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Our objectives were to investigate the utility of the Hachinski Ischemic Score (HIS) in differentiating patients with pathologically verified Alzheimer's disease (AD), multi-infarct dementia (MID), and "mixed" (AD plus cerebrovascular disease) dementia, and to identify the specific items of the HIS that best discriminate those dementia subtypes. Investigators from six sites participated in a meta-analysis by contributing original clinical data, HIS, and pathologic diagnoses on 312 patients with dementia (AD, 191; MID, 80; and mixed, 41). Sensitivity and specificity of the HIS were calculated based on varied cutoffs using receiver-operator characteristic curves. Logistic regression analyses were performed to compare each pair of diagnostic groups to obtain the odds ratio (OR) for each HIS item. The mean HIS (+/- SD) was 5.4 +/- 4.5 and differed significantly among the groups (AD, 3.1 +/- 2.5; MID, 10.5 +/- 4.1; mixed, 7.7 +/- 4.3). Receiver-operator characteristic curves showed that the best cutoff was < or = 4 for AD and > or = 7 for MID, as originally proposed, with a sensitivity of 89.0% and a specificity of 89.3%. For the comparison of MID versus mixed the sensitivity was 93.1% and the specificity was 17.2%, whereas for AD versus mixed the sensitivity was 83.8% and the specificity was 29.4%. HIS items distinguishing MID from AD were stepwise deterioration (OR, 6.06), fluctuating course (OR, 7.60), hypertension (OR, 4.30), history of stroke (OR, 4.30), and focal neurologic symptoms (OR, 4.40). Only stepwise deterioration (OR, 3.97) and emotional incontinence (OR, 3.39) distinguished MID from mixed, and only fluctuating course (OR, 0.20) and history of stroke (OR, 0.08) distinguished AD from mixed. Our findings suggest that the HIS performed well in the differentiation between AD and MID, the purpose for which it was originally designed, but that the clinical diagnosis of mixed dementia remains difficult. Further prospective studies of the HIS should include additional clinical and neuroimaging variables to permit objective refinement of the scale and improve its ability to identify patients with mixed dementia.

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BACKGROUND: Although risk factors for first stroke have been identified, the predictors of long-term stroke recurrence are less well understood. We performed the present study to determine whether dementia diagnosed three months after stroke onset is an independent risk factor for long-term stroke recurrence. METHODS: We examined 242 patients (age = 72.0 +/- 8.7 years) hospitalized with acute ischemic stroke who had survived the first three months without recurrence and followed them to identify predictors of long-term stroke recurrence. We diagnosed dementia three months after stroke using modified DSM-III-R criteria based on neuropsychological and functional assessments. The effects of conventional stroke risk factors and dementia status on survival free of recurrence were estimated using Kaplan-Meier analyses, and the relative risks (RR) of recurrence were calculated using Cox proportional hazards models. RESULTS: Dementia (RR = 2.71, 95% CI = 1.36 to 5.42); cardiac disease (RR = 2.18, CI = 1.15 to 4.12); and sex, with women at higher risk (RR = 2.03, CI = 1.01 to 4.10), were significant independent predictors of recurrence, while education (RR = 1.90, CI = 0.77 to 4.68), admission systolic blood pressure >160 mm Hg (RR = 1.80, CI = 0.94 to 3.44) and alcohol intake exceeding 160 grams per week (RR = 1.86, CI = 0.79 to 4.38) were weakly related. CONCLUSIONS: Our results suggest that dementia significantly increases the risk of long-term stroke recurrence, with additional independent contributions by cardiac disease and sex. Cognitive impairment may be a surrogate marker for multiple vascular risk factors and larger infarct volume that may serve to increase the risk of recurrence. Alternatively, less aggressive medical management of stroke patients with cognitive impairment or noncompliance of such patients with medical therapy may be bases for an increased rate of stroke recurrence.

