bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effects of long-term rehabilitation therapy on poststroke hemiplegic patients.
Authors: Dam M , Tonin P , Casson S , Ermani M , Pizzolato G , Iaia V , Battistin L 
Published: June 2011

Rehabilitation therapy is believed to be useful during the first few months after stroke when recovery usually takes place. However, evidence exists that this may not be the rule for all stroke victims. Therefore, we investigated, in a selected group of poststroke patients, the profile of recovery in response to long-term rehabilitation therapy.
Fifty-one hemiplegic subjects unable to walk 3 months after stroke were enrolled in this study. Patients underwent consecutive periods of rehabilitation up to 2 years after the cerebrovascular accident. Autonomy in daily living activities and the degree of neurological compromission were periodically assessed with the Barthel Index and a neurological scale designed for hemiplegic subjects. The main features of the patients were also evaluated as a possible predictor of outcome.
In a consistent percentage of the patients, significant gains in gait and daily living abilities were observed during the first year and, in individual cases, during the second year after stroke. At the end of the study, 74% of the patients regained their capacity to walk without assistance, and up to 79% had a Barthel Index score above 70. Sphincter function, level of neurological impairments, and capacity in daily living activities are significantly related to the outcome of the patients as a whole but were not useful to anticipate the outcome of each patient.
These results suggest that disabled poststroke subjects may attain significative functional improvements in response to prolonged restorative therapy. However, the possibility of predicting the outcome of individual patients appears the major problem to solve in order to assign to long-term rehabilitation programs only patients who will benefit from the therapy.
The effects of hypertension on cerebral atherosclerosis in the cynomolgus monkey.
Authors: Hollander W , Prusty S , Kemper T , Rosene D L , Moss M B 
Published: June 2011

There is substantial clinical, pathological, and experimental evidence that hypertension aggravates atherosclerosis of the extracranial vessels. The present study assesses the effects of hypertension on the development of cerebral atherosclerosis in nonhuman primates fed an atherogenic diet.
The extent and severity of cerebral atherosclerosis were evaluated morphologically, morphometrically, and biochemically in atherosclerotic monkeys with and without hypertension. Atherosclerosis was induced by feeding a hypercholesterolemic diet for 12 months; hypertension was produced by surgical coarctation of the thoracic aorta.
At autopsy, gross atherosclerotic lesions of the major cerebral arteries were observed in 15 of 16 atherosclerotic monkeys with hypertension compared with 5 of 16 atherosclerotic animals without hypertension. In the hypertensive-atherosclerotic group, 38.5% of the vessels examined showed gross involvement compared with only 3.4% of the vessels involved in the atherosclerotic group (P < .001). The lesions in the atherosclerotic group were generally mild, whereas those in the hypertensive-atherosclerotic group were severe and resulted in significant luminal narrowing and occlusion of vessels (P < .001). The small branches of the cerebral arteries also showed severe disease with luminal obstruction in the hypertensive-atherosclerotic group. The extent and severity of cerebral atherosclerosis were significantly related to the severity of the hypertension (P < .05).
Hypertension is an important factor in cerebral atherosclerosis because of its accelerating effect on the disease. Nonhuman primate models may be useful in clarifying the role of hypertension and atherosclerosis in cerebral vascular disease.
Cocaine-induced platelet defects.
Authors: Jennings L K , White M M , Sauer C M , Mauer A M , Robertson J T 
Published: June 2011

