bluuebunny/crossref_metadata_2025_split huggingface dataset:
Anterior choroidal artery territory infarcts. Study of presumed mechanisms.
Authors: Leys D , Mounier-Vehier F , Lavenu I , Rondepierre P , Pruvo J P 
Published: June 2011

A previous study suggested that occlusive diseases of small penetrating arteries account for most anterior choroidal artery (AChA) territory infarcts, but half of the patients did not have an echocardiogram. Cases of AChA territory infarcts associated with internal carotid artery stenosis or atrial fibrillation suggest that this hypothesis may be wrong. The aim of this study was to determine the mechanism of 16 nonselected consecutive AChA territory infarcts.
The study population consisted of 8 men and 8 women aged 17 to 89 years. They underwent a computed tomographic scan at the acute stage, Doppler ultrasonography and B-mode echotomography of the cervical arteries, bidimensional transthoracic echocardiography, and cerebral magnetic resonance imaging, replaced by a second computed tomographic scan in 3 patients. Ten patients underwent cerebral angiography. We defined the presumed cause of stroke according to the criteria used in the trial of Org 10172 in acute stroke treatment.
The presumed cause of stroke was definite cardio-embolism in 4 patients (atrial fibrillation in 2, paradoxical embolism in 1, and left ventricular akinesia in 1); definite large-vessel atherosclerosis in 2; dissection of the internal carotid artery in 2; and definite small-vessel occlusion in 1. Seven patients had a negative diagnostic workup. Six patients had no risk factors for small-vessel occlusion. The AChA was not visible on angiography in 4 patients. One patient had two arterial cutoffs, suggestive of emboli in other cerebral arteries.
This study suggests that AChA territory infarcts are rarely related to small-vessel occlusion and therefore require a complete diagnostic workup.
Diffusion-weighted imaging differentiates ischemic tissue from traumatized tissue.
Authors: Hanstock C C , Faden A I , Bendall M R , Vink R 
Published: June 2011

Diffusion-weighted magnetic resonance imaging (MRI) has been shown to be particularly effective in detecting early (0 to 4 hours) pathophysiological changes in localized brain regions after cerebral ischemia. The present study sought to establish whether diffusion-weighted MRI would be similarly effective in predicting outcome after traumatic brain injury.
Diffusion-weighted MRI images and T2-weighted MRI images were obtained over 4 hours after either moderate fluid percussion-induced traumatic brain injury or unilateral carotid ligation in rats.
Diffusion-weighted MRI images of traumatic brain injury demonstrated focal regions of image hypointensity as early as 1 hour after trauma. The relative diffusion coefficient in these hypointense regions was significantly increased (P < .005) by 4 hours after trauma compared with the noninjured hemisphere, but only in the transverse plane in the x direction. In contrast, induction of diffuse, nonfocal ischemia by unilateral carotid ligation resulted in scattered regions of hyperintensity with a significant (P < .001) decrease in relative diffusion coefficient as early as 1 hour after ligation compared with the noninjured hemisphere. This decrease exhibited no directionality.
We conclude that traumatic brain injury results in an increased water diffusion distance with the directionality indicative of bulk flow of extracellular fluid toward the lateral ventricles (vasogenic edema). In contrast, the decreased water diffusion distance with no apparent directionality observed in ischemia is most likely indicative of cytotoxic edema. Diffusion-weighted MRI therefore has the potential to differentiate cases of traumatic brain injury with no focal ischemia from those instances of traumatic brain injury in which focal ischemia is a complication.
Superoxide dismutase ameliorates neuronal death from hypoxia in culture.
Authors: Rosenbaum D M , Kalberg J , Kessler J A 
Published: June 2011

