bluuebunny/crossref_metadata_2025_split huggingface dataset:
A rapid, reliable, and valid method for measuring infarct and brain compartment volumes from computed tomographic scans.
Authors: Lyden P D , Zweifler R , Mahdavi Z , Lonzo L 
Published: June 2011

Clinical stroke trials require objective and reproducible end point variables. Morphometry of cerebral structures, including infarct volume, provides numerical measures that represent the amount of tissue damaged and potentially salvaged by therapy. However, morphometry may be time-consuming and labor-intensive, and it requires standardization across multiple centers, which may be difficult to achieve in large multicenter trials. We developed a brain morphometry method that is unbiased, rapid, reliable, and based on well-accepted stereological techniques. We now extend this method to analysis of routine computed tomographic (CT) scans such as might be obtained during a clinical stroke trial.
We studied CT scans from 18 stroke patients and 14 asymptomatic control patients obtained over 5 years at the San Diego Veterans Administration Medical Center. Three observers independently measured the volume of the cranial vault, cerebrum, cortex, white matter, deep gray structures, ventricle, sulcal cerebrospinal fluid space, visible infarction, and cerebellum/brain stem.
The two patient groups were well matched demographically. The intracranial volume of 1400 +/- 40 mL in control subjects was not different from the 1311 +/- 41 mL in patients. Cerebral volume was 1250 +/- 36 mL compared with 1070 +/- 36 mL (control subjects versus patients, P < .001), and infarction volume was 55 +/- 16 mL in patients. For all structures, intraclass correlation coefficients among the observers ranged from 0.87 to 0.03; the best agreement was found for lesion, ventricle, and intracranial volume. White matter and cortex volume predicted the National Institutes of Health Stroke Scale score but not the late outcome scores on the Barthel Index or Rankin Scale. Each scan required 70 to 90 minutes for analysis.
We developed a stereological method for cerebral morphometry from CT scans that is reliable, rapid, and simple. The measurements are unbiased, can be made on slices of any known thickness, and are independent of machine variables. Our results are remarkably similar to values obtained with more labor-intensive methods. This method should be of use in large-scale, multicenter trials of stroke therapy.
Transcranial color-coded duplex sonography in cerebral aneurysms.
Authors: Baumgartner R W , Mattle H P , Kothbauer K , Schroth G 
Published: June 2011

Diagnosis and successful therapy before rupture of cerebral aneurysms would be most desirable in view of the high mortality and morbidity rates of aneurysmal subarachnoid hemorrhage. Using transcranial color-coded duplex sonography, we studied radiologically proven cerebral aneurysms to define ultrasonographic criteria and sensitivity for their diagnosis and detection.
Twenty-nine consecutive patients with 30 radiologically proven cerebral aneurysms were prospectively examined using transcranial color-coded duplex sonography. The sonographer was aware of cerebral computed tomographic and magnetic resonance imaging findings but was blinded to the results of cerebral angiography.
Ultrasonographic findings for aneurysms studied were as follows: (1) Scanning planes that transsected approximately mid-aneurysm showed a round or oval mass that was divided by a "separation zone" into red and blue areas. (2) The "separation zone" was characterized by dark or no colors. (3) Peripheral scanning planes showed monochromatic images. (4) No turbulence was found. (5) No spontaneous fluctuations were detected. Twenty-three of 27 (85%) nonthrombosed aneurysms with a diameter of 6 to 25 mm were identified. The walls and three thrombosed and four nonthrombosed aneurysms (mean diameter, 5 mm) were missed.
Transcranial color-coded duplex sonography can provide the diagnosis of nonthrombosed aneurysm using the above-cited criteria because of its capacity to reveal flow phenomena. It is not the method of choice in the search for aneurysms because small and thrombosed aneurysms are missed. Careful visual inspection of the intracranial arteries to permit incidental detection of cerebral aneurysms should be part of every transcranial color-coded duplex examination.
Disturbance of retention of memory after focal cerebral ischemia in rats.
Authors: Hirakawa M , Tamura A , Nagashima H , Nakayama H , Sano K 
Published: June 2011

