bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cerebellar infarction. Clinical and anatomic observations in 66 cases.
Authors: Kase C S , Norrving B , Levine S R , Babikian V L , Chodosh E H , Wolf P A , Welch K M 
Published: June 2011

Cerebellar infarction displays different clinical features, depending on the vascular territory involved. We studied patients with infarcts in the territories of the posterior inferior cerebellar artery or the superior cerebellar artery to compare their clinical presentation, course, and prognosis.
We retrospectively analyzed the clinical features, laboratory data, and imaging studies of 66 patients with cerebellar infarction collected consecutively at five institutions. All the cerebellar infarcts were documented on computed tomographic scan or magnetic resonance imaging.
Two distinct profiles emerged, depending on the vascular territory involved. In 36 patients with posterior inferior cerebellar artery territory infarcts, a triad of vertigo, headache, and gait imbalance predominated at stroke onset. Computed tomography showed severe cerebellar mass effect in 11 cases (30%), with associated hydrocephalus in seven. In these seven patients (19%), postinfarct swelling led to brain stem compression that resulted in four deaths. In 30 patients with superior cerebellar artery infarcts, gait disturbance predominated at onset; vertigo and headache were significantly less common. The clinical course was usually benign. Computed tomography showed marked cerebellar mass effect, hydrocephalus, and brain stem compression in only two instances (7%). Presumed cerebral embolism was the predominant stroke mechanism in patients with superior cerebellar artery distribution infarcts, whereas in those with posterior inferior cerebellar artery distribution infarcts, the stroke mechanism was equally divided between cardiogenic embolism and posterior circulation arterial disease.
Cerebellar infarcts in the posterior inferior cerebellar artery and superior cerebellar artery distribution have distinct differences in clinical presentation, course, and prognosis. These differences should help in the selection of appropriate monitoring and treatment strategies.
Incidence of silent cerebral infarction in patients with major depression.
Authors: Fujikawa T , Yamawaki S , Touhouda Y 
Published: June 2011

There have been few studies of the incidence of silent cerebral infarction detected by magnetic resonance imaging in patients with presenile or senile major depression.
We examined silent cerebral infarction in patients with presenile and senile major depression who were diagnosed at Hiroshima Prefectural Hospital. The diagnostic criteria of the American Psychiatric Association (DSM-III-R) were used. Patients with stroke or focal neurological symptoms were excluded.
Silent cerebral infarction was observed in 51.4% of the patients with presenile-onset presenile depression, and the incidence was significantly higher than in patients with juvenile-onset presenile depression (P < .01). Among the patients with senile major depression, silent cerebral infarction was observed in 65.9% of those with presenile-onset depression and in 93.7% of those with senile-onset depression.
Our findings suggest that half of presenile-onset major depression and the majority of senile-onset major depression might be organic depression related to silent cerebral infarction. Because major depression occurring for the first time during or after the presenile period may be related to silent cerebral infarction, it is important to keep this possibility in mind when treating such patients.
Cerebral glucose metabolism as a predictor of rehabilitation after ischemic stroke.
Authors: Heiss W D , Emunds H G , Herholz K 
Published: June 2011

