bluuebunny/crossref_metadata_2025_split huggingface dataset:
Reactivity of cerebral blood flow to carbon dioxide in various types of ischemic cerebrovascular disease: evaluation by the transcranial Doppler method.
Authors: Maeda H , Matsumoto M , Handa N , Hougaku H , Ogawa S , Itoh T , Tsukamoto Y , Kamada T 
Published: June 2011

The response of cerebral blood flow to changes in the arterial carbon dioxide partial pressure (i.e., carbon dioxide reactivity) has been evaluated as a parameter of cerebral perfusion reserve in patients with cerebrovascular disease. In this study, variations in this reactivity in various ischemic cerebrovascular diseases were evaluated by a newly established method, a transcranial Doppler technique.
Thirty-three patients with symptomatic cerebrovascular disease, 13 patients with asymptomatic cerebral infarction, and 25 age-matched normal control subjects were investigated. The symptomatic patients were divided into three groups; those with unilateral carotid artery obstruction, those with cortical infarction, and those with lacunar infarction. The carbon dioxide reactivity of each subject was determined by simultaneously measuring the mean spatial Doppler frequency in the middle cerebral artery and the end-tidal carbon dioxide partial pressure under normocapnic, hypercapnic, and hypocapnic conditions.
In the patients with carotid obstruction, the carbon dioxide reactivity of the hemisphere ipsilateral to the obstruction was more impaired than the reactivity of the symptomatic hemispheres in any other group, and was significantly less than in the contralateral asymptomatic hemisphere (p < 0.01). In patients with cortical infarction, the carbon dioxide reactivity of the symptomatic hemisphere was significantly less than in normal control subjects (p < 0.05) and was also less than that of the contralateral asymptomatic hemisphere (p < 0.05). In patients with lacunar infarction, the carbon dioxide reactivity of both hemispheres was significantly less than that in normal controls (p < 0.01), although there was no difference between the symptomatic and asymptomatic hemispheres. In patients with asymptomatic infarction, the carbon dioxide reactivity was also less than that in normal controls (p < 0.01).
The carbon dioxide reactivity of cerebral blood flow measured by this transcranial Doppler technique may be useful for characterizing the hemodynamic changes that occur in various types of ischemic cerebrovascular disease.
Effect of the 21-aminosteroid tirilazad on cerebral pH and somatosensory evoked potentials after incomplete ischemia.
Authors: Maruki Y , Koehler R C , Kirsch J R , Blizzard K K , Traystman R J 
Published: June 2011

Postischemic evoked potential recovery correlates with acidosis during ischemia and early reperfusion. Acidosis promotes lipid peroxidation in vitro. We tested the hypothesis that the 21-aminosteroid tirilazad mesylate (U74006F), an inhibitor of lipid peroxidation in vitro, ameliorates somatosensory evoked potential recovery and acidosis during reperfusion after severe incomplete cerebral ischemia.
Cerebral perfusion pressure was reduced to 11 +/- 1 mm Hg (+/- SEM) for 30 minutes by cerebral ventricular fluid infusion in anesthetized dogs. Cerebral intracellular pH and high-energy phosphates were measured by magnetic resonance spectroscopy. Dogs were randomized to receive vehicle (citrate buffer; n = 8) or tirilazad (1 mg/kg; n = 8) before ischemia in a blinded study.
Cerebral blood flow was reduced to 6 +/- 1 mL/min per 100 g during ischemia, resulting in nearly complete loss of high-energy phosphates and an intracellular pH of 6.0-6.1 in both groups. Initial postischemic hyperemia was similar between groups but lasted longer in the vehicle group. Tirilazad accelerated mean recovery time of intracellular pH from 31 +/- 5 to 15 +/- 3 minutes and of inorganic phosphate from 13 +/- 2 to 6 +/- 1 minutes. Recovery of somatosensory evoked potential amplitude was greater with tirilazad (49 +/- 3%) than vehicle (33 +/- 6%). Fractional cortical water content was less with tirilazad (0.819 +/- 0.003) than vehicle (0.831 +/- 0.002).
Tirilazad attenuates cerebral edema and improves somatosensory evoked potential recovery after incomplete ischemia associated with severe acidosis. Accelerated pH and inorganic phosphate recovery indicates that this antioxidant acts during the early minutes of reperfusion.
Suppression of protein synthesis in the reperfused brain.
Authors: Krause G S , Tiffany B R 
Published: June 2011

