Increase in national intravenous thrombolysis rates for ischaemic stroke between 2005 and 2012: is bigger better?

BACKGROUND: Intravenous thrombolytic therapy after ischaemic stroke significantly reduces mortality and morbidity. Actual thrombolysis rates are disappointingly low in many western countries. It has been suggested that higher patient volume is related to shorter door-to-needle-time (DNT) and increased thrombolysis rates. We address a twofold research question: a) What are trends in national thrombolysis rates and door-to-needle times in the Netherlands between 2005-2012? and b) Is there a relationship between stroke patient volume per hospital, thrombolysis rates and DNT? METHODS: We used data from the Stroke Knowledge Network Netherlands dataset. Information on volume, intravenous thrombolysis rates, and admission characteristics per hospital is acquired through yearly surveys, in up to 65 hospitals between January 2005 and December 2012. We used linear regression to determine a possible relationship between hospital stroke admission volume, hospital thrombolysis rates and mean hospital DNT, adjusted for patient characteristics. RESULTS: Information on 121.887 stroke admissions was available, ranging from 7.393 admissions in 2005 to 24.067 admissions in 2012. Mean national thrombolysis rate increased from 6.4% in 2005 to 14.6% in 2012. Patient characteristics (mean age, gender, type of stroke) remained stable. Mean DNT decreased from 72.7 min in 2005 to 41.4 min in 2012. Volume of stroke admissions was not an independent predictor for mean thrombolysis rate nor for mean DNT. CONCLUSION: Intravenous thrombolysis rates in the Netherlands more than doubled between 2005 and 2012, in parallel with a large decline in mean DNT. We found no convincing evidence for a relationship between stroke patient volume per hospital and thrombolysis rate or DNT.

Depressive symptoms and executive functioning in stroke patients: a follow-up study.

BACKGROUND: Cognitive and emotional sequellae are commonly observed in stroke patients and these symptoms often co-occur. Diagnosis can be difficult since symptoms of depression and executive dysfunction overlap. OBJECTIVE: To study the longitudinal relationship between depressive symptoms and executive dysfunction in stroke patients. METHODS: The study comprises of 116 first-ever stroke patients who were followed-up for 2 years and who were assessed for emotional and cognitive sequellae after 1, 6, 12, and 24 months. Emotional disturbances were evaluated using the SCL-90 depression subscale. Executive functions were assessed using compound scores of a combination of the interference scores of the Stroop Colour Word Test and the Concept Shifting Test. RESULTS: Twenty-five patients suffered from both depressive symptoms and executive dysfunction, 28 patients were depressed with no signs of executive dysfunction, and 13 patients showed executive dysfunction with no depressive symptoms. Patients with executive dysfunction had higher mean SCL-90-D scores compared to patients with no executive dysfunction (30.9 (SD 11.7) versus 26.2 (SD 11.1, p = 0.037). Depressive symptoms were predictive for executive dysfunction in a regression analysis corrected for age, sex, and diabetes mellitus but not after additional correction for pre-existent brain damage and other vascular risk factors. After 2 years 66.6 and 53.3% of patients with both depressive symptoms and executive dysfunction at baseline still had depressive symptoms and executive dysfunctions respectively and had worse prognostic outcome than patients with depressive symptoms or executive dysfunction alone. CONCLUSIONS: Symptoms of depression and executive dysfunction are highly prevalent in stroke patients and often co-occur. These patients are more at risk for poor stroke outcome, chronic depression, and cognitive deterioration.

The effect of the APOE-epsilon4 allele and ACE-I/D polymorphism on cognition during a two-year follow-up in first-ever stroke patients.