Studies showing efficacy with free radical scavengers have been conflicting, and when protection was demonstrated it was attributed to action at the level of the vascular endothelium. The purpose of this study was to test the hypotheses that neuronal free radical formation plays a role in the ischemic cascade and occurs intracellularly and that free radical scavengers, if taken up intracellularly, will protect against hypoxic damage.
A tissue culture model of hypoxia followed by restoration of oxygen was employed, using both superior cervical ganglia and hippocampal neurons. Cells were exposed to an anoxic atmosphere of 95% N2 and 5% CO2 and examined 2 to 24 hours later after restoration of oxygen. Determination of survival was measured by trypan blue exclusion. Nitroblue tetrazolium stain was used to assess free radical formation.
Pretreatment with free superoxide dismutase did not decrease cell death after hypoxia as measured by trypan blue exclusion. However, when superoxide dismutase was taken up intracellularly under depolarizing conditions (55 mmol/L KCl in the medium), cell death was decreased significantly compared with hypoxic controls (28.7 +/- 4.34 versus 40.3 +/- 4.33; P < .03). During hypoxia neurons reduced nitroblue tetrazolium to form the blue precipitate formazan, and the color change was blocked in neurons pretreated with superoxide dismutase in depolarizing medium. Similar findings occurred in both superior cervical ganglia and hippocampal neurons.
These findings provide evidence to support the role of neuronal free radical formation in cell death secondary to hypoxia. In addition, free radical scavengers, if taken up intracellularly, may partially ameliorate their deleterious effect.
Surgically induced angiogenesis to compensate for hemodynamic cerebral ischemia.
Authors: Nariai T , Suzuki R , Matsushima Y , Ichimura K , Hirakawa K , Ishii K , Senda M 
Published: June 2011

The ischemic brain may stimulate angiogenesis to compensate for impaired circulation. We examined the conditions promoting such angiogenesis to provide the basis for surgical treatment.
The degree of cerebral hemodynamic stress was studied in patients with moyamoya disease using the stable xenon-enhanced computed tomographic acetazolamide tolerance test and positron emission tomography. Patients were subjected to surgery in which scalp arteries were placed on the cerebral cortex without vessel-to-vessel anastomosis. Formation of the newly vascularized collateral network connecting the implanted artery to cortical arteries was assessed angiographically 12 to 17 months after surgery.
Preoperative average resting cerebral blood flow for cortex that developed revascularization of cortical arteries was not significantly different from that for cortex that did not. However, cortex that developed revascularization had an average preoperative increase of blood flow by acetazolamide treatment of -3.29 +/- 4.6 mL/min per 100 cm3 (n = 20), which was significantly less (P = .0034) than that of cortex that did not show revascularization (20.7 +/- 4.3 mL/min per 100 cm3; n = 9). Good revascularization developed when the cortex showed increase of blood flow by acetazolamide treatment of less than 0 (steal phenomenon). Preoperative positron emission tomography data indicated that revascularization developed when the cortex was under "misery perfusion." Postoperative hemodynamics were ameliorated by revascularization.
Angiogenesis to connect the implanted scalp arteries to the cerebral cortical arteries was selectively initiated when ischemia of hemodynamic origin existed.
Cardiac arrhythmia associated with reversible damage to insula in a patients with subarachnoid hemorrhage.
Authors: Svigelj V , Grad A , Tekavcic I , Kiauta T 
Published: June 2011

The insular cortex has been shown experimentally to contain an arrhythmogenic center that may play an important role in the genesis of cardiac arrhythmias and electrocardiographic changes in patients with intracranial (eg, cerebrovascular) lesions. The description of our case is intended to substantiate this claim with a clinical observation.
A 37-year-old woman with subarachnoid hemorrhage suffered a severe reversible cardiac arrhythmia after neurosurgical clipping of an arterial aneurysm and removal of an intracerebral hematoma from the region of the left insula.
The observed association of a neurosurgical intervention in the region of the left insular cortex with a cardiac arrhythmia supports but does not prove the suggested role of the insulin in the causation of heart rhythm disturbances after stroke.
Long-term follow-up of cerebral infarction patients with proton magnetic resonance spectroscopy.
Authors: Gideon P , Sperling B , Arlien-Søborg P , Olsen T S , Henriksen O 
Published: June 2011

