bluuebunny/crossref_metadata_2025_split huggingface dataset:
Psychosocial function and life satisfaction after stroke.
Authors: Aström M , Asplund K , Aström T 
Published: June 2011

This prospective study was designed to describe different aspects of psychosocial function after stroke and the development of changes over time. A major aim has been to identify mental, functional, and social factors associated with low life satisfaction late after stroke.
Social network, functional ability, leisure-time activities, experience of ill health, major depression, and life satisfaction were assessed repeatedly over 3 years in a population-based sample of 50 long-term survivors of stroke (mean age 71.4 years).
Compared with a general elderly population, patients 3 years poststroke had more psychiatric symptoms, lower functional ability, and reduced life satisfaction. Contacts with children were maintained over the 3-year follow-up period, whereas contacts with friends and neighbors declined early after stroke and remained lower than in the general elderly population (p less than 0.05). When time dependency was analyzed, activities of daily living and somatic/neurological symptoms were found to change little after 3 months, while psychiatric symptoms showed changes later. Between 3 and 12 months poststroke, the prevalence of major depression decreased, leisure-time activities and social contacts were partly resumed, and life satisfaction improved (p less than 0.01). Once good life satisfaction was restored it was maintained, and poor life satisfaction at 1 year remained poor for the entire 3 years.
It is concluded that major depression early after stroke, functional disability, and an impaired social network interact to reduce life satisfaction for the long-term survivors of stroke.
Dietary nonprotein calories and cerebral infarction size in rats.
Authors: Robertson C , Goodman J C , Grossman R G , Claypool M , White A 
Published: June 2011

Conventional diets may cause hyperglycemia in patients with neurological injuries. The purpose of this study was to examine the effect on the severity of cerebral infarction of replacing carbohydrates as the primary dietary source of nonprotein calories.
Sixty-nine Long-Evans rats were either fasted for 24 hours, fed isocaloric amounts of a control diet containing 51.5% of the calories as carbohydrates, or fed one of five experimental diets before middle cerebral artery occlusion for 45 minutes. In the experimental diets, 60% of the carbohydrate calories were replaced with one or more of the following substrates: 1,3-butanediol, triacetin, tributyrin, and long- and medium-chain triglycerides.
The plasma glucose concentration in the fasted animals was 6.4 +/- 1.1 mumol/ml. In the animals receiving the control diet, which contained the greatest number of carbohydrate calories, plasma glucose was 9.1 +/- 1.4 mumol/ml. The 1,3-butanediol diet resulted in an intermediate plasma glucose concentration averaging 7.8 +/- 1.3 mumol/ml. Plasma beta-hydroxybutyrate levels were elevated in the fasted group and with the 1,3-butanediol diet. Plasma acetate levels were increased with the diets supplemented with triacetin. The smallest infarct volume (53 +/- 43 mm3) was found in the fasted group and the largest (162 +/- 56 mm3) in the control diet group. Infarct volumes that were significantly smaller were found with the 1,3-butanediol diet (98 +/- 41 mm3) and with the triacetin/tributyrin diet (105 +/- 53 mm3). The volume of the infarct was directly related to the plasma glucose concentration before ischemia (n = 69, r = 0.47, p less than 0.01), but not to plasma lactate, ketone body, or acetate levels.
It may be possible to develop a diet for patients with neurological injuries using noncarbohydrate calorie sources, such as 1,3-butanediol, triacetin, or tributyrin, that would supply systemic caloric and protein requirements without the adverse effect of conventional diets.
Transcranial Doppler in spontaneous attacks of migraine.
Authors: Zanette E M , Agnoli A , Roberti C , Chiarotti F , Cerbo R , Fieschi C 
Published: June 2011