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OBJECTIVE: To investigate the association between the apolipoprotein E (APOE) genotypes and dementia in patients with stroke, defined as either vascular dementia (VaD) or Alzheimer disease with cerebrovascular disease (AD with CVD). DESIGN AND SETTING: Population-based, case-control study from Rotterdam, the Netherlands, and New York City. PARTICIPANTS: A total of 187 patients with dementia and stroke were compared with 507 controls similar in age and ethnic group. MAIN OUTCOME MEASURES: The APOE allele frequencies in patients and controls; the odds ratio of dementia with stroke, VaD, and AD with CVD, adjusted for age, sex, residency, and education; and the percent attributable risk related to the APOE epsilon4 allele. RESULTS: Overall, patients with dementia and stroke had a higher APOE epsilon4 allele frequency than controls. Compared with APOE epsilon3 homozygote individuals, APOE epsilon4 homozygotes had a 7-fold increased risk of dementia with stroke (OR=6.9; 95% CI, 1.6-29.4), while APOE epsilon4 heterozygotes had nearly a 2-fold increase in risk (OR=1.8; 95% CI, 1.2-2.7). Risks associated with APOE epsilon4 were elevated regardless of the subtype of dementia with stroke or age or sex. The percent attributable risk related to the APOE epsilon4 allele among demented patients with stroke was 41% overall, 33% among those with VaD, and 44% among those with AD with CVD. CONCLUSION: The APOE epsilon4 allele is a genetic risk factor for dementia with stroke, including VaD and AD with CVD. This may imply shared genetic susceptibility to dementia associated with stroke and AD. Alternatively, the category of patients with dementia and stroke, including VaD as currently defined, may include patients with AD.

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Objectives. Both the number and type of higher cortical function deficits (HCFD) in acute stroke patients are important diagnostically and for gauging the extent of neurological deficits. Methods. The Stroke Data Bank (SDB) provided a large prospective data base for such evaluation. Thirty-one different HCFDs, each defined in the SDB manual, were considered. Results. Of 1,805 patients in the SDB, 641 instances of HCFD in 422 patients were recorded in alert patients at initial examination (within the first 7 to 10 days of ictus). Aphasia (41%) was the most commonly found HCFD, followed by neglect syndrome (27.2%), apraxia (11.7%), and anosognosia (11.1%). Agnosia (3.9%), alexia (3.3%), and aprosodia (1.5%) were less frequently found HCFDs. Cardioembolic infarct was most likely to have associated HCFDs (66%), and lacunar infarction was least likely to be accompanied by HCFDs (6%), with infarction caused by large artery thrombosis (50%) and infarct of undetermined cause (47%) having similar frequencies. The co-occurrence of sensory and motor deficits among the eight major subgroups of HCFD showed that neglect syndrome, apraxia, and anosognosia were most likely to be associated with long tract signs, whereas alexia, aprosodia, and agnosia invariably were not associated with sensorimotor impairment. Approximately half of aphasic patients had associated sensorimotor impairment. Conclusion. Our findings show that higher cortical function deficits are prevalent in the acute phase of stroke, particularly aphasia and neglect syndromes. They are more often associated with nonlacunar stroke and some are less likely to be associated with any sensorimotor deficits.

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BACKGROUND AND PURPOSE: Stroke significantly increases the risk of dementia in the elderly, yet the risk factors for incident dementia after ischemic stroke are not well understood. We attempted to determine whether hypoxic-ischemic (HI) disorders, which may result from comorbid medical conditions (eg. seizures, cardiac arrhythmias, pneumonia), would be an independent risk factor for the development of new dementia after stroke. METHODS: We prospectively followed 185 initially nondemented patients with ischemic stroke (age, 70.3 +/- 7.7 years) for a maximum of 52.8 months. We diagnosed the presence of dementia at annual examinations based on neuropsychological testing and modified DSM-III-R criteria. HI disorders were identified by record review or examination during hospitalization. We used Kaplan-Meier analysis to determine the cumulative proportion of patients with and without HI disorders who survived free of dementia and used Cox models to estimate the relative risk of dementia associated with HI disorders. RESULTS: The cumulative proportion (+/- SE) surviving without dementia was 51.7 +/- 10.9% in the HI group versus 78.2 +/- 4.3% in the non-HI group after 52.8 months of observation. The relative risk of incident dementia associated with HI events was 4.3 (95% confidence interval = 1.9 to 9.6) after we adjusted for demographic factors, recurrent stroke, and baseline cognitive function. CONCLUSIONS: We conclude that HI disorders may be a significant independent risk factor for incident dementia after stroke, even after adjustment for other recognized predictors of cognitive decline. Recognition of HI cerebral damage as a possible pathogenic mechanism for dementia after stroke may allow targeted therapeutic interventions to prevent subsequent cognitive deterioration.