Brain ischemia and reperfusion produce profound protein synthesis alterations, the extent and persistence of which are dependent on the nature of the ischemia, the brain region, the cell layer within a region, and the particular proteins studied. After transient ischemia, most brain regions recover their protein synthesis capability; however, recovery in the selectively vulnerable areas is poor. It is unknown whether this phenomenon itself provokes or is a consequence of the process of neuronal death.
Protein synthesis suppression during ischemia is due to energy depletion, but this is quickly reversed upon recirculation. Reperfusion does not appear to damage DNA or transcription mechanisms, although there are changes in the profile of transcripts being made. Similarly, purified ribosomes isolated from reperfused brains can make the normal repertoire of proteins and heat-shock proteins. However, during early reperfusion, newly synthesized messenger RNAs appear to accumulate in the nucleus; this alteration in RNA handling could reflect disruption at any of several steps, including posttranscriptional processing, nuclear pore transport, cytoskeletal binding, or formation of the translation initiation complex. Another mechanism that may be responsible for protein synthesis suppression during late reperfusion is progressive membrane destruction, with consequent shifts in the concentration of ions crucial for ribosomal function.
Protein synthesis suppression after ischemia likely involves a progression of multiple mechanisms during reperfusion. Although the recent work reviewed here offers new insight into the potential mechanisms disrupting protein synthesis, detailed understanding will require further investigation.
Pattern of cerebral atherosclerosis in Hong Kong Chinese. Severity in intracranial and extracranial vessels.
Authors: Leung S Y , Ng T H , Yuen S T , Lauder I J , Ho F C 
Published: June 2011

The clinical pattern of stroke and the angiographic distribution of cerebral atherosclerosis in Chinese are different from those in Caucasians. Pathological data from autopsy studies are lacking.
The intracranial and extracranial arteries supplying the brains of 114 consecutive Chinese patients undergoing autopsy in a regional general hospital were examined by computer-assisted morphometric analysis under a microscope as well as by macroscopic grading for atherosclerotic narrowing. The severity was correlated with various atherosclerosis-related factors.
Atherosclerosis of the intracranial cerebral vessels was more severe than that of the extracranial vessels. The distal branches of the intracranial vessels were also commonly involved. Hypertension and diabetes mellitus were identified as factors associated only with intracranial atherosclerosis (p < 0.001), whereas ischemic heart disease was associated with atherosclerosis in both the intracranial (p < 0.001) and extracranial (p = 0.012) vessels. Smoking was associated with narrowing of the extracranial vessels only (p = 0.0054).
Compared with figures from Caucasian and Japanese populations, the extent of intracranial atherosclerosis is much more severe in Hong Kong Chinese, whereas atherosclerotic narrowing of the extracranial carotid artery is less severe in Hong Kong Chinese than in Caucasians.
Paw-reaching, sensorimotor, and rotational behavior after brain infarction in rats.
Authors: Grabowski M , Brundin P , Johansson B B 
Published: June 2011

Functional tests that are stable and consistent over time are an advantage for long-term evaluation of treatment in experimental stroke research. Because little information on this subject is available in rodents with focal cerebral ischemia, we investigated the outcome of three behavioral tests for a period of 3 months after the insult.
Spontaneously hypertensive rats were sham-operated (n = 27) or underwent an occlusion (n = 36) of the right middle cerebral artery. Before surgery all rats were tested for amphetamine-induced rotational behavior, and half of the rats were trained in a paw-reaching task. One, 2, and 3 months after surgery the tests were repeated, together with a test for sensorimotor function. Infarct size was measured morphometrically.
In the lesion group, total hemisphere area was reduced by 22%, caudate putamen by 47%, and the thalamus by 24%. Contralateral to the lesion, paw-reaching was highly impaired, regardless of whether or not the rats had been pretrained, and lesion size correlated significantly to paw-reach performance. Ipsilateral rotation increased and sensorimotor function recovered with time in infarcted rats.
In contrast to amphetamine-induced rotation and sensorimotor behavior, the paw-reaching test provides a stable behavioral parameter after a middle cerebral artery occlusion. Moreover, the lesion-induced deficit in paw-reaching is highly correlated to the extent of the infarct, suggesting that this test is useful in evaluating treatment effects for a longer period of time.
A case of tinnitus and hearing loss after cerebellar hemorrhage.
Authors: Matsuda Y , Inagawa T , Amano T 
Published: June 2011