BACKGROUND: Cognitive impairment is commonly observed after stroke and has a negative impact on survival and rehabilitation. Some stroke patients deteriorate in cognitive functioning whereas others do not. Environmental and demographic risk factors cannot fully explain this. There is growing evidence that a genetic predisposition plays a role in the pathogenesis of post-stroke cognitive decline. OBJECTIVE: To study the influence of the APOE-epsilon4 allele and the ACE-I/D polymorphism on cognitive functioning after stroke. METHODS: We included 194 first-ever stroke patients of whom information about APOE genotyping and ACE-I/D polymorphism was available in 92 and 129 patients, respectively. Patients were cognitively assessed at 1, 6, 12 and 24 months after the event. Linear mixed models with slope estimates were used to study the influence of the APOE-epsilon4 allele and the ACE-I/D polymorphism on the MMSE score, CAMCOG, executive functioning, psychomotor speed, and verbal memory function during follow-up. RESULTS: Patients carrying the APOE-epsilon4 allele more often suffered a lacunar infarction than non-carriers. The APOE-epsilon4 allele had no effect on cognitive functioning during the follow-up. ACE-DD homozygosity was associated with a worse performance in executive functioning compared to patients with neither an APOE-epsilon4 allele nor the ACE-DD genotype. There was no interaction between the APOE-epsilon4 allele and the ACE-DD phenotype in the prediction of cognitive decline. CONCLUSION: The ACE-DD genotype may be associated with post-stroke cognitive decline while the APOE-epsilon4 allele is not. Further research is needed to examine the role of genetic risk factors for post-stroke cognitive decline and to determine why some patients deteriorate cognitively after stroke but others do not.

The symptomatology of post-stroke depression: comparison of stroke and myocardial infarction patients.

BACKGROUND: Depression is a frequent problem in stroke patients but, all too often, the problem goes unrecognized. How depression-like symptoms in post-stroke depression (PSD) should be interpreted is still subject to debate. If PSD has a distinct symptom profile of depression accompanying other chronic vascular somatic conditions then this could imply that PSD is a specific disease entity. OBJECTIVE: To study whether depressed stroke patients exhibit other signs and symptoms than patients suffering from depression after myocardial infarction (MI). METHODS: Depressive signs and symptoms were measured using the Hospital Anxiety and Depression Scale and the 17-item Hamilton Depression Rating Scale. The results of 190 stroke patients were compared with the results of 198 MI patients every 3 months during the first year after the event. RESULTS: Depressed stroke patients exhibited more loss of interest, psychomotor retardation, and gastro-intestinal complaints as compared to depressed MI patients. However, in multivariate analyses including both depressed and non-depressed stroke and MI patients, no specific symptom profile was found to differentiate between the two depressive syndromes by looking at the modifying effect of stroke vs MI on the occurrence of specific symptoms in depression. CONCLUSION: Although in their clinical presentation, depressed stroke patients exhibit a symptom profile different from depressed MI patients, this is not due to differences in the depressive syndrome in these two patient groups but it reflects differences between stroke and MI patients in general.

[Is there quality of life with locked-in syndrome?] / Kwaliteit van leven bij locked-in-syndroom: kan dat?

A 57-year-old man developed a locked-in state due to a brain stem stroke. He communicated through eye movements. The team suggested treatment should be discontinued, as there was no perspective of improvement. The family was very upset because they experienced sufficient quality of life. We investigated what 'quality of life' means. The literature shows that severely ill and completely care-dependent patients may experience high quality of life; this is called the disability paradox. Patients and families evaluate quality of life by looking for positive things to live for. Some quality-of-life tests, however, understand quality of life as 'functionality'. Healthy people evaluate the situation of people living with handicaps more negatively than the handicapped themselves do. Practitioners may overlook the instability of patients' evaluations: responses and situations may shift. Quality of life as an outcome in clinical trials may be different for individual patients. These insights may improve communication.

Sudden unexpected death in epilepsy patients: Risk factors. A systematic review.

INTRODUCTION: Several risk factors for sudden unexplained death in epilepsy patients (SUDEP) have been proposed, but subsequent work has yielded conflicting data. The relative importance of various risk factors for SUDEP was never explored. The aim of this study is to review systematically risk factors for SUDEP and also to determine their relevance for SUDEP by calculating relative risk factor ratios. METHODS AND MATERIALS: Authors performed a literature-search on "SUDEP" in Medline, the Cochrane Library and EMBASE. Studies with unknown number of SUDEP cases or with less than five SUDEP cases and reviews were excluded from further analysis. The value of each paper was assessed, based on the quality of the study and the reliability of the diagnosis of SUDEP. This value ranged from 1 (low quality) to 10 (high quality). Papers with a value below 7 were eliminated for further analysis. For each analysed factor, a risk factor ratio was determined, with a higher ratio for a stronger risk factor. RESULTS: A number of strong risk factors for SUDEP: young age, early onset of seizures, the presence of generalized tonic clonic seizures, male sex and being in bed. Weak risk factors for SUDEP: prone position, one or more subtherapeutic bloodlevels, being in the bedroom, a strucural brain lesion and sleeping. CONCLUSIONS: In this study, authors have designed a quality scale to select papers. The relative importance of risk factors for SUDEP is demonstrated.

