AIDS conferred an adjusted relative risk of 13.7 (95% confidence interval [CI], 6.1 to 30.8) for IS and 25.5 (95% CI, 11.2 to 58.0) for ICH. After exclusion of 5 cases of stroke in AIDS patients in whom other potential causes were identified, AIDS patients continued to have an increased risk of stroke with an adjusted relative risk of 9.1 (95% CI, 3.4 to 24.6) for IS and 12.7 (95% CI, 4.0 to 40.0) for ICH. CONCLUSIONS: This population-based study found that AIDS is strongly associated with both IS and ICH.

Antiphospholipid antibodies and stroke in young women.

BACKGROUND AND PURPOSE: Antiphospholipid antibodies have been associated with ischemic stroke in some but not all studies. METHODS: We performed a population-based case-control study examining antiphospholipid antibodies (anticardiolipin antibodies and lupus anticoagulants) using stored frozen sera and plasma in 160 cases and 340 controls enrolled in the Stroke Prevention in Young Women study. We evaluated for the presence of anticardiolipin antibody (IgG, IgM, and IgA isotypes) by an enzyme-linked immunosorbent assay and for the lupus anticoagulant using several phospholipid-dependent coagulation tests (activated partial thromboplastin time, dilute Russell's viper venom time) with mixing studies. If mixing studies were prolonged, confirmatory tests were performed. RESULTS: A positive anticardiolipin antibody level of any isotype was seen in 43 cases (26.9%) and 62 controls (18.2%) (P=0.03), lupus anticoagulant in 29 cases (20.9%) and 38 controls (12.8%) (P=0.03), and either anticardiolipin antibody or lupus anticoagulant in 61 cases (42.1%) and 86 controls (27.9%) (P=0.003). After adjustment for age, current cigarette smoking, hypertension, diabetes, angina, ethnicity, body mass index, and high-density lipoprotein levels, the relative odds of stroke for women with anticardiolipin antibody immunoreactivity of any isotype or a lupus anticoagulant was 1.87 (95% confidence interval, 1.24 to 2.83; P=0.0027). CONCLUSIONS: The results from this study support the importance of antiphospholipid antibodies as an independent risk factor for stroke in young women.

Outcome at 30 days in the New England Medical Center Posterior Circulation Registry.

BACKGROUND: Vertebrobasilar disease is generally considered a condition with a poor prognosis because of high rates of mortality and severe disability. OBJECTIVE: To compare the outcomes of 407 patients entered in the New England Medical Center Posterior Circulation Registry with the reported results of other studies. RESULTS: In contrast, among 407 patients prospectively and consecutively studied in the New England Medical Center Posterior Circulation Registry, we found a low mortality rate at 30 days after onset (3.6%) and relatively low rates of major disability (18% using a Modified Rankin Disability Scale score). Thirty days after stroke, 28% of the patients had no disability and 51% had only a minor disability. Stroke location, stroke mechanism, and arteries involved predicted outcome. Basilar artery involvement, embolic stroke mechanism, and multiple posterior circulation intracranial territory involvement correlated with poor outcome. Patients with lesions in the basilar artery were 5 times more likely to have a poor outcome independent of other factors. Lesions in the middle and distal territories were each associated with a poor outcome in one third of the patients. CONCLUSION: In contrast with previous reports, we found that vertebrobasilar occlusive disease consists of a variety of different stroke mechanisms and vascular lesions, many with a good prognosis.

Assessment of transient ischemic attack with diffusion- and perfusion-weighted imaging.

BACKGROUND: Diagnosing TIA can be difficult, since evidence of brain ischemia is habitually lacking on CT and conventional MR imaging. It has been suggested that patients with acute brain infarction on neuroimaging should be considered stroke cases instead of TIA, regardless of duration of symptoms, implying that optimal diagnostic methods need to be utilized. We therefore postulated that perfusion-weighted MR imaging (PW imaging) would be useful in the diagnosis of TIA. METHODS: Retrospective analysis of 22 patients with reversible neurologic symptoms lasting less than 24 hours, assessed with DW and PW imaging. RESULTS: MR imaging was abnormal in 15 patients (68%): 12 had abnormal DW imaging, four had both DW and PW imaging defects (all with a mismatch) and three had an isolated PW imaging abnormality. There were no differences in symptom duration, stroke etiology or cardiovascular risk factors between patients with abnormal MR imaging and those with unremarkable scan. Patients with mismatch were more likely to need conventional angiography or other cerebrovascular procedures. CONCLUSION: The combined use of DW imaging and PW imaging provided evidence of brain ischemia in most patients with clinical diagnosis of TIA. Prospective studies using follow-up MR imaging are required to determine the outcome of affected tissue, as well as the clinical implications of DW-PW imaging abnormalities.