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Central pontine myelinolysis (CPM) is a rare syndrome generally linked to hyponatremia. Autopsy and imaging studies described demyelination in the central pons, in some cases combined with thalamic, internal capsular, hemispheric and cerebellar white matter lesions. The clinical syndrome and prognosis spans from asymptomatic patients displaying only imaging lesions to coma and death. Frequent findings are pyramidal tract and pseudobulbar signs. No effective treatment is known. Alcohol abuse is often associated. The imaging pattern of CPM is unique and generally accepted as diagnostic when other causes such as ischemia, multiple sclerosis, tumors, radiation, or pharmacological effects are ruled out. However, the exact mechanism of this selective process of demyelination remains obscure. The current major controversy concerns the role of therapeutic efforts of sodium level restoration in the etiology of CPM. We present a case of CPM where no hyponatremia was found. We hypothesize that (1) iatrogenic sodium restoration may not in all cases of CPM be the putative mechanism, (2) the clinical onset of CPM may in some patients represent a delayed response to an initially asymptomatic demyelination, and (3) normal admission sodium levels do not exclude the diagnosis of CPM.

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Statistical methods traditionally used in the analysis of change (e.g., repeated measures ANOVA) may be inadequate for the investigation of cognitive decline if a study's effect size is small, the variance within groups is heterogeneous, or the statistical power is low. To examine an alternative approach to the determination of clinically meaningful cognitive decline and investigate whether such decline occurs during the first year after stroke, we administered a neuropsychological test battery to 172 patients (age = 70.3 +/- 7.6 years; education = 10.3 +/- 4.7 years) 3 and 12 months after stroke and 199 nondemented stroke-free control subjects (age = 71.1 +/- 6.4 years; education = 12.8 +/- 4.2 years) on two occasions 12 months apart. Two neuropsychologists classified each subject's test performance as having declined, improved, or remained stable based solely on clinical judgment. Reliability of the rating of decline versus the pooled rating of improvement/stability was excellent (kappa = 0.79). The two rating groups differed significantly and in the appropriate directions in change on most tests. While a MANOVA comparing the stroke and control groups on change in test scores was not significant, logistic regression analysis determined that a rating of clinically meaningful cognitive decline was associated with stroke status (Odds Ratio = 1.8, 95% Confidence Interval = 1.0 to 3.2), while adjusting for demographic factors. We propose that this alternative approach to the analysis of cognitive change can facilitate the recognition of decline in subgroups of subjects. It would be valuable as an adjunct to studies of the incidence of dementia, for example, in which the recognition of cognitive decline might be difficult in highly educated patients whose baseline level of performance is far above the cutoffs operationalized for the diagnosis of dementia.

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A 55 year old man with bilateral internal carotid and unilateral vertebral artery occlusions presented subacutely with profound behavioural and cognitive changes featuring frontal lobe deficits. Neuropsychological testing showed severe cognitive impairment compatible with dementia. Anatomical imaging showed only a small right superior frontal infarction. Cerebral blood flow was severely reduced, with profound hypofrontality and limited hypercapnic reactivity, and cerebral metabolism was reduced primarily in the medial frontal lobes. After right sided extracranial to intracranial cerebral bypass surgery, both flow and metabolism improved, as did behavioural and neuropsychological deficits. Perfusion insufficiency from bilateral carotid occlusions, with secondarily reduced metabolism in the frontal zones bilaterally, may be an unusual cause of a reversible frontal dementia syndrome.

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BACKGROUND AND PURPOSE: This study was an attempt to determine whether CT and MRI are comparable or if one is superior to the other in the early detection of ischemic stroke or hematoma. METHODS: Patients with acute stroke were sought within 3 hours of onset for clinical examination and prospective evaluation by concurrently performed CT and MRI. Repeated clinical and imaging studies were undertaken when possible immediately after imaging and at 24 hours, 3 to 5 days, and 3 months. The study neurologists were blinded to the results of imaging, as were the study radiologists to the clinical findings. The study radiologists read the scans in sequence, mapping each imaging on standard templates before viewing a later scan. No retrospective revisions of imaging mapping of earlier images were undertaken. RESULTS: Sixty-eight patients were recruited within 4 hours and an additional 12 patients within 24 hours. Seventy-five strokes were due to infarction and five to hemorrhage. The median time to first scan was 132 minutes. Although some of the infarctions in 75 patients were detected within 1 hour, the fraction of positive first scans approached an asymptote at 2 to 3 hours. Overall, with the use of conventional non-contrast-enhanced CT and T1- and T2-weighted MRI, neither was superior in the very early detection of either hematoma or infarction. There was a marginally significant correlation between early positive brain imaging and the severity of the stroke. Some patients had initially positive CT and/or MRI scans, but their neurological examination had returned to normal by 24 hours. Overall, CT was better than baseline MRI at predicting 24-hour outcome. After 24 hours, both CT and MR more conspicuously defined the lesion limits than they did at baseline. CONCLUSIONS: With the technology available through 1991, neither CT nor MRI proved superior in the detection of the earliest signs of stroke.