Numerous studies have demonstrated an association between acute cardiac events, cerebrovascular accidents, and cocaine use. The underlying mechanisms leading to these complications have not been well defined. Using various in vitro model systems, it has been reported that cocaine, up to or greater than an order of magnitude of the lethal dose, causes either inhibitory or proaggregatory effects on platelet function.
To address these reported discrepancies, we examined the effect of cocaine and its carrier on the activation and aggregation of human platelets in vitro.
We found that cocaine inhibited platelet aggregation when platelets were challenged with ADP, collagen, or arachidonic acid. This inhibition was due to a direct effect on fibrinogen binding to the activated platelet. Cocaine also caused the dissociation of preformed platelet aggregates. At these same concentrations, cocaine did not inhibit agonist-mediated increases in cytosolic calcium or inhibit platelet shape change, suggesting that its effect on platelet aggregation was a selective process and not due to a total destruction of platelet function. Interestingly, the organization of the cytoskeleton of activated platelets, a secondary event critical to cell receptor clustering and clot retraction, was disrupted by cocaine treatment. In addition, alterations in platelet protein electrophoretic patterns were observed on preincubation of platelets with cocaine.
We conclude that cocaine may have a direct inhibitory effect on the ability of platelets to participate in thrombus formation. The contribution of this effect as an underlying mechanism of sudden death in cocaine abusers is unknown.
The prognostic value of admission blood pressure in patients with acute stroke.
Authors: Carlberg B , Asplund K , Hägg E 
Published: June 2011

Patients with acute stroke are often found to have high blood pressures at hospital admission. Previous studies have shown variable results regarding the prognostic value of high blood pressure in acute stroke. The aim of this study was to investigate the prognostic value of admission blood pressure in a population-based sample of patients with acute stroke.
Eighty-five patients with intracerebral hemorrhage and 831 with ischemic disease were included in the study. The relations between admission blood pressure and 30-day mortality were studied by logistic regression analyses.
High blood pressure in patients with impaired consciousness on hospital admission was significantly related to 30-day mortality in patients with intracerebral hemorrhage (P = .037) and in patients with ischemic disease (P < .0001). In patients without impaired consciousness, high blood pressure at time of admission was not related to increased mortality at 30 days.
High admission blood pressure in alert stroke patients was not related to increased mortality. Stroke patients with impaired consciousness showed higher mortality rates with increasing blood pressure. However, this does not provide a basis for recommending antihypertensive therapy for such patients.
Screening for neuroborreliosis in patients with stroke.
Authors: Hammers-Berggren S , Gröndahl A , Karlsson M , von Arbin M , Carlsson A , Stiernstedt G 
Published: June 2011

Borrelia burgdorferi, the etiologic agent of Lyme disease, can cause different neurological manifestations. We studied the prevalence of Lyme neuroborreliosis in patients with stroke.
During a 1-year period, sera from patients with cerebral thrombosis or transient ischemic attack without cardioembolism were investigated for antibodies against B burgdorferi.
One of 281 patients had a positive serum immunoglobulin M titer and 23 of 281 (8%) had positive serum immunoglobulin G titers against B burgdorferi. One of the 24 seropositive patients, with a diagnosis of transient ischemic attack due to dysphasia, had a lymphocytic pleocytosis and intrathecal antibody production against B burgdorferi. The medical history revealed a 9-month period of general and neurological symptoms compatible with Lyme neuroborreliosis before the strokelike incidents.
We conclude that Lyme neuroborreliosis may imitate stroke, but screening for antibodies against B burgdorferi seems to be of little value and may be replaced by a careful medical history.
Subcortical infarction in children.
Authors: Powell F C , Hanigan W C , McCluney K W 
Published: June 2011

This report examines the occurrence of subcortical infarction in 5 children, reviews the English literature, and discusses evaluation of this uncommon childhood illness.
Clinical characteristics and neurological follow-up were examined in children who presented with subcortical infarction within the past 7 years. The English literature over the previous 20 years was reviewed to identify similar patients with radiological documentation of subcortical infarction.
Mean age of the patients in this series was 4.8 years (range, 4 months to 12 years); 3 children were female. Three patients presented with the sudden onset of hemiparesis, 1 with dystonia, and 1 with fever and focal seizures. Protein C deficiencies were demonstrated in 2 children; a cardiomyopathy was seen in 1 patient. Mean follow-up was 1.5 years. Two patients were neurologically normal, mild residual symptoms persisted in 2, and 1 patient showed severe dystonia. The literature analysis indicated that specific risk factors were described in 79 patients; complete clinical analysis was available for 51 patients. In the latter group, the mean age was 5.7 years; 26 children were female. Forty-six presented with hemiplegia, 4 with dystonia, and 1 with focal seizures. Follow-up greater than 5 months in 29 patients showed complete or good resolution of deficits in 23. Specific risk factors such as infection, trauma, hematologic disorders, or cardiac or vascular abnormalities were identified in 62 of 79 children.
This analysis indicates that children with subcortical infarction usually presented with acute hemiparesis. Risk factors were identified in the majority of children, and follow-up demonstrated good or complete resolution of neurological deficits in 80% of the patients.
Responses of cerebral arterioles to activation of beta-adrenergic receptors during diabetes mellitus.
Authors: Mayhan W G 
Published: June 2011