Permanent neurological deficits after ischemic stroke are primarily determined by the location and size of an infarct, but social recovery and rehabilitation also depend on the functional status of brain tissue outside the infarct. Since neuronal loss and functional deactivation in peri-infarct tissue are reflected as changes in flow and metabolism, measurement of glucose consumption may yield an additional measure of rehabilitative capacity.
Seventy-six nondiabetic patients (48 men, 28 women; mean age, 56.7 +/- 14.37 years) with a first unilateral supratentorial ischemic infarct were consecutively enrolled. At stable neurological and clinical condition 9 +/- 7.2 days after the attack, cerebral metabolic rate of glucose (CMRglu) in noninfarcted brain regions was measured by positron emission tomography of fluorodeoxyglucose. Outcome was assessed 21 to 77 (mean, 50.5 +/- 11.7) months after the stroke with a rehabilitation index for daily life activities.
At time of assessment of outcome 16 patients had died (score, 0), 22 were completely recovered (score, 200), and 38 had partially improved (rehabilitation score, 5 to 195). Younger age, absence of arterial hypertension and cardiac disease, but also higher global, ipsilateral, and contralateral CMRglu were significantly related to a better final outcome (P = .001), whereas sex and neurological deficits in the subacute stage after stroke were not related to final outcome. To evaluate the significance of CMRglu further after adjustment for clinical prognostic variables, a multiple regression analysis of the effect of age and CMRglu on rehabilitation score in homogeneous subgroups of partially recovered patients was performed. It revealed a significant positive correlation of CMRglu (P = .016) with recovery in hypertensive subjects, while age was the dominant prognostic factor (P = .07) in patients with normal blood pressure.
These results demonstrate that outcome after stroke is significantly influenced by several factors incapacitating brain function in addition to the ischemic attack. In addition to age and cardiac disease, hypertension is an important factor leading to widespread arteriopathy with neuronal loss and tissue damage. The significant correlation of CMRglu outside the infarct with functional recovery in hypertensive subjects probably reflects the extent of hypertensive tissue damage and subsequently reduced capacity to compensate for the focal ischemic insult.
Early temporal variation of cerebral metabolites after human stroke. A proton magnetic resonance spectroscopy study.
Authors: Graham G D , Blamire A M , Rothman D L , Brass L M , Fayad P B , Petroff O A , Prichard J W 
Published: June 2011

Proton magnetic resonance spectroscopy has documented declines in normal metabolites and long-term elevation of lactate signal after stroke in humans. Within days of stroke, leukocytes infiltrating the infarct zone may produce much of the lactate seen in the subacute and chronic periods.
We examined 10 patients by localized proton magnetic resonance spectroscopy with one-dimensional spectroscopic imaging within the first 60 hours after acute nonhemorrhagic cerebral infarction, a period before abundant leukocyte infiltration. Follow-up studies on day 8 to 17 after stroke were performed on 7 of these patients.
Initially, the lactate magnetic resonance signal was elevated in all patients. The N-acetyl-aspartate peak within the lesion was reduced below contralateral normal brain in all but two. At subsequent examination, significant declines had occurred in lesion maximum lactate and N-acetyl-aspartate signals, with average changes of -36 +/- 11% per week and -29 +/- 9% per week, respectively. Declines in lesion creatine/phosphocreatine and in choline-containing compound peaks occurred in some patients but did not attain statistical significance for the group as a whole. Estimated lesion volume correlated positively with both total (r = .75, P = .012) and lesion maximum (r = .74, P = .015) lactate signal.
Elevated lactate signal is reliably detectable by magnetic resonance spectroscopy after acute cerebral infarction in humans. Clearance of lactate occurs despite the potential contribution of lactate-producing leukocytes in the subacute stage. Delayed loss of N-acetyl-aspartate signal in second examinations suggests that late death of viable cells may occur within the first 2 weeks after cerebral infarction.
Comparative histopathologic consequences of photothrombotic occlusion of the distal middle cerebral artery in Sprague-Dawley and Wistar rats.
Authors: Markgraf C G , Kraydieh S , Prado R , Watson B D , Dietrich W D , Ginsberg M D 
Published: June 2011

We have developed a minimally invasive model of photothrombotic occlusion of the distal middle cerebral artery in rats and have evaluated the patterns and features of the resulting histopathologic injury in two normotensive strains.
Food-deprived male Sprague-Dawley (n = 14) and Wistar (n = 10) rats anesthetized with halothane/nitrous oxide underwent a small craniotomy to expose the right distal middle cerebral artery just above the rhinal fissure. The animals were injected intravenously with the photosensitizing dye rose bengal, and the distal middle cerebral artery was irradiated with light from an argon laser-activated dye laser at three separate points to induce thrombotic occlusion. The ipsilateral common carotid artery was then permanently occluded, and the contralateral common carotid artery was occluded for 60 minutes. Three days later, the brains were perfusion-fixed and prepared for histopathologic examination, and infarct volume was determined by quantitative planimetry.
In Sprague-Dawley rats, a large consistent temporoparietal cortical infarct was observed; mean +/- SD infarct volume was 130.5 +/- 40.0 mm3 (coefficient of variation, 30.7%) and a relatively small adjacent zone of selective neuronal necrosis ("incomplete infarction"), amounting to only 9.1% of the total injury volume, was also seen. By contrast, Wistar rats had smaller and more variable cortical infarcts (volume, 48.4 +/- 26.9 mm3; coefficient of variation, 55.6%) but displayed a much more substantial zone of incomplete cortical infarction (volume, 20.8 +/- 10.1 mm3; 30.1% of the total injury volume). In neither strain was infarct size related to alterations of blood pressure. In both strains, infarcts were limited to the cortex, typically involving the parietal cortex, somatosensory cortex, and forelimb region. Three rats exhibited infarcts in the contralateral hemisphere.
This model has the advantages of necessitating only minimal surgery, allowing the dura to remain intact, and avoiding mechanical trauma to the brain surface. In Sprague-Dawley rats, the resulting large cortical infarct exhibited relatively small interanimal variation, making the model suitable, for example, for replicate studies of pharmacotherapy. In Wistar rats, the large zone of incomplete infarction, a unique feature heretofore undescribed in rodent models of permanent focal ischemia, lends the model to the study of the pathomechanisms underlying graded cortical ischemic injury.
Dexamethasone prevents cerebral infarction without affecting cerebral blood flow in neonatal rats.
Authors: Tuor U I , Simone C S , Barks J D , Post M 
Published: June 2011