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The mechanisms of dementia resulting from small deep infarctions are incompletely understood. The thesis underlying the concept of "multi-infarct dementia" is that multiple lesions have a synergistic effect on mental functions, resulting in dementia irrespective of specific location or volume. In this report, we summarize our experience with six patients reported previously along with additional patients examined subsequently, whose clinical features and brain imaging findings allow an alternative formulation for dementia resulting from lacunar stroke. The six initial patients presented with an abrupt change in behavior after acute infarction involving the inferior genu of the internal capsule documented by computed tomography (CT) and magnetic resonance imaging (MRI). The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia were evident in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients using 133xenon regional cerebral blood flow (rCBF) and single photon emission computed tomography (SPECT) showed focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. Perfusion was also defective in the medial and laterial temporal cortex. Important pathways of the limbic system traverse the inferior capsule in the region of the genu. Corticothalamic and thalamocortical fibers form the thalamic peduncles which detach from the internal capsule and enter the thalamus at its rostral and caudal poles and along its dorsal surface. The anterior thalamic peduncle, conveys reciprocal connections between the dorsomedial nucleus and the cingulate gyrus, as well as the prefrontal and orbitofrontal cortex. The inferior thalamic peduncle carries fibers which connect the thalamus with orbitofrontal, insular, and temporal cortex, as well as the amygdala via the ansa peduncularis to the ventral amygdalofugal pathway. Thus, damage to one or both white-matter tracts may occur with infarctions in the region of the inferior genu, causing striking frontal behavioral effects and memory loss in our patients associated with functional deactivation of the ipsilateral frontal and temporal cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

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To investigate the frequency, course, and clinical correlates of disorientation following stroke, we administered the Mini-Mental State Examination orientation subtest to 177 alert patients 7-10 days and 3 months after stroke and 240 stroke-free nondemented subjects. Disorientation was defined as a score < or = 8/10. Seventy-two (40.7%) of the patients were disoriented 7-10 days after stroke and 39 patients (22.0% of the sample) remained disoriented 3 months later. A logistic regression analysis determined that persistent disorientation was significantly related to stroke status [odds ratio (OR) = 5.8], after adjusting for memory and attentional deficits and demographic variables. Among stroke patients, disorientation was associated with severe hemispheral stroke syndromes (OR = 7.7), but not infarct location or vascular risk factor history, after adjusting for memory and attentional deficits and demographic variables. Sensitivity and specificity analyses determined that disorientation was an inaccurate marker for dementia or deficits in memory or attention, while intact orientation was associated with a low probability of dementia or memory dysfunction in most patients but not preserved attention. We conclude that disorientation is common and persistent following stroke and associated with severe hemispheral stroke syndromes but not infarct location. While disorientation is a poor marker for dementia or deficits in memory or attention, intact orientation should suggest that cognitive functions are likely to be preserved.

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Stroke is considered the second most common cause of dementia, but the magnitude of the risk posed by stroke has not been fully clarified. The aim of this study was to determine the long-term risk of developing dementia after stroke onset in a hospitalized cohort. We prospectively examined 185 nondemented patients aged > or = 60 years hospitalized with ischemic stroke and 241 age-matched nondemented controls without stroke from the same community using neurologic, neuropsychological, and functional assessments given annually. Using criteria modified from the DSM-III-R, we diagnosed incident dementia based on the annual examination findings. We used life-table methods to estimate incidence in the two groups, Kaplan-Meier analysis to determine the proportion surviving without dementia, and Cox proportional-hazards analysis to compute the relative risk (RR) of dementia after 1 to 4 years of follow-up. The incidence of dementia was 8.4 per 100 person-years in the stroke group and 1.3 per 100 person-years in the control group. After 52 months of follow-up, the cumulative proportion (+/- SE) surviving without dementia was 66.3 +/- 5.5% for stroke and 90.3 +/- 4.3% for control subjects. The RR of dementia associated with stroke compared with controls was 5.5 (95% CI, 2.5 to 11.1) after adjusting for demographic factors. Older age at stroke onset and fewer years of education were significant covariates, but sex and race were not. A low score on the Mini-Mental State Examination at baseline was a significant predictor when added to this model.(ABSTRACT TRUNCATED AT 250 WORDS)