Our aim in this study was to compare headache-free and spontaneous migraine measurements of blood flow velocity and the pulsatility index in the anterior cerebral artery, middle cerebral artery, and posterior cerebral artery.
Thirty-one patients (nine having experienced migraine with aura and 22 migraine without aura) were studied in headache-free periods and during spontaneous migraine attacks with transcranial Doppler ultrasonography.
During attacks of migraine with aura, blood flow velocities (particularly the diastolic velocity [p = 0.05]) were reduced while the pulsatility index increased (p = 0.05), whereas a generalized increase in diastolic velocity (p less than 0.02) and a decrease in the pulsatility index (p = 0.05) were observed during attacks of migraine without aura. Significant variations of blood pressure and heart rate were never found.
These findings are consistent with constriction of resistance vessels in migraine with aura and dilatation of the vessels in migraine without aura. This disparity could be due to a difference between the two migraine types or could be related to the fact that in this study the time interval between headache onset and transcranial Doppler was shorter in the migraine-with-aura group. The latter explanation would apply if, in fact, both types of migraine evolve from hypoperfusion to hyperperfusion during their time course, although perhaps with a difference in intensity.
Cerebellar infarction in the young.
Authors: Rosman N P , Wu J K , Caplan L R 
Published: June 2011

Ischemic cerebrovascular disease in children and young adults usually affects the anterior circulation.
We describe two cases of cerebellar infarction in the territory of vertebral artery supply, associated with physical exertion, in a young adult and in a child. Review of 31 previous cases of cerebellar infarction occurring in the first 2 decades of life demonstrated a mostly obscure causation; where a likely cause was found, trauma was most frequent. In 12 of the 31 patients, a vertebral artery (usually the left) was occluded. Patients were sometimes predisposed to such occlusions by subluxation between the first and second cervical vertebrae, allowing abnormal neck movements that can cause arterial injury and thromboembolism. Some of these cerebellar infarcts, like those of our patients, have followed physical exertion.
Cerebellar infarction can be life-threatening, but half of the patients, including ours, have had complete or near-complete recovery.
Evaluation of vasomotor reactivity by transcranial Doppler and acetazolamide test before and after extracranial-intracranial bypass in patients with internal carotid artery occlusion.
Authors: Karnik R , Valentin A , Ammerer H P , Donath P , Slany J 
Published: June 2011

The aim of this trial was to evaluate the effectiveness of extracranial-intracranial bypass with respect to vasomotor reactivity in patients with internal carotid artery occlusions and absent vasomotor reactivity, comparing them with a control group treated conservatively.
To test vasomotor reactivity in 104 patients with unilateral occlusion of the internal carotid artery, we measured blood flow velocity in the middle cerebral artery by transcranial Doppler sonography both at rest and after injection of acetazolamide. Among the 39 patients who failed to show increased mean blood flow velocity after the acetazolamide test distal to an occluded internal carotid artery by greater than or equal to 10%, 14 subjects subsequently underwent extracranial-intracranial bypass surgery (group A) and 14 age- and sex-matched subjects in whom no such procedure was done composed the control group (group B). Follow-up examinations were performed 3-6 months postoperatively and in the control group 3-6 months after initial examination.
Baseline values of the mean blood flow velocity at rest on the affected side were reduced in both groups compared with the contralateral healthy side (group A, 46.0 +/- 15.1 cm/sec; group B, 48.1 +/- 16.7 cm/sec) and revealed only a marginal increase after acetazolamide. The contralateral side showed a normal blood flow velocity at rest and an adequate response to acetazolamide in both groups. On the follow-up examination group A demonstrated a normalized vasodilatory capacity. Blood flow velocity increased significantly after acetazolamide from 41.9 +/- 13.1 cm/sec to 53.5 +/- 16.0 cm/sec (p less than 0.002). In group B, the compromised vasomotor reactivity remained unchanged.
Our results demonstrate that transcranial Doppler sonography together with the acetazolamide test can identify subjects with reduced vasomotor reactivity distal to an occluded internal carotid artery, who may improve hemodynamically by an extracranial-intracranial bypass.
Emergency reversal of anticoagulation after intracerebral hemorrhage.
Authors: Fredriksson K , Norrving B , Strömblad L G 
Published: June 2011