We recently demonstrated that pretreatment with the synthetic glucocorticoid dexamethasone prevents hypoxic-ischemic brain damage in neonatal rats. Presently, we examine whether this protective effect of dexamethasone is due to an improvement in local cerebral blood flow.
Neonatal rats were treated with either vehicle or 0.1 mg/kg i.p. dexamethasone 24 hours before hypoxia-ischemia (right carotid artery occlusion +3 hours of 8% O2). Cerebral blood flow was measured with [14C]iodoantipyrine autoradiography after either 2 (n = 17) or 3 (n = 15) hours of hypoxia-ischemia. Additional animals (n = 20) were perfusion-fixed 3 days after hypoxia-ischemia. The area of cerebral pathological changes was measured from hematoxylin and eosin-stained coronal sections taken at three different levels.
Pathological outcome differed between groups. In vehicle-treated rats, sections from anterior, mid, and posterior portions of the cerebrum all had extensive infarction or cellular necrosis ipsilateral to the occlusion (mean areas of damage were 62.6 +/- 10%, 70.2 +/- 9%, and 54.2 +/- 8%, respectively). However, in dexamethasone-treated animals, brain damage in sections at corresponding levels was minimal (0%, 1.6 +/- 2%, and 1.5 +/- 1%, respectively; p < 0.0002). In contrast to the pathological results, cerebral blood flow was equivalent in the dexamethasone- and vehicle-treated groups. After either 2 or 3 hours of hypoxia, cerebral blood flow was reduced 60-80% ipsilateral to the carotid artery occlusion in animals treated with either vehicle or dexamethasone.
Despite ischemic levels of cerebral blood flow, pretreatment with dexamethasone prevents cerebral damage in neonatal rats. Instead of improving local cerebral perfusion, dexamethasone presumably acts via peripheral or central glucocorticoid receptors to produce some alteration in the brain that decreases its susceptibility to hypoxia-ischemia.
Questions people ask about stroke.
Authors: Hanger H C , Mulley G P 
Published: June 2011

We sought to identify the type and frequency of questions asked about stroke by patients, relatives, and caregivers.
All stroke-related inquiries made to Stroke Association Advice Centers in the United Kingdom during a 4-month period were recorded.
During the study period, 1,397 people asked 1,908 questions. Nearly one quarter needed more information about the nature of stroke. The other most common inquiries concerned help at home (with many expressing concern about their current level of community support), requests for information about stroke clubs, speech difficulties, rehabilitation, personality changes, and depression.
Knowledge of the questions asked should enable health professionals to provide better information to stroke victims and allow modification of stroke information pamphlets.
Silent brain infarctions in patients with first-ever stroke. A community-based study in Umbria, Italy.
Authors: Ricci S , Celani M G , La Rosa F , Righetti E , Duca E , Caputo N 
Published: June 2011