Evidence-based re-engineering: re-engineering the evidence--a systematic review of the literature on business process redesign (BPR) in hospital care.

PURPOSE: Business process redesign (BPR) is used to implement organizational transformations towards more customer-focused and cost-effective care. Ideally, these innovations should be carefully described and evaluated so that "best practices" can be re-applied. To investigate this, available evidence was collected on patient care redesign projects. DESIGN/METHODOLOGY/APPROACH: The Ebsco Business Source Premier, Embase and Medline databases were searched. Studies on innovations related to re-engineering patient care that used before-after design as minimum prerequisites were selected. General characteristics, logistic parameters and other outcome measures to determine the objectives and results and interventions used were looked at. FINDINGS: A total of 86 studies that conformed to the criteria were found: a minority mentioned measurable parameters in their objectives. In the majority of studies, multiple interventions were combined within single studies, making it impossible to compare the effects of individual interventions. Only three randomized controlled trials were found. Furthermore, inconsistencies were noted between the study objectives and the reported results. Many more issues were reported in the results than were mentioned in the study aims. It would appear that publications were hard to find owing to a lack of specific MeSH headings. Nearly 7,500 abstracts were scanned and from these it was concluded that clear and univocal research methods, terms and reporting guidelines are advisable and must be developed in order to learn and benefit from BPR innovations in health care organizations. ORIGINALITY/VALUE: This appears to be the first time available evidence about redesign projects in hospitals has been systematically collected and assessed.

Impairment of cerebrovascular reactivity in long-term type 1 diabetes.

The early preclinical detection of cerebrovascular complications in individuals with diabetes is one of the goals of care described in the St. Vincent Declaration. In accordance with this goal, the aim of the present work was to investigate whether altered cerebral microvascular function in patients suffering from type 1 diabetes can be detected with a transcranial Doppler probe after the administration of acetazolamide. A total of 72 type 1 diabetic patients and 40 healthy control subjects entered the study. Patients were divided into two groups: those with long-term diabetes (disease duration of >10 years, n = 37) and those with short-term diabetes (disease duration of < or =10 years, n = 35). Mean blood-flow velocity in the middle cerebral artery (MCAV) was measured at rest and at 5, 10, 15, and 20 min after intravenous administration of 1 g acetazolamide with a transcranial Doppler probe and expressed as the percentage change from the pretest measurement. The percentage increase in MCAV (cerebrovascular reactivity) was calculated at each time point and compared between the groups. Cerebrovascular reserve capacity (CRC), expressed as the maximal percentage increase of the MCAV, was compared between the groups. Additionally, a reproducibility study of CRC was performed in 10 patients, using intraclass correlations. Cerebrovascular reactivity in the long-term diabetes group was lower (means +/- SD: 5 min, 23.4 +/- 15.4%; 10 min, 28.8 +/- 17.0%; 15 min, 30.0 +/- 15.6%; 20 min, 24.2 +/- 17.8%) than that of the control subjects (5 min, 43.5 +/- 23.9%; 10 min, 55.3 +/- 24.0%; 15 min, 56.7 +/- 23.8%; 20 min, 54.8 +/- 25.9%) and the short-term diabetic patients (5 min, 43.6 +/- 25.9%; 10 min, 52.2 +/- 27.7%; 15 min, 55.3 +/- 32.2%; 20 min, 45.8 +/- 35.8%). CRC was lower in the long-term diabetes group than in the control group or the short-term diabetes group. Impairment of cerebrovascular reactivity was associated with retino- and nephropathy and increased levels of fibrinogen. In contrast, CRC was independent from actual glucose, insulin, glycosylated hemoglobin, von Willebrand factor antigen, and alpha-2 macroglobulin levels. Transcranial Doppler measurements of the changes in MCAV after stimulation with acetazolamide can detect altered cerebral microvascular function in patients with diabetes. Cerebrovascular reactivity and reserve capacity are reduced in patients with long-term diabetes. Further prospective studies should delineate the clinical significance of our results.