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BACKGROUND AND PURPOSE: The aim of this study was to determine whether dementia after stroke adversely influences long-term survival. METHODS: Subjects were 251 patients > or = 60 years of age with ischemic stroke who were given neurological, neuropsychological, and functional examinations 3 months after hospitalization and were followed up prospectively. Using criteria modified from the Diagnostic and Statistical Manual of Mental Disorders-III-R, dementia was found in 66 (26.3%) patients at the 3-month baseline examination. Life-table methods were used to estimate mortality rates in the groups with and without dementia after 1 to 5 years of follow-up, Kaplan-Meier curves to estimate the cumulative proportion surviving with and without dementia, and Cox proportional-hazards analysis to compute the relative risk of mortality associated with dementia at baseline, after adjusting for other potential predictors of stroke mortality. RESULTS: The mortality rate was 19.8 deaths per 100 person-years with dementia compared with 6.9 deaths per 100 person-years without dementia. The cumulative proportion surviving after a median follow-up of 58.6 months was 38.9 +/- 0.08% for those with dementia and 74.5 +/- 0.04% for those without dementia. The relative risk associated with dementia was 3.11 (95% confidence interval, 1.79 to 5.41) after adjusting for the effects of demographic factors, cardiac disease, severity of stroke (Barthel Index), stroke type (lacunar versus nonlacunar), and recurrent stroke (examined as a time-dependent variable). When the Mini-Mental State Examination score at baseline was examined instead of the diagnosis of dementia, the results of the model were similar. CONCLUSION: Our study is the first to demonstrate that dementia or cognitive impairment adversely influences long-term survival after stroke, even after adjusting for other commonly accepted predictors of stroke mortality. Impairment in intellectual function after stroke, independent of physical disability, has a significant impact on prognosis. Both cognitive and physical functions should be assessed in clinical studies of stroke outcome.

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BACKGROUND: The pathophysiology of stroke-like episodes in MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) is uncertain. CASE DESCRIPTION: We studied a 24-year-old man with MELAS who had fluent aphasia and right hemianopia. Magnetic resonance imaging and computed tomography showed a large infarction in the parietal, temporal, and occipital lobes. We performed serial planar 133Xe regional cerebral blood flow studies and single-photon emission computed tomography. Fifteen and 26 days after the stroke-like episode, there was generalized hyperperfusion, highest in infarcted areas. Four and 8 months after the stroke-like episode, the brain was still hyperemic, with highest flow in noninfarcted tissue. Reactivity to CO2 was less than normal within the infarct at 26 days but improved thereafter. In the noninfarcted region, vasomotor reactivity was impared at 4 months, when resting flows were at their peak. CONCLUSIONS: We observed generalized cerebral hyperemia and fluctuating CO2 reactivity in MELAS, possibly a consequence of local lactic acid production. In addition, this case suggests that nonquantitative functional imaging may be misleading in MELAS.

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OBJECTIVE: Several cross-sectional studies have found an association between Alzheimer's disease (AD) and limited educational experience. It has been difficult to establish whether educational experience is a risk factor for AD because educational attainment can influence performance on diagnostic tests. This study was designed to determine whether limited educational level and occupational attainment are risk factors for incident dementia. DESIGN: Cohort incidence study. SETTING: General community. PARTICIPANTS: A total of 593 nondemented individuals aged 60 years or older who were listed in a registry of individuals at risk for dementia in North Manhattan, NY, were identified and followed up. INTERVENTIONS: We reexamined subjects 1 to 4 years later with the identical standardized neurological and neuropsychological measures. MAIN OUTCOME MEASURES: Incident dementia. RESULTS: We used Cox proportional hazards models, adjusting for age and gender, to estimate the relative risk (RR) of incident dementia associated with low educational and occupational attainment. Of the 593 subjects, 106 became demented; all but five of these met research criteria for AD. The risk of dementia was increased in subjects with either low education (RR, 2.02; 95% confidence interval [Cl], 1.33 to 3.06) or low lifetime occupational attainment (RR, 2.25; 95% Cl, 1.32 to 3.84). Risk was greatest for subjects with both low education and low life-time occupational attainment (RR, 2.87; 95% Cl, 1.32 to 3.84). CONCLUSIONS: The data suggest that increased educational and occupational attainment may reduce the risk of incident AD, either by decreasing ease of clinical detection of AD or by imparting a reserve that delays the onset of clinical manifestations.