The relative frequency of computed tomographic evidence of old cerebral infarctions without prior history of stroke, and their effect on short- and long-term outcome of patients with first-ever ischemic stroke, are currently unknown. Silent infarctions may relate to specific risk factors and may influence the rate of survival free of handicap.
We studied the prevalence of such lesions in patients registered with SEPIVAC, a community-based survey of stroke incidence and outcome in the Sixth Local Health Unit of Umbria, Italy. Of 375 first-ever strokes, 209 patients with cerebral infarction (computed tomogram done within 30 days after the stroke) were included in this study. Computed tomograms were reviewed blindly, and cases were classified as having a single lesion or multiple lesions; in the latter case, it was assumed that at least one silent brain infarction was present. The two groups were compared in terms of risk factors and outcome. To avoid a selection bias, these patients were also compared with 68 patients who were not submitted to computed tomography but were judged on clinical grounds to have a > 90% probability of having suffered a cerebral infarction.
Risk factors and outcome did not differ between patients without and with a computed tomogram. In the latter group, 80 patients (38.3%; 95% confidence interval, 31.7%-44.9%) had silent brain infarction. Male sex (odds ratio, 1.84; 95% confidence interval, 1-3.4), ischemic changes on an electrocardiogram (odds ratio, 2.5; 95% confidence interval, 1.3-4.9), and--in the multivariate analysis--hypertension (odds ratio, 1.46; 95% confidence interval, 1.1-2) were significantly more frequent in these patients. Outcome at 1, 6, and 12 months was not influenced by the presence of silent infarctions.
This community-based study shows that silent brain infarctions in patients with first-ever stroke are not significantly related to risk factors commonly described in hospital-based series (atrial fibrillation, transient ischemic attack, etc.); rather, silent infarctions seem to be a marker of widespread vascular disease.
Stroke trends in an aging population. The Technology Assessment Methods Project Team.
Authors: Niessen L W , Barendregt J J , Bonneux L , Koudstaal P J 
Published: June 2011

Trends in stroke incidence and survival determine changes in stroke morbidity and mortality. This study examines the extent of the incidence decline and survival improvement in the Netherlands from 1979 to 1989. In addition, it projects future changes in stroke morbidity during the period 1985 to 2005, when the country's population will be aging.
A state-event transition model is used, which combines Dutch population projections and existing data on stroke epidemiology. Based on the clinical course of stroke, the model describes historical national age- and sex-specific hospital admission and mortality rates for stroke. It extrapolates observed trends and projects future changes in stroke morbidity rates.
There is evidence of a continuing incidence decline. The most plausible rate of change is an annual decline of -1.9% (range, -1.7% to -2.1%) for men and -2.4% (range, -2.3% to -2.8%) for women. Projecting a constant mortality decline, the model shows a 35% decrease of the stroke incidence rate for a period of 20 years. Prevalence rates for major stroke will decline among the younger age groups but increase among the oldest because of increased survival in the latter. In absolute numbers this results in an 18% decrease of acute stroke episodes and an 11% increase of major stroke cases.
The increase in survival cannot fully explain the observed mortality decline and, therefore, a concomitant incidence decline has to be assumed. Aging of the population partially outweighs the effect of an incidence decline on the total burden of stroke. Increase in cardiovascular survival leads to a further increase in major stroke prevalence among the oldest age groups.
Extracranial vertebral artery pseudoaneurysm presenting as subarachnoid hemorrhage.
Authors: Kaplan S S , Ogilvy C S , Gonzalez R , Gress D , Pile-Spellman J 
Published: June 2011

True aneurysms of the extracranial vertebral artery are rare. The usual pathogenesis of aneurysms in this location is either penetrating or blunt trauma with resultant pseudoaneurysm formation. We report a postpartum patient with a presumed traumatic pseudoaneurysm of the extracranial vertebral artery presenting with subarachnoid hemorrhage.
A 41-year-old woman had three episodes of neck stiffness 1 month after an uncomplicated vaginal delivery. The last episode, 3 days before admission, was accompanied by intense neck and head pain and paresthesias that extended into the left arm, thumb, and forefinger.
Lumbar puncture showed subarachnoid hemorrhage. Angiography revealed a left vertebral artery dissection from C6-7 to C3 with pseudoaneurysm at C5-6. Computed tomography demonstrated impingement of the C6 root at the foramen by this lesion. The lesion was successfully treated by balloon occlusion of the vertebral artery.
We present a patient with an extracranial vertebral pseudoaneurysm with subarachnoid hemorrhage and cervical root impingement. To our knowledge, this is the first case of such a lesion presenting as subarachnoid hemorrhage. The lesion was successfully treated using endovascular techniques.
Gait outcome in ambulatory hemiparetic patients after a 4-week comprehensive rehabilitation program and prognostic factors.
Authors: Hesse S A , Jahnke M T , Bertelt C M , Schreiner C , Lücke D , Mauritz K H 
Published: June 2011