The purpose of this study was to investigate the behavioral changes, in particular retention of memory, after focal cerebral ischemia in rats.
Ischemia was produced by permanent occlusion of the left middle cerebral artery (MCA). For quantitative behavioral analysis, one-trial passive avoidance response and active avoidance response with the discrete lever-press avoidance procedure were observed. One group of animals was trained once to learn the passive avoidance task 1 day before surgery. The response latency was examined 4 and 14 days after surgery. The second group was trained to learn the active avoidance task for 2 weeks before surgery. The avoidance rate was examined 3 and 14 days after surgery.
The MCA-occluded group showed significant failure of memory retention in both of these tasks (P < .01). The nonoperated group and sham-operated group showed no definite memory failure.
Retention of memory in the passive avoidance response and the active avoidance response was disturbed after left MCA occlusion in the rat. These results strongly suggest that this model can be used to assess memory disturbance after focal cerebral ischemia.
Prothrombotic states in young people with idiopathic stroke. A prospective study.
Authors: Barinagarrementeria F , Cantú-Brito C , De La Peña A , Izaguirre R 
Published: June 2011

Although 4% of cerebral infarcts in the young can be attributed to hematologic disturbances that predispose to thrombosis, the frequency of cerebral infarcts caused by prothrombotic states is not known. Recently, the association between cerebral infarction and deficiencies of elements of the natural anticoagulant system has been recognized.
Thirty-six consecutive patients under 40 years of age with cerebral infarction of undetermined cause were prospectively studied. Quantitation of natural anticoagulants was done at least 3 months after the cerebral infarction. The following activity tests were performed, all by the chromogenic method: antithrombin III, protein C, plasminogen, tissue plasminogen activator, and inhibitor of tissue plasminogen activator. Protein S was quantified by the Laurell rocket method. All patients underwent a complete cardiological examination, including two-dimensional echocardiography, as well as four-vessel cerebral angiography. Some patients were also studied by transesophageal echocardiography.
Of 36 patients, 17 were male, with a mean age of 28 years. Mean age for women was 25 years. Nine patients (25%; 5 women, 4 men) had a deficiency of one natural anticoagulant and constituted group I. In these patients, isolated protein S deficiency was detected in five cases (13.8%); in one case, we observed the association between protein S deficiency and antiphospholipid antibodies; and deficiency of protein C was seen in one case (2.7%), of antithrombin III in one case (2.7%), and of plasminogen in one case (2.7%). Instances of cerebral infarction without natural anticoagulant deficiency (group II) included 12 women and 15 men. There were no differences in clinical and radiological findings between the two groups.
Considering the importance of prothrombotic state, especially caused by deficiency of protein S, in the development of cerebral infarcts, we suggest that it should be looked for in every young patient affected by this pathological entity and in whom no etiologic factors can be determined.
Medical and neurological complications during inpatient stroke rehabilitation.
Authors: Dromerick A , Reding M 
Published: June 2011

We sought to assess the type, frequency, and clinical predictors of neuromedical complications occurring during inpatient rehabilitation after stroke.
One hundred consecutive patient records were reviewed. All medical and neurological complications requiring a physician's order for further evaluation or treatment were recorded.
Complications were urinary tract infection (44 cases), depression (33), musculoskeletal pain (31), urinary retention (25), falls (25), fungal dermatitis (24), hypotension (19), diabetes mellitus (16), hypertension (15), and other neuromedical problem (194). The mean +/- SD numbers of medical and neurological complications per patient were 3.6 +/- 2 and 0.6 +/- 0.8, respectively. Complications were independently related to both the severity of functional disability as judged by Barthel score (r = -.42, P < .001) and length of rehabilitation hospital stay (r = .54, P < .001). Cardiac complications were predicted by New York Heart Association class 3 or 4 symptomatology on admission (P < .05). The age, sex, interval from stroke to rehabilitation hospital admission, and ischemic versus hemorrhagic etiology of the stroke were unrelated to the number of complications observed. Thirteen patients required transfer back to an acute-care hospital, one of whom died within 24 hours of transfer. There were no deaths on the rehabilitation unit.
We have defined the type and frequency of neuromedical complications during inpatient rehabilitation after stroke. Their frequency varies with the severity of stroke, cardiovascular comorbidity, and length of stay.
Usefulness of an intravenous contrast medium in the characterization of high-grade internal carotid stenosis with color Doppler-assisted duplex imaging.
Authors: Sitzer M , Fürst G , Siebler M , Steinmetz H 
Published: June 2011