Although intracerebral hemorrhage is one of the most serious complications during oral anticoagulant therapy, there are no guidelines on emergency treatment with respect to reversal of anticoagulation effect in these patients.
We retrospectively compared laboratory data and clinical features in 17 cases of anticoagulant-related intracerebral hemorrhage treated with prothrombin complex concentrate (n = 10) or fresh-frozen plasma (n = 7).
In the group of patients treated with prothrombin complex concentrate, the mean prothrombin time decreased from 2.83 to 1.22 International Normalized Ratio within 4.8 hours, compared with a decrease from 2.97 to 1.74 within 7.3 hours in those given fresh-frozen plasma (i.e., four to five times more rapidly after treatment with prothrombin complex concentrate) (p less than 0.001). Symptoms and signs of intracerebral hemorrhage, measured on an eight-graded Reaction Level Scale, progressed on average 0.2 grades in patients given prothrombin complex concentrate compared with 1.9 grades in those given fresh-frozen plasma (p less than 0.05). In patients with prothrombin values above 1.46, clinical progression within 12 hours occurred in five of six cases.
Treatment with prothrombin complex concentrate reverses anticoagulation more rapidly than fresh-frozen plasma, which might be of importance for the prevention of further bleeding.
Pressure-flow relations in canine collateral-dependent cerebrum.
Authors: Muhonen M G , Sawin P D , Loftus C M , Heistad D D 
Published: June 2011

The pressure-flow relation has been characterized in normal cerebrum, but it has not been studied in cerebrum dependent on collateral flow. The purpose of this investigation was to examine the relation between systemic pressure, regional cerebral blood flow, and middle cerebral artery branch pressure in collateral-dependent and normal brain.
In 10 anesthetized dogs, we cannulated a branch of the middle cerebral artery and identified collateral-dependent tissues using the shadow flow technique. We measured pressure in normal and cannulated branches of the middle cerebral artery and regional cerebral blood flow. The common carotid arteries were occluded, and hemorrhage reduced mean arterial pressure to 50 and 25 mm Hg.
When aortic pressure was 25 mm Hg, blood flow to the collateral-dependent zone decreased from a baseline of 87 +/- 5 to 6 +/- 1 ml/100 g per minute (mean +/- SE), and pressure in the cannulated branch of the middle cerebral artery decreased from 49 +/- 4 to 2 +/- 0.4 mm Hg (p less than 0.05). Small-vessel resistance in the collateral-dependent region decreased from 0.56 +/- 0.09 to 0.38 +/- 0.04 mm Hg/ml/100 g per minute (p less than 0.05) after carotid occlusion but did not change significantly during hypotension. In normal brain, however, small-vessel resistance continued to decrease as systemic pressure was reduced.
This study provides pressure-flow relations in normal and collateral-dependent cerebrum during carotid occlusion and progressive hypotension. In collateral-dependent tissue, concurrent occlusion of middle cerebral and carotid arteries produces autoregulatory dilatation of small vessels, resistance fails to decrease as mean arterial pressure is reduced to 25 mm Hg, and profound focal hypoperfusion is produced.
Some epidemiological aspects of stroke: mortality/morbidity trends, age, sex, race, socioeconomic status.
Authors: Modan B , Wagener D K 
Published: June 2011

The reasons for decreasing stroke mortality could be related to either decreasing incidence and/or improved prognosis. Thus far, secular trends of stroke have been analyzed either through mortality or morbidity data. This report examines both aspects simultaneously, on a nationwide basis, for the period 1968-1988.
Mortality statistics were based on the Compressed Mortality File. Estimates of morbidity were based on the National Hospital Discharge Survey. The Area Resource File was used to obtain county-specific socioeconomic statistics.
The decline in stroke mortality continued through the 1970s and 1980s, whereas morbidity remained constant and possibly even increased. Mortality and morbidity rates were similar in both sexes, higher in blacks, and lower in other (primarily Asian) Americans. There was an inverse correlation between death rates and socioeconomic status, which was particularly marked in blacks. Temporal decline occurred in all strata.
The observed decrease in stroke mortality rates results most probably from an improved survival rather than from a decline in incidence. The abundance of new drugs and screening programs may not have affected the overall morbidity of stroke, possibly because of inefficient treatment regimens.
Relationship of cardiac disease to stroke occurrence, recurrence, and mortality.
Authors: Broderick J P , Phillips S J , O'Fallon W M , Frye R L , Whisnant J P 
Published: June 2011