Although gait training is prominent in the rehabilitation of hemiparetic stroke patients, little is known about its outcome and prognostic factors in mildly affected patients. We therefore intended to assess gait in ambulatory stroke patients before and after a 4-week inpatient rehabilitation program based on the neurodevelopmental technique.
We measured vertical ground reaction forces by force plates in 148 stroke patients. Variables were stance durations, peak vertical ground reaction forces at heel strike (Fz1) and toe-off (Fz2), loading and deloading rates, time to Fz1, and time to Fz2. The absolute changes for both legs and symmetry outcome were calculated. In addition, we assessed maximal walking speed, walking endurance, stair climbing ability, and the Motricity Index.
Stance duration, weight acceptance, push-off of both legs, and the stance duration symmetry improved independent of changes of gait velocity. The symmetry of the ground reaction forces did not improve. Results were even worse for Fz1 and the loading rate at the end of treatment. Sex, age, side of hemiparesis, motor strength, stroke interval, and sensory impairment had no influence on the outcome of symmetry. Functional performance did not improve considerably.
The absolute changes of the ground reaction forces indicated better weight acceptance and push-off of both legs and thus confirmed the efficacy of the neurodevelopmental technique. The symmetry outcome and the functional performance at the end of treatment, however, challenge the efficacy of intensive rehabilitation therapy for 4 weeks in its attempts to restore physiological gait in these mildly affected patients.
Ethnic differences in stroke mortality between non-Hispanic whites, Hispanic whites, and blacks. The National Longitudinal Mortality Study.
Authors: Howard G , Anderson R , Sorlie P , Andrews V , Backlund E , Burke G L 
Published: June 2011

Although US blacks are known to have an excess stroke mortality compared with US whites, little is known about the stroke burden of the Hispanic white population. This report will provide estimates of the relative burden of stroke mortality in the US black and Hispanic population relative to the white population and examine the consistency of this relation across age.
Data were from participants aged > 45 years from the National Longitudinal Mortality Study. There were 1844 stroke deaths among 239,734 non-Hispanic whites, 46 deaths among 12,527 Hispanic whites, and 234 deaths among 23,468 black participants. Standard statistical methods were used to examine the ethnic differences in stroke mortality.
The hazard ratios for black men and women (relative to non-Hispanic whites) were nearly identical, at > 4.0 at age 45 but marginally < 1.0 by age 85. For both Hispanic men and women, the hazard ratios (relative to non-Hispanic whites) were approximately 1.0 at age 45 but were marginally significantly < 1.0 at older ages. The ethnic differences in stroke death rates reveal differences in age distributions of age at fatal stroke between these groups. Approximately 6% of fatal strokes for non-Hispanic whites occurred before age 60, whereas > 15% occurred in both Hispanic whites and blacks.
These results suggest that (1) for Hispanics, stroke risk is similar to that for non-Hispanic whites at young ages but is marginally lower at older ages, (2) the excess stroke mortality in blacks mainly occurs at younger ages (between 45 and 55 years), and (3) the relation between stroke risk for blacks and Hispanics relative to whites is similar by sex. The impact of age on relative stroke mortality would argue against simple age adjustment for describing ethnic differences in stroke mortality. Finally, proportionally, more strokes occur at older ages in non-Hispanic whites than in either US blacks or Hispanic whites.
Racial disparities in severity of cerebrovascular events.
Authors: Kuhlemeier K V , Stiens S A 
Published: June 2011

This study was conducted to determine if blacks hospitalized for cerebrovascular events had more severe cerebrovascular events than whites similarly hospitalized.
Data from the Maryland Health Services Cost Review Commission were used to determine incidence of coma, death rates, age at death of those who died, and length of stay for acute hemorrhagic and occlusive stroke in hospitalized blacks and whites after adjusting for sex and, if appropriate, age.
With a single exception (number of patients with hemorrhagic stroke who died during short-term hospitalization), all indices indicated that blacks incurred more severe cerebrovascular events than whites (P < .05 or less).
Maryland state data from hospitalized patients indicate that blacks had more severe strokes than whites.