With proton magnetic resonance spectroscopy it is possible to measure the content of various brain metabolites in vivo, including N-acetylaspartate (which may be used as a neuronal marker), creatine, choline, and lactate. The content of these brain metabolites was measured serially from the acute stage to the chronic stage of infarction. Regional cerebral blood flow was also measured within the affected areas. These factors were compared with the clinical outcome.
Six patients with ischemic stroke were examined serially from the acute stage (< or = 2 days) to the chronic stage (> 6 months) with proton magnetic resonance spectroscopy. Cerebral blood flow was measured with single-photon emission-computed tomography with 99mTc-labeled d,l-hexamethylenepropyleneamine oxime as flow tracer.
Lactate was found in all patients in the acute stage of stroke. Lactate was also found in the 3 largest lesions in the chronic stage; in 2 of these patients lactate was not found in the subacute stage. Reduced levels of N-acetylaspartate were found in 5 patients; in the sixth patient with a small lesion no reduction was found. In all lesions reduced blood flow was found in the acute and chronic stage, whereas hyperemia was found in 4 patients in the subacute stage.
In this preliminary study no clear correlation was found between the level of N-acetylaspartate or lactate in the acute stage of stroke and the clinical outcome; however, there does appear to be some connection between the reduction of cerebral blood flow and the spectroscopic findings in the chronic stage and to some extent the clinical outcome. Studies of larger clinical groups will be necessary to further elucidate the prognostic potential of proton magnetic resonance spectroscopy in human stroke.
Extent of pontine pyramidal tract Wallerian degeneration and outcome after supratentorial hemorrhagic stroke.
Authors: Fukui K , Iguchi I , Kito A , Watanabe Y , Sugita K 
Published: June 2011

Pyramidal tract Wallerian degeneration has been detected on magnetic resonance imaging (MRI) as T2-weighted high-intensity areas. We analyzed the relation between the extent of brain stem Wallerian degeneration and activities of daily living (ADL) after supratentorial hemorrhagic stroke.
Twenty-six patients with supratentorial hemorrhage were examined on the coronal T2-weighted image of the pons 3 months or later after stroke, and the percentage of Wallerian degeneration in the pons was calculated. The patients were divided into three groups. In group A (n = 6), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 2 months from the MRI. In group B (n = 11), MR films were taken 3 to 6 months from the onset, and the ADL assessment was done within 10 months from the MRI (mean, 15.5 months from the onset). In group C (n = 9), MR films were taken after 10 to 17 months (mean, 12.0 months) from the ictus, and the ADL assessment was done simultaneously. Barthel Index score was used for quantitative ADL assessment.
All patients showed various degrees of pontine pyramidal tract Wallerian degeneration associated with capsular involvement by the hematoma. In group A, the percentage of degeneration did not correlate with the Barthel Index score (r = .2101, P = .6895). An inverse relation between percentage of degeneration and Barthel Index score was seen in groups B (r = .7354, P = .0099) and C (r = .888, P = .0014). In groups B and C, Wallerian degeneration was higher in patients with Barthel scores less than 60 (P = .005).
The extent of pontine Wallerian degeneration on MRI 3 months or later after the stroke correlated with the patient's Barthel Index score 1 year after the stroke.
Cerebral blood flow in migraine accompaniments and vertebrobasilar ischemia.
Authors: Ramadan N M , Levine S R , Welch K M 
Published: June 2011

Transient neurological symptoms of brain stem or occipital lobe origin may be caused by transient ischemic attack in the vertebrobasilar territory (VB-TIA) or late-onset (or late-life) migraine accompaniment (LOMA). It is often clinically difficult to distinguish between VB-TIA and LOMA.
Cerebral blood flow of 23 patients with VB-TIA, 24 with LOMA, and 28 age-matched control subjects was measured using the 133Xe inhalation regional cerebral blood flow (rCBF) technique.
After adjusting for differences in baseline variables such as blood pressure, hematocrit, and PCO2, patients with VB-TIA had (1) lower mean rCBF than control subjects (P < .003) as measured by the initial slope index method; (2) more frequent anterior rCBF asymmetries than control subjects and patients with LOMA (P < .03 for both comparisons); and (3) higher mean interhemispheric rCBF differences compared with patients with LOMA (P = .08) and control subjects (P < .02).
Regional CBF patterns in patients with VB-TIA and LOMA differ, with lower rCBF and more asymmetry of the anterior blood flows in patients with VB-TIA, probably reflecting the effects of stroke risk factors on the cerebral circulation. Patients with LOMA have rCBF patterns more closely resembling those of age-matched healthy subjects. rCBF measurements may assist in the clinical diagnosis of VB-TIA and late-onset migrainous events.
Brain ischemia decreases phosphatidylcholine-phospholipase D but not phosphatidylinositol-phospholipase C in rats.
Authors: Nishida A , Emoto K , Shimizu M , Uozumi T , Yamawaki S 
Published: June 2011