Diabetes mellitus impairs reactivity of large peripheral arteries and arterioles to activation of beta-adrenergic receptors. The goal of this study was to determine whether diabetes mellitus alters dilatation of cerebral arterioles to activation of beta-adrenergic receptors.
In vivo diameter of pial arterioles was measured in nondiabetic and diabetic (streptozotocin 50 to 60 mg/kg IP) rats during superfusion with isoproterenol, forskolin, and nitroglycerin. In addition, we examined the contribution of nitric oxide or a nitric oxide-containing compound in dilatation of pial arterioles in response to the agonists.
Dilatation of pial arterioles in response to isoproterenol was significantly less in diabetic compared with nondiabetic rats (3 +/- 2% versus 14 +/- 1%, respectively, for 1.0 mumol/L isoproterenol). In contrast, dilatation of pial arterioles in response to nitroglycerin and forskolin was similar in nondiabetic and diabetic rats. Furthermore, dilatation of pial arterioles in nondiabetic rats in response to isoproterenol and forskolin was not related to the synthesis and release of nitric oxide or a nitric oxide-containing compound.
The findings of the present studies suggest that diabetes mellitus impairs dilatation of cerebral resistance arterioles in response to activation of beta-adrenergic receptors. Impairment of beta-adrenergic-mediated dilatation of cerebral arterioles during diabetes mellitus does not appear to be related to an alteration in cyclic adenosine monophosphate, since forskolin produced similar vasodilatation in nondiabetic and diabetic rats.
Impaired relaxation of the carotid artery during activation of ATP-sensitive potassium channels in atherosclerotic monkeys.
Authors: Faraci F M , Orgren K , Heistad D D 
Published: June 2011

This study examined the hypotheses that (1) atherosclerosis impairs relaxation of the carotid artery in response to activation of adenosine triphosphate (ATP)-sensitive potassium channels and (2) regression of atherosclerosis restores the response toward normal.
Isometric tension was measured in rings of carotid artery taken from normal, atherosclerotic, and regression monkeys and precontracted submaximally with prostaglandin F2 alpha.
Relaxation in response to acetylcholine was less in atherosclerotic compared with normal arteries (5 +/- 6% versus 54 +/- 4% [mean +/- SE] in response to 3 x 10(-8) mol/L acetylcholine, P < .01). Relaxation in response to aprikalim, a direct activator of ATP-sensitive potassium channels, was also less in atherosclerotic than in normal arteries (32 +/- 7% versus 69 +/- 5% during 10(-6) mol/L aprikalim, P < .01). Relaxation in response to aprikalim but not to acetylcholine or nitroprusside was inhibited almost completely by glibenclamide (4 mumol/L), a selective inhibitor of ATP-sensitive potassium channels. Relaxation in response to low but not high (10(-6) to 10(-5) mol/L) concentrations of sodium nitroprusside was less in atherosclerotic than in normal arteries. Regression of atherosclerosis tended to restore responses to acetylcholine, but not responses to nitroprusside or aprikalim, toward normal.
These findings suggest that atherosclerosis impairs relaxation of the carotid artery in response to activation of ATP-sensitive channels. Impaired responses may be due, in part, to nonspecific impairment of relaxation. Regression of atherosclerosis did not restore responses of the carotid artery toward normal.
Blood pressure treatment slows the progression of carotid stenosis in patients with isolated systolic hypertension.
Authors: Sutton-Tyrrell K , Wolfson S K , Kuller L H 
Published: June 2011