This is a study of cardiac diseases associated with the 1,382 cases of first cerebral infarction in residents of Rochester, Minn., during 1960-1984.
This is a population-based study in Rochester, Minn., for which the medical record-linkage system was used to identify cardiac disease among patients with first cerebral infarction.
There were 318 patients (23%) who had at least one major potential cardiac source of emboli. The proportion of patients with a cardiac source of emboli was significantly higher among patients older than age 75 years (29%) than among younger patients (17%). The 30-day stroke recurrence rate among patients with a cardiac source of emboli (2%) was not significantly different than that among those without a cardiac source of emboli (2%). Among patients with a cardiac source of emboli, there was no difference in the probability of stroke at 30 days and at 90 days for those treated or not treated with anticoagulants. During the first 30 days after cerebral infarction, the risk of death in patients with a cardiac source of emboli (23%) was 14 times that of recurrent stroke. The risk of death at 30 days in patients without a cardiac source of emboli was 8%.
Significant independent predictors of death (Cox proportional-hazards analysis) were age, prior myocardial infarction, atrial fibrillation present at onset of stroke, congestive heart failure before the stroke, and an age x congestive heart failure interaction. The only significant independent predictors of recurrent stroke were cardiac valve disease and congestive heart failure.
Distribution of the 72-kd heat-shock protein as a function of transient focal cerebral ischemia in rats.
Authors: Li Y , Chopp M , Garcia J H , Yoshida Y , Zhang Z G , Levine S R 
Published: June 2011

The significance and physiological implications of the expression of the 72-kd heat-shock protein in ischemic tissue are unknown. To enhance our understanding of the relation between ischemic cell damage and 72-kd heat-shock protein expression, we evaluated the cellular expression and the anatomic distribution of 72-kd heat-shock protein in conjunction with the morphological analysis of rat brain, as a function of the duration of a single arterial occlusion.
Adult Wistar rats were subjected to graded transient middle cerebral artery occlusion (for a duration of 10, 20, 30, 60, 90, and 120 minutes and sham; n = 4 per group). Forty-eight hours after reopening the artery, brain tissue sections were analyzed to determine the extent of neuronal damage (hematoxylin and eosin staining), the extent of astrocytic reactivity (immunohistochemistry, using anti-glial fibrillary acidic protein), and the distribution of 72-kd heat-shock protein (immunohistochemistry, using a monoclonal antibody to 72-kd heat-shock protein).
We found that 72-kd heat-shock protein was sequentially expressed in morphologically intact neurons, microglia, and endothelial cells with increasing duration of ischemia; 72-kd heat-shock protein immunoreactivity was not detected in astrocytes. The duration of ischemia required to evoke a 72-kd heat-shock protein response in neurons was dependent on the anatomic site and followed a pattern of increasing neuronal sensitivity to ischemic cell damage with duration of ischemia: 72-kd heat-shock protein and neuronal damage were sequentially detected in the caudate putamen, globus pallidus, cerebral cortex, amygdala, and hippocampus with increasing duration of ischemia. With ischemia of long duration (greater than or equal to 90 minutes), neurons expressing 72-kd heat-shock protein were localized to a zone peripheral to the severely damaged ischemic core.
These studies suggest that 1) the expression of 72-kd heat-shock protein in neurons precedes the development of ischemic cellular alterations detectable by conventional hematoxylin and eosin light microscopy methods; 2) there is a hierarchy of cell types and anatomic sites that express 72-kd heat-shock protein, and this hierarchy reflects cellular and anatomic vulnerability to ischemic cell damage; and 3) 72-kd heat-shock protein induction in neurons bordering a necrotic ischemic core may be the morphological equivalent of the ischemic penumbra.
Reversible focal ischemic injury demonstrated by diffusion-weighted magnetic resonance imaging in rats.
Authors: Minematsu K , Li L , Sotak C H , Davis M A , Fisher M 
Published: June 2011