Phosphatidylcholine (PC)-phospholipase D (PLD) is an important intracellular signaling pathway in response to a variety of agonists, but little is known about the effects of brain ischemia on the PC-PLD system. We thus have examined the effects of global cerebral ischemia on PLD in rats.
We have examined the effects of global ischemia (decapitation or four-vessel occlusion) on PLD and PLC activity in the membrane fraction of rat brains. We measured the PLD and PLC activity in detergent-mixed micelle assay systems using 3H-labeled exogenous substrate.
The results demonstrate that basal PLD activity showed a gradual decrease with increased duration (5 to 30 minutes) of ischemia by decapitation in the hippocampus; after 30 minutes of ischemia, PLD activity was significantly decreased compared with the control. Lineweaver-Burk plots showed that the apparent Vmax value of PLD in ischemia was one half of that in the control without changes in Km value. Ischemia by decapitation significantly decreased PLD activity in the brain stem as well as the hippocampus, whereas in four-vessel occlusion study, ischemia significantly decreased PLD activity in the hippocampus but not in the brain stem. Lowered temperature (30 degrees C and 22 degrees C) during ischemic incubation did not reverse the ischemia-induced PLD activity decrease. In contrast to PLD, ischemia by decapitation had no effect on basal phosphatidylinositol-phospholipase C activity or the amount of phospholipase C beta 1 in the membrane fractions from 30-minute ischemic hippocampus by immunoblots probed with the antibody.
These results suggest that PC-PLD is one of the target enzymes of ischemia; its decrease may cause a perturbation of PC hydrolysis and/or disorders of intracellular transduction of signals or choline metabolism for acetylcholine formation in brain.
Vertebrobasilar junction fenestration associated with dissecting aneurysm of intracranial vertebral artery.
Authors: Zhang Q J , Kobayashi S , Gibo H , Hongo K 
Published: June 2011

Vertebrobasilar junction fenestration is considered to be a subtype of fenestration of the proximal basilar artery, which has been described only in autopsy cases. The fenestration associated with a dissecting vertebral aneurysm is extremely rare.
A 47-year-old man presented with subarachnoid hemorrhage. The four-vessel angiogram showed a fusiform dilatation with an intimal flap of the left vertebral artery distal to the origin of the posterior inferior cerebellar artery and a fenestration at the vertebrobasilar junction, in which a small limb of the fenestration arising from the distal portion of the left vertebral artery bridged the proximal basilar trunk, while another limb had a large diameter showing the same diameter as the basilar artery. The dissecting aneurysm was treated with body clipping by directly clipping the ruptured portion of the aneurysm via a suboccipital approach in an early operation 48 hours after the ictus. The patient had a good recovery and returned to his work. He is well at a 5-year follow-up.
The relevant angiographic features of the vertebrobasilar junction fenestration and the surgical treatment of such associated aneurysms are discussed.
Bilateral infarction in the anterior cerebral artery vascular territory due to an unusual anomaly of the circle of Willis.
Authors: Borggreve F , De Deyn P P , Mariën P , Cras P , Dierckx R A 
Published: June 2011

Bilateral infarction in the anterior cerebral artery vascular territory is rare and usually results from rupture of an aneurysm of the anterior communicating artery. In the case of an anomaly of the anterior part of the circle of Willis, thrombosis also may lead to bilateral infarction.
A 73-year-old right-handed man presented with a complete loss of communicative behavior and an almost complete quadriplegia. 99mTc-hexamethylpropyleneamine oxime single-photon emission-computed tomography (HMPAO SPECT) of the brain showed a "horseshoe" image, reflecting bilateral perfusion defects in areas supplied by the anterior cerebral arteries. Postmortem examination of the brain revealed an unusual anomaly of the circle of Willis in which the postcommunicating part of the right anterior cerebral artery was absent.
In our patient a unique developmental anomaly of the circle of Willis indirectly contributed to bilateral infarction in the territory of the anterior cerebral artery. The patient's neuropsychological profile, dominated by akinetic mutism, was highly suggestive of involvement of the receptive language modalities. For the first time, 99mTc-HMPAO SPECT of the brain revealed a horseshoe image in bilateral infarction in the territory of the anterior cerebral artery.
Comparison of clinical and neuroradiological findings in first-ever stroke. A population-based study.
Authors: Lindgren A , Norrving B , Rudling O , Johansson B B 
Published: June 2011