Calcium antagonists for ischemic stroke: a systematic review.

BACKGROUND AND PURPOSE: Stroke is a common disease, and many trials with calcium antagonists as possible neuroprotective agents have been conducted. The aim of this review is to determine whether calcium antagonists reduce the risk of death or dependency after acute ischemic stroke. METHODS: Acute stroke trials were identified with help of the Cochrane Collaboration Stroke Group and personal contacts. All randomized trials (published and unpublished) investigating a calcium antagonist (acting on voltage-sensitive calcium channels) were included. Poor outcome, defined as death or dependency in activities of daily living, was used as main outcome. Analyses were, if possible, "intention-to-treat"; pooled relative risks with 95% CIs were calculated. RESULTS: Forty-seven trials were identified, of which 29 were included (7665 patients). No effect of calcium antagonists on poor outcome at the end of follow-up (relative risk, 1.04; 95% CI, 0.98 to 1.09) or on death at end of follow-up (relative risk, 1.07; 95% CI, 0.98 to 1.17) was found. Sensitivity analyses on route of administration and time interval between stroke and start of treatment showed no effect on outcome. In subgroups of unpublished and methodologically sound trials, a statistically significant negative effect for calcium antagonists was found. This contrasts with results of published trials and trials of moderate or poor methodological quality. CONCLUSIONS: The presented evidence rules out a clinically important effect of calcium antagonists after ischemic stroke. The large amount of data leads to narrow CIs with no significant heterogeneity, and the overall results are therefore likely to be statistically robust.

Very Early Nimodipine Use in Stroke (VENUS): a randomized, double-blind, placebo-controlled trial.

BACKGROUND AND PURPOSE: The Very Early Nimodipine Use in Stroke (VENUS) trial was designed to test the hypothesis that early treatment with nimodipine has a positive effect on survival and functional outcome after stroke. This was suggested in a previous meta-analysis on the use of nimodipine in stroke. However, in a recent Cochrane review we were unable to reproduce these positive results. This led to the early termination of VENUS after an interim analysis. METHODS: In this randomized, double-blind, placebo-controlled trial, treatment was started by general practitioners or neurologists within 6 hours after stroke onset (oral nimodipine 30 mg QID or identical placebo, for 10 days). Main analyses included comparisons of the primary end point (poor outcome, defined as death or dependency after 3 months) and secondary end points (neurological status and blood pressure 24 hours after inclusion, mortality after 10 days, and adverse events) between treatment groups. Subgroup analyses (on final diagnosis and based on the per-protocol data set) were performed. RESULTS: At trial termination, after inclusion of 454 patients (225 nimodipine, 229 placebo), no effect of nimodipine was found. After 3 months of follow-up, 32% (n=71) of patients in the nimodipine group had a poor outcome compared with 27% (n=62) in the placebo group (relative risk, 1.2; 95% CI, 0.9 to 1.6). A treatment effect was not found for secondary outcomes and in the subgroup analyses. CONCLUSIONS: The results of VENUS do not support the hypothesis of a beneficial effect of early nimodipine in stroke patients.

Clinical meaning of the Stroke-Adapted Sickness Impact Profile-30 and the Sickness Impact Profile-136.