The remaining limitations of ultrasonographic imaging in accurately quantifying internal carotid stenosis or diagnosing internal carotid occlusion may be overcome by enhancing the echogenicity of flowing arterial blood with contrast agents. This study assessed the usefulness of the intravenous (transpulmonary) contrast medium SH U 508 A in improving the characterization and quantification of severe internal carotid stenosis.
We examined 32 patients (30 had vessels with a stenosis of greater than 70% luminal narrowing and 2 had vessel occlusions) using a 7.5-MHz linear-array transducer for color Doppler-assisted duplex imaging before and after injection of the contrast medium.
The SH U 508 A-induced increase in carotid blood echogenicity began 11 +/- 2 (mean +/- SD) seconds after the start of the bolus injection, peaked at 21 +/- 2 dB, and showed a half-life of 75 seconds. Quantitative vascular measurements (cross-sectional luminal area reduction and plaque length, respectively) obtained before and after contrast application were highly correlated (r > .90). Visualization of the entire length of the intrastenotic residual flow lumen, however, was significantly improved by contrast enhancement (52% versus 83%, P = .01).
This pilot study on patients with extracranial carotid artery disease suggested that ultrasonic contrast media may be most useful in improving the ultrasonography-based diagnosis of internal carotid occlusion.
Tissue-type plasminogen activator improves neurological functions in a rat model of thromboembolic stroke.
Authors: Sakurama T , Kitamura R , Kaneko M 
Published: June 2011

The capacity of an intravenous infusion of double-stranded tissue-type plasminogen activator to salvage neurological functions in a rat model of thromboembolic stroke was studied.
The model of thromboembolic stroke was induced by the intracarotid injection of 2-hour-old homologous blood clots to rats. Neurological functions were scored on a 5-point scale 48 hours after the injection of the clots. Infarction size was determined by triphenyltetrazolium chloride staining, and cerebral hemorrhage was examined macroscopically.
Intravenous infusion of tissue-type plasminogen activator (1 or 5 x 10(5) IU/kg) within 3 hours after embolization significantly improved neurological functions (P < .01) and reduced infarction size (P < .05). Tissue-type plasminogen activator treatment 6 hours after embolization failed to attenuate the neurological status score. Treatment with tissue-type plasminogen activator did not increase the incidence of intracerebral hemorrhage and was not associated with a systemic fibrinolytic state. In comparison with tissue-type plasminogen activator treatment, although urokinase treatment (5 x 10(5) IU/kg) improved neurological functions, it was associated with a systemic fibrinolytic state and a tendency to increase the incidence of intracerebral hemorrhage.
These findings in this model suggest that tissue-type plasminogen activator should be given early after the onset of ischemic symptoms to effectively prevent or limit pathological infarction and improve neurological functions without an increase in the incidence of cerebral hemorrhage.
Effects of clentiazem on cerebral ischemia induced by carotid artery occlusion in stroke-prone spontaneously hypertensive rats.
Authors: Kikkawa K , Yamauchi R , Suzuki T , Banno K , Murata S , Tetsuka T , Nagao T 
Published: June 2011