To determine how a recently proposed clinical stroke subclassification corresponds to specific findings on computed tomography (CT) and magnetic resonance imaging (MRI) of the brain.
Two hundred twenty-eight patients with first-ever stroke were divided into four clinical subgroups: (1) total anterior circulation syndrome: both cortical and subcortical symptoms from anterior and middle cerebral artery territory; (2) partial anterior circulation syndrome: more restricted and predominantly cortical symptoms from the same arterial territories; (3) lacunar syndrome; and (4) posterior circulation syndrome: vertebrobasilar or posterior cerebral artery symptoms. The imaging protocol included CT of the brain on day 0 through 15 and a second CT and an MRI of the brain on day 16 through 180 after acute stroke onset.
There were 200 patients with cerebral infarction and 28 patients with intracerebral hemorrhage. Intracerebral hemorrhage was found in 19% of patients with total anterior circulation syndrome and in no patients with lacunar syndrome (chi 2 test; P < .01 for the difference between the four clinical subgroups). Of the 200 patients with cerebral infarction, 27% had total anterior circulation, 30% partial anterior circulation, 26% lacunar, and 16% posterior circulation syndromes. CT within 2 days revealed a visible lesion in about two thirds of patients with infarctions of total or partial anterior circulation syndrome type, compared with only 22% of patients with lacunar infarction (chi 2 test; P = .02 for the difference between the four subgroups). The mean volume of the symptomatic infarction on CT within 15 days was 95 mL for total anterior circulation, 20 mL for partial anterior circulation, and 2.5 mL for lacunar syndrome (one-factor ANOVA; P = .0001). A cortical involvement of the infarction on CT day 16 through 180 was seen in 81% of patients with total anterior circulation syndrome and 58% of those with partial anterior circulation syndrome, compared with only 8% of patients with lacunar syndrome (chi 2 test; P = .0001). MRI more often than CT showed a cortical involvement of lacunar infarctions and also revealed more silent lesions.
The described clinical subgroups significantly differed in frequencies of intracerebral hemorrhage, cortical involvement, and lesion volume on CT and MRI.
Spectrum of lateral medullary syndrome. Correlation between clinical findings and magnetic resonance imaging in 33 subjects.
Authors: Kim J S , Lee J H , Suh D C , Lee M C 
Published: June 2011

Computed tomography is insufficient in evaluation of medullary lesions. Although lateral medullary infarction is a relatively common type of cerebrovascular disease, detailed correlation between clinical findings and magnetic resonance imaging (MRI) has not yet been reported.
We studied 33 consecutive patients with lateral medullary infarction who showed appropriate MRI lesions and correlated their clinical findings with the MRI results.
Gait ataxia (88%), vertigo/dizziness (91%), nausea/vomiting (73%), dysphagia (61%), hoarseness (55%), Horner sign (73%), and facial (85%) and hemibody (94%) sensory changes were frequent clinical findings. MRI results showed that the lesions located in the rostral part of the medulla were usually diagonal band-shaped and were associated with more severe dysphagia, hoarseness, and the presence of facial paresis, whereas the caudal lesions, situated usually in the lateral surface of the medulla, appeared to correlate with more marked vertigo, nystagmus, and gait ataxia. Nausea/vomiting and Horner sign were common regardless of the lesion location, and lesions extending ventromedially correlated with facial sensory change on the contralateral side of the lesion.
Analysis of MRI findings in rostrocaudal and dorsoventral aspects allows us, although not unequivocally, to make anatomicoclinical correlations in the evaluation of patients with lateral medullary stroke syndrome.