Approximately 10% of cases of hypertensive intracerebral hemorrhage are cerebellar hemorrhage. We report a case of intracerebellar hemorrhage in which the initial symptoms were hearing loss and tinnitus.
A 45-year-old man suddenly complained of hearing loss and tinnitus on the right side. Computed tomography demonstrated a high-density area 1.2 cm in diameter in the right cerebellar peduncle. Because of enlargement of the high-density area, the patient underwent surgery based on the diagnosis of hypertensive intracerebellar hemorrhage, and the hematoma was evacuated. The right-sided acoustic nerve was remarkably swollen by a subpial hematoma.
In this case, hemorrhage of the right cerebellar peduncle extended to the eighth nerve through the subpial space, causing hearing loss and tinnitus.
Left atrial spontaneous echo contrast is highly associated with previous stroke in patients with atrial fibrillation or mitral stenosis.
Authors: Chimowitz M I , DeGeorgia M A , Poole R M , Hepner A , Armstrong W M 
Published: June 2011

Spontaneous echo contrast is a dynamic smokelike signal that is detected by transesophageal echocardiography in patients with stasis of blood in the left atrium. We designed this study to determine if spontaneous echo contrast is associated with an increased risk of previous stroke or peripheral embolism.
Forty-two patients with spontaneous echo contrast were identified (34 had atrial fibrillation or mitral stenosis; 8 had neither). Control subjects comprised 40 patients randomly selected from patients with atrial fibrillation or mitral stenosis who did not have spontaneous echo contrast at transesophageal echocardiography. The frequency of vascular risk factors, echocardiographic features, and stroke or peripheral embolism within 1 year of echocardiography were compared in the two groups.
The frequency of traditional risk factors for stroke were the same in both groups, yet 9 of 42 patients with spontaneous contrast had stroke or peripheral embolism compared with only 1 of 40 control subjects (P < .02; relative risk, 10.6; 95% confidence interval, 1.3 to 88.4). In patients with nonvalvular atrial fibrillation, 6 of 12 patients with spontaneous contrast had a stroke or peripheral embolism compared with 1 of 28 patients without spontaneous contrast (P < .001; relative risk, 27.0; 95% confidence interval, 2.7 to 267.8).
Spontaneous echo contrast is highly associated with previous stroke or peripheral embolism in patients with atrial fibrillation or mitral stenosis. Transesophageal echocardiography may enable stratification of cardioembolic risk in patients with nonvalvular atrial fibrillation.
BW619C89, a glutamate release inhibitor, protects against focal cerebral ischemic damage.
Authors: Leach M J , Swan J H , Eisenthal D , Dopson M , Nobbs M 
Published: June 2011

The excitatory amino acid neurotransmitter glutamate is involved in excitotoxic brain injury and neurodegeneration after cerebral ischemia. Therefore, compounds that block the release of glutamate may be useful as cerebroprotective agents. The purpose of this study was to evaluate the cerebroprotective properties of a glutamate release inhibitor, BW619C89.
In the studies reported here, the effect of BW619C89 [4-amino-2-(4-methyl-1-piperazinyl)-5-(2,3,5-trichlorophenyl)pyrimidine] on neurotransmitter release (endogenous amino acids, gamma-aminobutyric acid, and acetylcholine) from slices of rat brain cerebral cortex in vitro has been determined. The neuroprotective efficacy of BW619C89 has been evaluated using the middle cerebral artery occlusion model of focal cerebral ischemia in the Fischer 344 rat.
In the in vitro studies, BW619C89 inhibited veratrine- (but not potassium-) evoked release of both endogenous glutamate and aspartate from rat cerebral cortex slices with IC50 values of approximately 5 microM. BW619C89 was approximately 10-fold less potent to inhibit veratrine-evoked 3H-gamma-aminobutyric acid release (IC50 = 51 microM), fourfold less potent to inhibit 3H-acetylcholine release (IC50 = 21 microM), and at 10 microM had only weak activity at excitatory amino acid (N-methyl-D-aspartate, kainate, and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites. When administered intravenously to Fischer 344 rats 5 minutes after permanent middle cerebral artery occlusion, BW619C89 produced marked reductions of both total (cortex and basal ganglia) and cortical infarct volumes. Cortical infarct size was reduced by 20% at a dose of BW619C89 of 5 mg/kg (n = 6, not significant); 43% at 10 mg/kg (n = 8, P < .01); 59% at 20 mg/kg (n = 8, P < .001); 61% at 30 mg/kg (n = 8, P < .001), and 53% at 40 mg/kg (n = 8, P < .001). BW619C89 at doses of 20 and 30 mg/kg also significantly reduced noncortical (basal ganglia) infarct volumes, demonstrating that a proportion of this tissue also appears to be salvageable. Behavioral effects observed were dose related, generally minor, and at doses of 20 mg/kg IV and above consisted of body tremor and mild ataxia lasting approximately 2 hours.
These results suggest that glutamate release inhibitors such as BW619C89 may provide an alternative to excitatory amino acid receptor antagonists in the treatment of focal cerebral ischemia and stroke.
Associations of serum total cholesterol, different types of stroke, and stenosis distribution of cerebral arteries. The Akita Pathology Study.
Authors: Konishi M , Iso H , Komachi Y , Iida M , Shimamoto T , Jacobs D R , Terao A , Baba S , Sankai T , Ito M 
Published: June 2011