BACKGROUND AND PURPOSE: Handicap or health-related quality of life (HRQL) measures are seldom used in stroke trials, although the importance of these measures has been stressed frequently. We studied the clinical meaning of the Stroke-Adapted Sickness Impact Profile-30 (SA-SIP30) and the original SIP136 for use in stroke research. METHODS: We included 418 patients who had had a stroke 6 months earlier. We studied the associations between the SA-SIP30 and SIP136 scores versus other frequently used outcome measures from the International Classification of Impairments, Disabilities, and Handicaps (ICIDH) (Barthel Index, Rankin Scale) and the HRQL model (health perception items, Euroqol). To interpret the continuous SA-SIP30 and SIP136 scores, we used receiver operating characteristic curve analysis with the aforementioned measures as external criteria. RESULTS: The psychosocial dimension scores of both SIP versions remained largely unexplained. The physical dimension and total scores of both SIP versions were mainly associated with the disability measures derived from the ICIDH model, as well as with the physical HRQL domains. Most patients with an SA-SIP30 total score >33 or an SIP136 total score >22 had poor health profiles. There were no major differences between the SA-SIP30 and the SIP136, although the SA-SIP30 scores were less skewed toward the healthier outcomes than the SIP136. CONCLUSIONS: Our study showed that (1) both SIP total scores primarily represent aspects of physical functioning and not HRQL; (2) both SIP versions provide more clinical information than the frequently used disability measures; and (3) the SA-SIP30 should be preferred over the SIP136.

Nimodipine in animal model experiments of focal cerebral ischemia: a systematic review.

BACKGROUND AND PURPOSE: Based on the results of animal experiments, clinical trials were performed with nimodipine, which did not demonstrate a beneficial effect on outcome after stroke. The aim of this study was to determine whether the evidence from animal experiments with nimodipine supported the use of nimodipine in clinical trials. METHODS: - We performed a systematic review of animal experiments with nimodipine in focal cerebral ischemia. Studies were identified by searching Medline and Embase. We assessed whether these studies showed a beneficial effect of active treatment. In-depth analyses were performed on infarct size and amount of edema, and subgroup analyses were performed on the length of the time window to the initiation of treatment and the methodological quality of the studies. RESULTS: - Of 225 identified articles, 20 studies were included. The methodological quality of the studies was poor. Of the included studies, 50% were in favor of nimodipine. In-depth analyses showed statistically significant effects in favor of treatment (10 studies). No influence of the length of time to the initiation of treatment or of the methodological quality on the results was found. CONCLUSIONS: - We conclude that the results of this review did not show convincing evidence to substantiate the decision to perform trials with nimodipine in large numbers of patients. There were no differences between the results of the animal experiments and clinical studies. Surprisingly, we found that animal experiments and clinical studies ran simultaneously.

Genome-wide linkage in a large Dutch consanguineous family maps a locus for intracranial aneurysms to chromosome 2p13.

BACKGROUND AND PURPOSE: Familial occurrence of intracranial aneurysms suggests a genetic factor in the development of these aneurysms. In this study, we present the identification of a susceptibility locus for the development of intracranial aneurysms detected by a genome-wide linkage approach in a large consanguineous pedigree. METHODS: Patients with clinical signs and symptoms of intracranial aneurysms, confirmed by radiological, surgical, or postmortem investigations, were included in the study. Magnetic resonance angiography was used to detect asymptomatic aneurysms in relatives. RESULTS: Seven out of 20 siblings had an intracranial aneurysm. Genome-wide multipoint linkage analysis showed a significant logarithm of the odds score of 3.55. CONCLUSIONS: In a large consanguineous pedigree intracranial aneurysms are linked to chromosome 2p13 in a region between markers D2S2206 and D2S2977.

Anticipation in familial intracranial aneurysms in consecutive generations.

Intracranial aneurysms (IA) are the major cause of subarachnoid haemorrhages (SAH). A positive family history for SAH is reported in 5-10% of the patients. The mode of inheritance is not unambiguously established; both autosomal dominant and recessive modes have been reported. In sporadic as well as in familial SAH, approximately 60% of the SAH patients are female. Recently, anticipation has been described in familial SAH. Since up to 15% of the SAHs are not caused by an IA, we have analysed anticipation, sex ratio and mode of inheritance only in families with patients with a proven IA in two consecutive generations. A total of 10 families were studied in which at least two persons in consecutive generations were affected by SAH, a symptomatic IA (SIA) or a presymptomatic IA (PIA). We also analysed published data from families with a proven IA in two consecutive generations on age of SIA onset and sex ratios among affected family members (both SIA and PIA). The age of SIA onset in the parental generation (mean 55.5 years) differed significantly from the age of onset in their children (mean 32.4 years). In the parental generation 11 men and 37 women were affected (both SIA and PIA), in the consecutive generation these numbers were 28 men and 32 women. There is a significant difference in sex ratio of affected family members when the generations are compared (P<0.02). No family could be found in which three consecutive generations were affected by an IA (SIA or PIA).