The Systolic Hypertension in the Elderly Program (SHEP) was a randomized trial testing the efficacy of treating systolic hypertension in older adults. A significant reduction in stroke risk was observed among participants assigned to active treatment. Serial carotid duplex scans were performed on 129 participants at the University of Pittsburgh center, and rates of progression and regression of carotid stenosis were observed.
Changes in blood flow velocity ratios were used to detect progression because they can be reliably measured and their relation to degree of residual lumen is known. Progression required the development of a 40% to 50% diameter stenosis when stenosis was not initially present or, if already present, further reduction in the lumen diameter. Regression required the absence of a 40% to 50% diameter stenosis when stenosis was initially present or a stenosis significantly less severe than that initially seen.
Progression occurred in 22% (28/129) of participants and regression in 16% (8/49). Progression of carotid stenosis occurred more often among participants randomized to placebo as compared with active treatment (31% versus 14%, P = .020). All eight patients exhibiting-regression were randomized to active treatment. In multivariate analysis, participants assigned to placebo had 4.3 times greater odds of progressing than participants assigned to active treatment. Other factors significantly related to progression were higher degree of plaque at baseline, low high-density lipoprotein-3, high lipoprotein(a), and younger age.
Treating systolic hypertension appears to slow progression of carotid stenosis. Similar effects occurring in the intracranial vessels may be one reason for the substantial decrease in stroke among SHEP participants assigned to active treatment.
A comparison of lesions in small intracerebral arteries among Japanese men in Hawaii and Japan.
Authors: Reed D , Jacobs D R , Hayashi T , Konishi M , Nelson J , Iso H , Strong J 
Published: June 2011

This report examines the hypothesis that the higher risk of stroke among Japanese men in Japan compared with those in Hawaii is related to pathology in small intracerebral arteries by comparing the prevalence of such lesions in autopsied participants from two cohorts of Japanese men in Japan and Hawaii.
Existing histological sections from the left basal ganglia from 232 men from Japan and 175 men of Japanese ancestry in Hawaii were examined for selected abnormalities in arteries between 100 and 300 microns in diameter by three pathologists. The presence of lacunar infarcts was also noted, and information about cerebral infarcts, cerebral hemorrhages, and atherosclerosis in the circle of Willis was available for the Hawaii group.
Lacunar infarcts and all small intracerebral artery lesions except medial fibrosis were more common at every age in Japan than in Hawaii. By cause of death, all lesions were three or more times more prevalent among men who died of stroke than of noncardiovascular causes in both areas. In the Hawaii group, the small intracerebral artery lesions were significantly associated with autopsy evidence of cerebral and lacunar infarcts, and with atherosclerosis in the large arteries of the circle of Willis. Among a large number of risk factors measured at the baseline examination in Hawaii, only high blood pressure and reported usual Asian diet were significantly associated with one or more measures of small intracerebral artery lesions.
An overview of the accumulated data indicated that small intracerebral artery pathology plays an important role in the high risk of stroke in Japanese men in Japan compared with those in Hawaii. These studies support the idea that hypertension is a necessary factor in the causal pathway, but also indicate that some other factors are involved. Some aspect of an Asian diet continues to be of importance for future research.
What causes false clinical prediction of small deep infarcts?
Authors: Lodder J , Bamford J , Kappelle J , Boiten J 
Published: June 2011