The relation between serum total cholesterol levels and stroke is controversial. The Akita Pathology Study provides data on the association of serum total cholesterol, different types of stroke, and distribution of stenosis in cerebral arteries.
The data are based on 750 autopsied men aged 30 years and older who were admitted to a local hospital in northeast Japan between 1966 and 1984. The overall autopsy rate was 88%. The grade of stenosis in the cerebral arteries was determined blindly by one pathologist using Baker's method for basal cerebral arteries (atherosclerosis scores) and using microscopic examination of a single basal ganglion slide for the intracerebral penetrating arteries (arteriolosclerosis scores).
The age-adjusted mean value of serum total cholesterol concentration was 164 mg/dL for cerebral hemorrhage, 177 mg/dL for infarction in penetrating artery regions, and 200 mg/dL for infarction in cortical artery regions. Mean serum cholesterol was lower in deaths caused by cerebral hemorrhage than in those caused by myocardial infarction and other cardiovascular disease. Mean atherosclerosis score of basal cerebral arteries was low for cerebral hemorrhage, intermediate for penetrating artery infarction, and high for cortical artery infarction. Stenosis of both basal and penetrating arteries was minimum or absent in cases of cerebral hemorrhage. Only the basal arteries were stenotic in cases of cortical artery infarction, whereas both basal and penetrating arteries were stenosed in cases of penetrating artery infarction. There were positive associations of serum cholesterol with stenosis of basal and penetrating arteries. Among cases of cerebral hemorrhage, serum total cholesterol levels were even lower in men with no significant stenosis in either basal or penetrating arteries than in men with stenosis in either type of artery.
The association of serum cholesterol with pathogenesis varies among stroke types. Elevated serum cholesterol levels were associated with the presence of cortical artery infarction, while low serum cholesterol levels were associated with cerebral hemorrhage.
High serum lipoprotein(a) levels are an independent risk factor for cerebral infarction.
Authors: Shintani S , Kikuchi S , Hamaguchi H , Shiigai T 
Published: June 2011

This study was conducted to evaluate the role of high serum lipoprotein(a) levels in a group of patients with a relatively early onset of cerebral infarction as a whole and in a subgroup with the perforating artery occlusion subtype of cerebral infarction.
Fifty-four patients with cerebral infarction, the onset of which was before age 65 years (37 men, 17 women; mean age, 61.9 +/- 7.7 years) were examined in this study. When patients with atrial fibrillation were excluded to omit cardiac embolic strokes from analysis, the group consisted of 45 patients. The patients were classified into two subtype groups, the perforating artery occlusion group and the cortical artery occlusion group, by using magnetic resonance imaging. Lipoprotein(a) levels were measured by an enzyme-linked immunosorbent assay. Four biochemical variables (serum levels of lipoprotein(a), high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, and triglycerides) and other potential risk factors such as hypertension, diabetes mellitus, smoking habits, alcohol intake, and family history were analyzed by stepwise logistic regression to determine the independent and significant risk factors for cerebral infarction without atrial fibrillation.
The incidence of subjects with serum lipoprotein(a) levels > or = 42.6 mg/dL, which is the 95th percentile level of the control subjects, was significantly increased in the total cerebral infarction group (P < .025) and the perforating artery occlusion group (P < .025) compared with the control group. In addition, by using stepwise logistic regression analysis in the total and perforating artery occlusion patient groups we identified three independent and significant risk factors: hypertension, a low high-density lipoprotein cholesterol level, and a high serum lipoprotein(a) level. In the cortical artery occlusion group, the sample size was not large enough for the statistical analysis. Diabetes mellitus is the only known factor that correlates with serum lipoprotein(a) levels, but there were no significant correlations between serum lipoprotein(a) levels and history of diabetes mellitus or fasting blood sugar.
These findings indicate that high serum lipoprotein(a) levels are an independent risk factor in the development of cerebral infarction when subjects with atrial fibrillation were excluded from the total group and the perforating artery occlusion subtype group.
Fibrinogen and the albumin-globulin ratio in recurrent stroke.
Authors: Beamer N , Coull B M , Sexton G , de Garmo P , Knox R , Seaman G 
Published: June 2011