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Cognitive function was examined in 227 patients three months after admission to hospital for ischaemic stroke, and in 240 stroke-free controls, using 17 scored items that assessed memory, orientation, verbal skills, visuospatial ability, abstract reasoning, and attentional skills. After adjusting for demographic factors with standardised residual scores in all subjects, the fifth percentile was used for controls as the criterion for failure on each item. The mean (SD) number of failed items was 3.4 (3.6) for patients with stroke and 0.8 (1.3) for controls (p < 0.001). Cognitive impairment, defined as failure on any four or more items, occurred in 35.2% of patients with stroke and 3.8% of controls (p < 0.001). Cognitive domains most likely to be defective in stroke compared with control subjects were memory, orientation, language, and attention. Among patients with stroke, cognitive impairment was most frequently associated with major cortical syndromes and with infarctions in the left anterior and posterior cerebral artery territories. Functional impairment was greater with cognitive impairment, and dependent living after discharge either at home or nursing home was more likely (55.0% with, v 32.7% without cognitive impairment, p = 0.001). In a logistic model examining the risks related to dependent living after stroke, cognitive impairment was a significant independent correlate (odds ratio, OR = 2.4), after adjusting for age (OR = 5.2, 80 + v 60-70 years) and physical impairment (OR = 3.7, Barthel index < or = 40 v > 40). It is concluded that cognitive impairment occurs frequently after stroke, commonly involving memory, orientation, language, and attention. The presence of cognitive impairment in patients with strike has important functional consequences, independent of the effects of physical impairment. Studies of stroke outcome and intervention should take into account both cognitive and physical impairments.

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PURPOSE: To characterize cerebral hemodynamics in patients immediately before microsurgical resection of moderate to large arteriovenous malformations during isoflurane anesthesia. METHODS: In angiographically defined arteriovenous malformation feeding and nonfeeding arteries, transcranial Doppler studies were performed in 25 surgeries on 22 patients. The mean blood flow velocity and pulsatility index were recorded in the middle, anterior, and posterior cerebral arteries. Transcranial Doppler velocities were measured at end-tidal carbon dioxide tensions (PetCO2) of about 25 and 35 mm Hg. Carbon dioxide reactivity was calculated as percentage mean blood flow velocity change per mm Hg PetCO2 change. RESULTS: Patient demographic and clinical data for the arteriovenous malformation group followed the expected strata of a large arteriovenous malformation population. All patients were neurologically stable before surgery. A total of 43 feeding arteries and 55 nonfeeding arteries were studied. Compared with nonfeeders, feeders exhibited higher mean blood flow velocity (68 +/- 5 vs 31 +/- 3 cm/sec, P < 0.0001) and lower pulsatility index (0.64 +/- 0.03 vs 0.88 +/- 0.04, P < 0.001); anterior and middle cerebral artery velocities at normo- and hypocapnia were significantly higher than posterior cerebral arteries for both feeders and nonfeeders (P < 0.001). Carbon dioxide reactivity was 0.2 +/- 0.2%/mm Hg in feeders and 2.1 +/- 0.2%/mm Hg in nonfeeders, with no significant difference between arteries. In four of eight patients with lesions fed by the anterior circulation (middle cerebral artery with or without anterior cerebral artery feeders), posterior cerebral artery nonfeeders exhibited low reactivity. In 2 of 5 patients with ipsilateral posterior cerebral artery feeders, contralateral posterior cerebral artery nonfeeders exhibited impaired reactivity. CONCLUSIONS: Quantitative transcranial Doppler studies are technically feasible in the operating room or interventional suite during anesthesia. Hemodynamic assessment using physiologic challenges of arteriovenous malformation feeders as well as angiographically uninvolved vessels may be useful as criteria in the assessment of malformations and arteriovenous malformation patients may exhibit abnormal vasoreactivity in distant uninvolved perfusion territories, suggesting a deranged neural control mechanism.

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