Diffusion-weighted magnetic resonance imaging (DWI) can quantitatively display focal brain abnormalities within minutes after the onset of ischemia. We performed the present study to determine the effects of 1 and 2 hours of temporary ischemia on DWI.
We examined DWI and T2-weighted magnetic resonance images (T2WI) during and after 1 and 2 hours of temporary middle cerebral artery occlusion in rats (n = 10 for each group). In a subgroup of four animals from each group, we employed perfusion magnetic resonance imaging to monitor cerebral perfusion. Neurological outcome and infarct size after survival for 24 hours were compared between the groups and correlated with DWI and T2WI studies.
Perfusion studies qualitatively documented hypoperfusion and reperfusion during and after temporary occlusion. Lesion size on DWI during reperfusion was significantly less than that during ischemia for 1 (55% decline, p less than 0.02) but not 2 hours of occlusion. The DWI signal intensity ratio (intensity compared with that in the contralateral homologous area) just before withdrawal of the occluder was significantly less in regions where the hyperintensity disappeared after withdrawal than in regions with persistent hyperintensity (p less than 0.002). The T2WI studies revealed few or no abnormalities, except after 2 hours of occlusion. The neurological outcome was significantly better in the 1-hour than in the 2-hour group (p less than 0.05). Postmortem infarct volume was significantly smaller in the 1-hour group than in the 2-hour group (p less than 0.05). The postwithdrawal DWI accurately predicted infarct size (R = 0.96, p less than 0.0001).
The present study indicates that DWI can rapidly display not only irreversible but also reversible ischemic brain damage and enhances the importance of DWI as a diagnostic modality for stroke.
Edema, cation content, and ATPase activity after middle cerebral artery occlusion in rats.
Authors: Yang G Y , Chen S F , Kinouchi H , Chan P H , Weinstein P R 
Published: June 2011

Reduction of cerebral blood flow results in several acute metabolic disturbances, including a reduction in Na,K-ATPase activity. The relation between this reduction and the onset of edema is unknown, as is the effect of restoration of blood flow. Therefore, we investigated the role of decreased Na,K-ATPase activity in the pathogenesis and time course of ischemic brain edema and reperfusion.
The middle cerebral arteries of rats were occluded by cannulation with a nylon suture for 30, 60, 120, or 240 minutes. The animals were then decapitated (permanent occlusion) or the suture was withdrawn to allow 24 hours of reperfusion before decapitation (temporary occlusion). Na,K-ATPase activity and Na+, K+ and water contents were measured at various intervals.
In the ischemic hemisphere, Na,K-ATPase activity was significantly decreased at 30, 60, 120, and 240 minutes of permanent occlusion (p less than 0.05). There was also a significant decrease in rats subjected to 60 or 120 minutes of temporary occlusion followed by 24 hours of reperfusion. Water content increased after 60, 120, or 240 minutes of permanent occlusion (p less than 0.01); after 24 hours of reperfusion, water content remained elevated (p less than 0.01). The Na+ content increased after both permanent and temporary occlusion, and the K+ content decreased only after permanent occlusion. Increases in water content correlated with decreases in Na,K-ATPase activity after temporary occlusion and with the Na+:K+ ratio after permanent occlusion.
Reduction in Na,K-ATPase activity resulting in disruption of cellular ionic homeostasis may account for early development of cytotoxic brain edema after permanent occlusion of the middle cerebral artery. Such edema is also present 24 hours after 60 and 120 but not 30 minutes of temporary occlusion.
Sudden bilateral hearing impairment in vertebrobasilar occlusive disease.
Authors: Huang M H , Huang C C , Ryu S J , Chu N S 
Published: June 2011

Bilateral hearing impairment is rare in vertebrobasilar occlusive disease.
Between 1986 and 1991, we encountered seven patients (four men, three women; median age, 61 years; range, 46-71 years) who had sudden bilateral hearing impairment among 503 patients with vertebrobasilar occlusive disease. The main initial neurological symptoms were sudden bilateral hearing impairment, tinnitus, and vertigo. Acute labyrinthitis or Ménière's disease was the initial diagnosis until subsequent brain stem or cerebellar signs appeared. Brain stem auditory evoked potentials were abnormal bilaterally in six patients but had unilateral attenuation of the IV-V complex in the remaining one patient. Computed tomographic scans in all six patients showed multiple hypodense lesions in the brain stem and the cerebellum. Cerebral angiography showed complete occlusion on both vertebral arteries in one patient, occlusion on the left with small caliber on the right in another, and severe stenosis on both sides in a third. There was no opacification of internal auditory arteries in these three patients. The remaining patient had arteriosclerotic changes with faint opacification of the bilateral internal auditory arteries. Five patients had a poor prognosis, with locked-in state in four and severe truncal ataxia in one.
We conclude that sudden bilateral hearing impairment in vertebrobasilar occlusive disease is more common than previously recognized and that it may indicate a grave prognosis.