We examined metabolic and functional changes when forebrain ischemia was induced in stroke-prone spontaneously hypertensive rats by bilateral carotid artery occlusion. In addition, the protective effect of clentiazem was evaluated in this model.
Rats were anesthetized with urethane. Cerebral blood flow was measured with a laser Doppler flowmeter. Cerebral high-energy phosphates and intracellular pH were measured by phosphorus magnetic resonance spectroscopy. Electroencephalographic activity was evaluated as the summation of its amplitude. These parameters were monitored during a 30-minute period of ischemia and recirculation. Clentiazem was given orally as pretreatment (10 mg/kg twice a day for 3.5 days).
Bilateral carotid occlusion caused a decrease in cerebral blood flow to approximately 5% of the preischemic level and the disappearance of electroencephalographic activity. Occlusion also caused a decrease in ATP and phosphocreatine (to 48.7 +/- 4.3% and 23.7 +/- 2.2% of preischemic levels, respectively) as well as intracellular pH (from 7.3 +/- 0.1 to 6.0 +/- 0.1). During recirculation the reversal of these changes was variable: high-energy phosphates were partially restored, but electroencephalographic activity and intracellular pH showed little improvement. Hypoperfusion (55.7 +/- 11.5% of the preischemic flow) developed after reactive hyperemia. Pretreatment with clentiazem lessened the decrease in cerebral blood flow (control, 4.8 +/- 1.4%; clentiazem, 14.1 +/- 4.1% of the preischemic level; P < .05) and prevented the disappearance of electroencephalographic activity in some rats during ischemia. Clentiazem also prevented postischemic hypoperfusion and accelerated the restoration of high-energy phosphates, intracellular pH, and electroencephalographic activity during recirculation.
Carotid artery occlusion induced stable forebrain ischemia in stroke-prone spontaneously hypertensive rats. Clentiazem improved the metabolic and functional disturbances that occurred in this ischemic model, and its beneficial effect appeared to be due mainly to the relative preservation of cerebral blood flow during carotid occlusion.
Variations in the anatomy of the rabbit cervical carotid artery.
Authors: Lee J S , Hamilton M G , Zabramski J M 
Published: June 2011

A model for cerebral ischemia that requires injection of emboli into the internal carotid artery of the rabbit is commonly used. However, in our experience we have found the anatomy of the cervical carotid to be highly variable. If not appreciated, this may result in unexpectedly high variability in the severity of ischemic injury. We undertook this experimental protocol to determine whether it was possible to characterize the anatomy of the rabbit cervical carotid artery.
We examined and recorded the architecture of the cervical carotid arteries of 105 consecutive rabbits involved in experimental protocols to evaluate the role of tissue-type plasminogen activator during embolic stroke.
Two basic patterns of origin of the internal carotid artery were identified: lateral origin, classified as type I, and dorsomedial origin, classified as type II. In addition, there were three subsequent variations in the origin and morphology of the occipital artery in relation to the internal carotid artery: origin from the external carotid artery (subtype A); origin proximal on the internal carotid artery (subtype B); and origin distal on the internal carotid artery (subtype C).
The classification of the anatomy of the cervical carotid artery of the rabbit into these easily recognized types will assist those attempting to use this embolization model. Failure to recognize the origin of the occipital artery from the internal carotid artery can result in the misdirection of embolic material into the occipital artery and significantly reduce the effectiveness of this stroke model.
Effects of cocaine on carotid vascular reactivity in swine after balloon vascular injury.
Authors: Núñez B D , Miao L , Ross J N , Núñez M M , Baim D S , Carrozza J P , Morgan J P 
Published: June 2011