Ischemic stroke after surgical procedures: clinical features, neuroimaging, and risk factors.

OBJECTIVE: To describe risk factors and explore mechanisms of ischemic strokes after general surgery. BACKGROUND: Strokes follow general surgery in about 0.08% to 2.9% of cases. Patients with previous cerebrovascular disease, atrial fibrillation, hypertension, advanced age, or atherosclerosis were found to have an increased risk. Knowledge of factors involved may guide physicians in determining the overall risk of surgery. METHODS: This case-control study was performed in a referral center. A total of 61 patients identified through a computerized database with ischemic strokes after surgical procedures-excluding heart, brain, vessels, or neck-between July 1986 and July 1996 were studied. Procedures included 11 urogenital, 16 gastrointestinal, 17 orthopedic, 12 pulmonary, and 5 other. A total of 122 randomly selected controls were matched for age, sex, procedure, and year of procedure. Main outcome measures included arterial territory, timing, risk factors, and perioperative events. Differences were expressed as adjusted odds ratios (AOR) with 95% confidence limits (CL), using multivariate conditional logistic analyses for matched case-control design. RESULTS: Arterial territory included 37 middle cerebral artery, 11 posterior circulation, 7 borderzone, and 6 multiple. Median procedure to stroke interval was 2 days (range, 0 to 16); 10 patients had intraoperative strokes. Three major risk factors emerged: previous cerebrovascular disease (AOR 12.57, 95% CL 2.14/73.70), chronic obstructive pulmonary disease (COPD) (7.51, 1.87/30.12), and peripheral vascular disease (PVD) (5.35, 1.25/22.94). After adding stroke-related factors, PVD (14.70, 2.01/107.71) and COPD (10.04, 1.90/53.14) remained the strongest variables; blood pressure (1.05, 1.01/1.10) and urea (1.04, 1.01/1.07) contributed slightly. Hypotension did not contribute. Four patients (6.6%) and no controls had diffuse intravascular coagulation (p = 0.01). Four stroke patients had myocardial infarction (6.6% versus 0%; p = 0.01). CONCLUSIONS: Ischemic strokes after general surgery most commonly occur after an asymptomatic interval. Previous cerebrovascular disease, COPD, and PVD greatly increase the risk. Hypotension rarely accounts for postoperative strokes. Major comorbidity of the patient at risk seems more important than complicating events during surgery.

Some patients with intracranial aneurysms have a reduced type III/type I collagen ratio. A case-control study.

A reduced production of type III collagen has been reported in previous studies to be associated with intracranial aneurysms. The purpose of this prospective case-control study was to assess the possible role of a reduced type III collagen production as a risk factor for having an intracranial aneurysm. The study group consisted of 41 consecutively admitted patients with intracranial aneurysms. Intracranial aneurysms were demonstrated by intraarterial digital subtraction cerebral angiography or during operation. The control group consisted of 41 healthy volunteers matched for age and sex. Fibroblasts were cultured from skin biopsies from patients and control subjects, and the type III/type I collagen ratios were determined. The type III/type I collagen ratios in the controls ranged from 5.5 to 19.8%, with a median ratio of 10%, and none had a ratio below 5.5%. The type III/type I collagen ratios in patients ranged from 1.1 to 25.1%, with a median ratio of 10.5%, and eight patients (19.5%) had a low (< 5.5%) ratio (p = 0.005, Fisher's exact test). Our findings support the hypothesis that a reduced production of type III collagen may contribute to the formation of intracranial aneurysms in some patients.

rCBF-SPECT in brain infarction: when does it predict outcome?