Our goal was to identify factors that play a role in false clinical diagnosis of small deep infarcts.
In 350 prospectively registered patients with a first supratentorial ischemic stroke, we clinically differentiated between lacunar and nonlacunar syndromes. Using computed tomography (CT), we distinguished small deep and territorial infarcts and also recorded leukoaraiosis and asymptomatic infarcts. Degree of initial handicap, potential source of cardioembolic stroke, and hypertension were also noted.
One hundred forty-seven patients had a lacunar and 203 a nonlacunar syndrome. Forty-two (12%) had a lesion visualized by CT that was compatible with a recent infarct but was considered inappropriate for the clinical syndrome: nineteen had a nonlacunar syndrome but a small deep infarct, and 23 had a lacunar syndrome but a territorial infarct. Patients with a nonlacunar syndrome but a small deep infarct were more severely disabled (a modified Rankin scale rating of 5) (odds ratio [OR], 4.31; 95% confidence interval [CI], 1.25 to 14.88) and had a cardioembolic source (OR, 4.07; 95% CI, 1.04 to 15.95), leukoaraiosis (OR, 3.79; 95% CI, 1.32 to 10.05), or asymptomatic infarcts visualized by CT (OR, 4.13; 95% CI, 1.45 to 11.71) compared with 124 patients with a correctly diagnosed small deep infarct. Twelve of 19 patients with a nonlacunar syndrome but a small deep infarct had a lesion in the left hemisphere, and 9 of these 12 had "aphasia." Patients with a lacunar syndrome but a territorial infarct more often had a cardioembolic source (OR, 4.02; 95% CI, 1.15 to 14.03) and a pure motor syndrome (OR, 4.52; 95% CI, 1.55 to 13.18) than those with lacunar syndrome but a small deep infarct, although 21 (91%) were in the right hemisphere. Of the first 103 patients with lacunar stroke diagnosed by two of the study neurologists, 5 had an inappropriate lesion compared with 14 of the later 40 diagnosed by colleagues without a specific interest in cerebrovascular diseases (OR, 0.09; 95% CI, 0.03 to 0.26).
(1) Diagnosis of lacunar syndromes should not be influenced by deficit severity or the presence of a potential cardiac source of embolism. (2) Speech disorders should carefully be classified. (3) Routine tests of nondominant higher functions may be inadequate. (4) Doctors interested in cerebrovascular neurology have a lower failure rate in differentiating small deep infarcts from territorial infarcts than those less well-trained or interested in neurology. (5) Among the lacunar syndromes, pure motor syndrome may be the least specific predictor of a small deep infarct.
Pure motor hemiparesis and sensorimotor stroke. Accuracy of very early clinical diagnosis of lacunar strokes.
Authors: Toni D , Del Duca R , Fiorelli M , Sacchetti M L , Bastianello S , Giubilei F , Martinazzo C , Argentino C 
Published: June 2011

Clinical differentiation of lacunar from nonlacunar strokes in the very early phase could help to exclude patients with lacunar stroke from pharmacologic trials designed for nonlacunar strokes, namely, those with thrombolytic agents. In a continuous series of acute ischemic stroke patients, we evaluated how accurately a clinical diagnosis of pure motor hemiparesis or sensorimotor stroke formulated in the first hours from onset predicts a lacunar stroke documented by cerebral computed tomography or by autopsy.
We examined 517 patients (299 men, 218 women; mean +/- SD age, 67 +/- 10 years) within 12 hours (mean +/- SD, 6.1 +/- 3.2 hours) of the event. At hospital admission, we observed 151 (29%) patients with pure motor hemiparesis and 68 (13%) patients with sensorimotor stroke.
Computed tomography or autopsy was compatible with a lacunar stroke (ie, detection of a lacune or permanently negative computed tomography) in 170 (33%) patients, of whom 123 (72%) had pure motor hemiparesis and 47 (28%) had sensorimotor stroke. This led to a sensitivity of 72%, a specificity of 72%, a positive predictive value of 56%, and a negative predictive value of 84%. Overall positive predictive value of pure motor hemiparesis was 58% (60% for two areas and 58% for three areas involved), and that of sensorimotor stroke was 51% (87% for two areas and 40% for three areas involved). By separately evaluating the sides of lesions, we found a positive predictive value of 46% for right-side infarcts and of 72% for left-side infarcts. Right-side lesions constituted 51% of lesions in lacunar syndrome patients with lacunar stroke, 76% in those with nonlacunar stroke, 19% in nonlacunar syndrome patients with lacunar stroke, and 31% in those with nonlacunar stroke (P < .0001). During the first days of hospital stay we observed a deterioration of 21% of lacunar syndrome patients with nonlacunar stroke and an improvement of 49% of nonlacunar syndrome patients with lacunar stroke, with appearance and disappearance of symptoms of cortical involvement, respectively. The examination of these patients after the occurrence of these clinical changes would have led to a daily increase of the positive predictive value up to a maximum of 66% at day 7.
Pure motor hemiparesis and sensorimotor stroke diagnosed within 12 hours of the event are poorly predictive of lacunar strokes. Hence, the very early identification of these syndromes cannot be used for patient selection in therapeutic trials.