The use of cocaine has been associated with stroke. To evaluate carotid vasospasm as a potential mechanism of cocaine-induced stroke, we studied 12 swine immediately and 10 weeks after angioplasty.
We compared the short- and long-term vasoconstrictor responses of normal and injured arterial segments to nitroglycerin, histamine, and cocaine in vivo by carotid angiography. We also compared the isometric contractile force responses to different vasoactive substances in normal and injured vascular rings in vivo, and we tested the direct action of cocaine on both arterial segments.
In in vivo studies, immediately after angioplasty, luminal diameter in the control segment decreased by 30% with histamine 30 micrograms/kg and by 23% with cocaine 10 mg/kg (P < .001). In contrast, neither histamine nor cocaine produced vasoconstriction in the angioplasty segment. Thus, a transient loss of vasoconstriction occurred at the angioplasty site. Ten weeks later, histamine 30 micrograms/kg significantly (P < .001) decreased luminal diameter by 34% in the control and by 33% in the angioplasty segment; similarly, cocaine 10 mg/kg significantly (P < .001) decreased luminal diameter by 26% in the control and by 34% in the angioplasty segment. Thus, 10 weeks after angioplasty, the transitory loss of carotid vasoconstriction in response to histamine and cocaine reverted, and a moderate generalized vasoconstriction occurred in both segments without localized vasospasm. In vitro, the maximal isometric tension responses to KCl, acetylcholine, histamine, and phenylephrine were similar in vascular rings from normal and angioplasty segments. The median effective doses to histamine and phenylephrine were similar. In contrast, cocaine in concentrations from 10(-7) to 10(-3) mol/L failed to produce any isometric contraction in vitro.
Cocaine in vivo produced a generalized carotid vasoconstriction without evidence of localized vasospasm; since there was no response to cocaine in vitro, the in vivo effect was most likely mediated by neurohumoral factors rather than by a direct action of cocaine on vascular smooth muscle.
Effect of nilvadipine on the development of neurological deficits in stroke-prone spontaneously hypertensive rats.
Authors: Takakura S , Furuichi Y , Yamamoto T , Ogawa T , Satoh H , Mori J 
Published: June 2011

Several types of antihypertensive drugs have been reported to protect stroke-prone spontaneously hypertensive rats from stroke. However, the clinical relevance remains unclear. This study was performed to investigate the effect of nilvadipine, a calcium channel blocker, on the development of neurological deficits in stroke-prone spontaneously hypertensive rats. In addition, plasma levels of nilvadipine were measured to determine the clinical relevance.
Salt-loaded stroke-prone spontaneously hypertensive rats were orally administered nilvadipine mixed with a powder diet (0.01% and 0.03%, wt/wt). Non-salt-loaded rats were maintained on tap water. Chronological changes in neurological deficit scores and systolic blood pressure were recorded. After 6 weeks of medication, measurement of plasma levels of nilvadipine, serum biochemical analysis, and pathological observation of both the brain and the kidney were performed.
In the salt-loaded control group, both severe hypertension and neurological deficit developed, and the final survival rate was 30%. Systolic blood pressure decreased significantly in the high-dose nilvadipine-treated group but not in the low-dose nilvadipine-treated group. However, the development of neurological deficit was almost completely inhibited in both nilvadipine-treated groups that had no deaths (P < .01). The mean plasma levels of nilvadipine in the low-dose group and in the high-dose group at the time of death were 0.21 ng/mL and 0.61 ng/mL, respectively.
Nilvadipine inhibited the development of neurological deficit in stroke-prone spontaneously hypertensive rats at plasma concentrations lower than that in clinical use. Thus, nilvadipine might prevent cerebral vascular disorders at doses routinely used for essential hypertension.
Cardiac sources of embolism in patients with pial artery infarcts and lacunar lesions.
Authors: Mast H , Thompson J L , Völler H , Mohr J P , Marx P 
Published: June 2011

On the assumption that the majority of lacunes are caused by small-vessel diseases and that pial artery infarcts arise from cardio-embolic or large-vessel diseases, 194 patients from the Berlin Cerebral Ischemia Data Bank with either lacunar or pial artery infarcts were analyzed for the frequency of cardiac sources of embolism. The primary hypothesis was that the frequency of cardiac sources of embolism is higher among pial artery infarct subjects.
The presence of cardiac sources of embolism was estimated by electrocardiographic and transthoracic and transesophageal echocardiographic studies. Cranial computed tomography scans were evaluated by two masked observers.
The overall rate of cardiac sources of embolism did not differ significantly between the lacunar and the pial artery infarct group (66% versus 71%; odds ratio, 0.80; confidence interval, 0.43 to 1.50). Echocardiographic evidence of cardiac thrombi was positively associated with pial artery infarcts (odds ratio, 0.18; confidence interval, 0.04 to 0.80); atrial fibrillation and all other cardiac sources were not.
Left cardiac thrombi are significantly associated with pial artery infarcts. Other presumed cardiac sources of embolism, including atrial fibrillation, may often represent coincidental findings or have a less strong tendency to result in pial artery infarcts.