We prospectively studied 26 patients with ischemic stroke within 24 hr, after 2 wk, and after 6 mo with thallium-201-diethyldithiocarbamate single-photon emission computed tomography (SPECT) and neurologic and functional assessments. The admission flow deficits correlated with outcome. The admission and 6-mo scores correlated with clinical conditions at each time. At 2 wk, the flow deficits were smaller and did not correlate with clinical parameters. Nor did the presence or absence of hyperfixation of the radiopharmaceutical. Six months after the infarct, the flow defect had decreased in 9 of 15 patients in whom three serial scans were available, with better clinical improvement than in the remaining six whose flow deficits increased. More patients in the first group had been treated randomly with the calcium-entry blocker flunarizine. SPECT imaging of rCBF within 24 hr after stroke correlates with clinical outcome and condition, whereas rCBF imaging at 2 wk after the stroke shows no clinical correlation.

Cerebral blood flow imaging with thallium-201 diethyldithiocarbamate SPECT.

Thallium-201 diethyldithiocarbamate ([201TI]DDC) was studied in humans as an agent for cerebral blood flow imaging. Brain uptake proved to be complete 90 sec after injection with no appreciable washout or redistribution for hours. Intracarotid injection suggested an almost 100% extraction during the first passage. Whole-body distribution studies demonstrated a brain uptake of 4.3% of the dose compared with 0.9% for [201TI]chloride. No differences were found in the distribution of [201TI]DDC versus [201TI]chloride in other organs. After the injection of 3 mCi 201TI, good quality single photon emission computed tomographic (SPECT) images of the brain were obtained with both a rotating gamma camera and a multidetector system. In ischemic brain disease, perfusion defects were easily demonstrated. We conclude that [201TI]DDC is a suitable radiopharmaceutical for SPECT studies of cerebral blood flow.

The role of cognitive impairment in the quality of life after ischaemic stroke.

Many patient- and disease-related factors influence the quality of life (QL) after stroke. Few studies address the direct relation between cognition and quality of life. The objective of this study was to investigate the role of cognitive impairment in the QL of patients after stroke. We evaluated several variables including age, degree of paralysis, cognitive deficits and volume of infarcts, in 129 patients (64 men, 65 women; mean age 63.2, SD 14.6 years), who had been hospitalized a mean of 2.3 (range 0.25-4) years previously with ischaemic stroke. Cognitive function was assessed with the CAMCOG and QL with a visual analogue scale (VAS). Ninety-seven patients (75%) of our sample completed all the tests. Univariate analysis showed that substantial infarct volume, aphasia, impaired motor function, disability relating to activities of daily life, disturbed global functional health and impaired cognitive function were significantly associated with poorer QL. Age, sex and education of the patient, co-morbidity and location of the infarcts were not related to QL. Linear regression analysis revealed that disturbed global functional health, larger volume of infarcts and severity of aphasia were significant independent explanatory factors for poorer QL (adjusted R2 = 22%). In conclusion, we did not find a significant impact of cognitive impairment on the patients' QL. However, this conclusion is restricted to a relatively well group of stroke survivors.

Feasibility of cognitive screening of patients with ischaemic stroke using the CAMCOG. A hospital-based study.

Brief screening tests would be convenient for the measurement of cognitive impairment in stroke patients. In these patients aphasia can interfere with test procedures. To evaluate the feasibility of examining cognitive functions in stroke patients we examined 129 patients with an ischaemic stroke using the CAMCOG, a standardised neuropsychological screening test, after an interval of at least 3 months. Most patients (88%) were able to complete the CAMCOG. Patients with severe aphasia were significantly more likely to have an abnormal CAMCOG score than patients without aphasia [relative risk (RR) 4.0, 95% confidence interval (CI) 2.8-5.8]. The group of patients with moderate aphasia was not at higher risk of having an abnormal CAMCOG score than patients without aphasia (RR 1.4, 95% CI 0.6-2.8). Looking for other factors that might correlate with the scores, logistic regression analysis revealed age as the only significant factor for the prediction of the CAMCOG score (odds ratio 4.0, 95% CI 1.2-13.2). We concluded that the CAMCOG can conveniently be used for screening cognitive functions in patients with cerebral infarcts, even if there is moderate aphasia.