In following patients initially recruited for a cross-sectional study of blood viscosity in ischemic cerebrovascular disease, it was noted that those having a low albumin-globulin ratio appeared to experience the majority of subsequent vascular events. Accordingly, a prospective study in which subjects were assigned to a high or low albumin-globulin cohort was undertaken to examine the relation between a low albumin-globulin ratio, the presence of clinical risk factors for stroke, and the occurrence of subsequent stroke, myocardial infarction, or vascular death.
Three groups of subjects were followed for an average of 1.5 +/- 0.8 years to ascertain vascular end points. Group 1 consisted of 126 patients with acute ischemic stroke; group 2 included 109 subjects matched with group 1 for age, medications, and recognized clinical risk factors for stroke; and group 3 was composed of 84 healthy volunteers, matched for age with groups 1 and 2. The median albumin-globulin ratio for group 1 at enrollment, 1.45, was used to dichotomize patients into two cohorts: all subjects with an albumin-globulin ratio of 1.45 or less were assigned to the "low" albumin-globulin cohort; those whose ratio was greater than 1.45 were assigned to the "high" albumin-globulin cohort. The occurrence of vascular end points was verified during subsequent hospitalizations and outpatient clinic visits and by telephone interviews of patients and providers.
A total of 51 vascular events occurred, including 39 in group 1, 8 in group 2, and 4 in group 3. Subjects in either group 1 or 2 who were in the low albumin-globulin cohort had at least double the risk for a subsequent vascular event compared with their counterparts in the high albumin-globulin cohort (P < .01 and P < .03, respectively). In comparison with the high albumin-globulin cohort, significantly more patients in the low albumin-globulin cohort in group 1 had a history of prior stroke (P < .03). When groups 1 and 2 were combined, both a low albumin-globulin ratio and diabetes had a significant independent association with increased risk for subsequent vascular events in a Cox proportional-hazards model (P < .01 and P < .03, respectively).
The results of this study indicate that significantly increased risk for subsequent vascular events in stroke patients and in subjects with clinical risk factors for stroke is associated with a shift in the concentrations of blood proteins to a prothrombotic environment characterized by lower levels of albumin and an increased concentration of globulins and fibrinogen.
Factors influencing return to work after stroke in Japan.
Authors: Saeki S , Ogata H , Okubo T , Takahashi K , Hoshuyama T 
Published: June 2011

Few studies have identified factors that predict return to work after stroke in Japan. Our aim in this study was to determine the predictors of return to work after stroke in Japan.
We performed a retrospective cohort study on the association between patients' characteristics at admission and return to work in 230 first-stroke patients, adjusting for potential confounding factors. The patients were all aged younger than 65 years and were working, students, or housewives at the time of their stroke. Return to work was evaluated by a follow-up questionnaire. Data were analyzed using forward logistic regression analysis to compute odds ratios of return to work.
The adjusted odds ratios (and 95% confidence intervals) for patients with normal muscle strength vs severe muscle weakness, without apraxia vs with apraxia, and with white-collar vs blue-collar occupation were 4.50 (1.04 to 19.42), 4.87 (1.28 to 18.54), and 3.33 (1.34 to 8.30), respectively.
Significant predictors of return to work after stroke were no muscle weakness, absence of apraxia, and white-collar occupation.