bluuebunny/crossref_metadata_2025 huggingface dataset:
Age-related spontaneous intracerebral hematoma in a German community.
Authors: Schütz H , Bödeker R H , Damian M , Krack P , Dorndorf W
Published: June 2011

We investigated incidence, age distribution in relation to etiology, and localization of spontaneous intracerebral hematoma in 100 consecutive cases. Incidence in the total population of the Giessen area was estimated to be greater than 11/100,000 inhabitants/yr and increased with age. There was a trend toward higher incidence in males. Overall mortality was 27%, 22% of 58 patients aged less than 70 years and 33% of 42 patients aged greater than or equal to 70 years. Hypertensive putaminal hematoma showed the highest mortality rate (42%, 10 of 24 cases). Chronic alcoholism and anticoagulant medication influenced the mortality rate unfavourably. We found the following localizations and etiologies to have a specific relation with age: 1) lobar hematomas from vascular malformations, group aged less than 40 years; 2) hypertensive putaminal hematomas and hypertensive thalamic hematomas, group aged 40-69 years; and 3) lobar hematomas, group aged greater than or equal to 70 years. Alcoholism was an additional factor in 38% of the 13 middle-aged men with hypertensive putaminal hematomas. Fourteen cases of spontaneous intracerebral hematoma were possibly due to cerebral amyloid angiopathy. Six of these 14 patients had recurrent lobar hematomas, but only three of the six could be histologically investigated. In these three cases, cerebral amyloid angiopathy was proven.
Differences in ischemia-induced accumulation of amino acids in the cat cortex.
Authors: Shimada N , Graf R , Rosner G , Heiss W D
Published: June 2011

It is well established that excitatory amino acid neurotransmitters are extensively liberated during ischemia and that they have neurotoxic properties contributing to neuronal injury. To study changes in the liberation of excitatory and other amino acids during cerebral ischemia, we measured their extracellular concentrations and related them to blood flow levels and electrophysiologic activity (electrocorticogram and auditory evoked potentials) before and for up to 2 hours after multiple cerebral vessel occlusion in 14 anesthetized cats. Blood flow levels between 0 and 43 ml/100 g/min were reached. Concentrations of the excitatory amino acid neurotransmitters increased most (aspartate 10-fold, glutamate 30-fold, and gamma-aminobutyric acid 300-fold compared with control values) below a blood flow threshold of 20 ml/100 g/min. The total power of the electrocorticogram and the amplitude of the auditory evoked potentials were affected below the same blood flow threshold. In contrast, concentrations of the nontransmitter amino acids taurine, alanine, asparagine, serine, and glutamine increased 1.5-5-fold as blood flow decreased, while concentrations of the essential amino acids phenylalanine, valine, leucine, and isoleucine did not change during cerebral ischemia. The great increases in concentrations of the excitatory amino acid neurotransmitters below a blood flow threshold close to that for functional disturbance is in accordance with the role of these amino acids in ischemic cell damage. Their release at blood flow levels compatible with cell survival and the increase in their concentrations with severity and duration of cerebral ischemia imply that excitotoxic antagonists may have potential as therapeutic agents.
Remote effect of deep-seated vascular brain lesions on cerebral blood flow.
Authors: Attig E , Capon A , Demeurisse G , Verhas M
Published: June 2011

We measured regional cerebral blood flow using the xenon-133 inhalation method, at approximately 1 month after onset, in 60 stroke patients who had no evidence of major carotid artery stenosis or occlusion. Their single lesions (43 infarcts and 17 hematomas) were located in the capsulothalamolenticular region, sparing the cortex. Hemispheric mean cerebral blood flow was reduced on the side of the lesion in 25 patients and on both sides in 20. Regional hypoperfusion was observed in 46 patients (ipsilaterally in 34, bilaterally in 10, and contralaterally in two). Regional hypoperfusion was observed most frequently in the frontal lobe, particularly in the motor and premotor cortices of the prerolandic area. The 46 patients with regional hypoperfusion were compared with the 14 patients without regional hypoperfusion, considering the size and location of the lesion as well as the functional and analytic motor performances. As a rule, the lesion was slightly smaller and more posterior and the functional (p less than 0.001) and analytic (p less than 0.05) motor performances were significantly better in the 14 patients without regional hypoperfusion. Since the xenon-133 inhalation method examines cortical blood flow, we can attribute blood flow reductions resulting from deep-seated lesions to a functional depression akin to diaschisis. Interpretation of the clinical consequences and pathogenesis of this phenomenon requires further sequential and pathologic studies.
Embolic stroke after smoking "crack" cocaine.
Authors: Petty G W , Brust J C , Tatemichi T K , Barr M L
Published: June 2011

A 39-year-old woman had an embolic upper division middle cerebral artery branch occlusion 3 hours after smoking the free base of cocaine ("crack"). Radionuclide ventriculography demonstrated cardiomyopathy, and echocardiography documented a left atrial thrombus. This case demonstrates that embolism is one mechanism of ischemic stroke after cocaine use, and that cardiomyopathy, possibly cocaine induced, may be the source of embolus. A cardiac source of embolus should be sought in patients with cocaine-associated cerebral infarction.
Diagnostic significance of flow separation within the carotid bifurcation demonstrated by digital subtraction angiography.
Authors: Schuierer G , Huk W J
Published: June 2011

The presence of an area of reversed blood flow due to flow separation in the interval carotid artery is a normal finding in Doppler ultrasound studies in vivo as well as in model carotid bifurcations. This flow separation phenomenon is caused by the geometry of the carotid bifurcation and the fluid dynamics of blood. We demonstrated the flow separation phenomenon on lateral-projection intra-arterial digital subtraction angiograms in 99 of 100 carotid bifurcations. The mean duration of flow separation was 5.8 seconds, with values up to 14 seconds in normal carotid bifurcations. The presence of this flow separation phenomenon is almost independent of atherosclerotic lesions and is not correlated with cerebral ischemia. Therefore, the angiographic finding of a flow separation has no diagnostic value. However, our results refer to a factor that may be important in the genesis of atherosclerosis at the carotid bifurcation, namely the duration of the stay of blood and its components within the area of flow separation.
Transcranial Doppler ultrasonographic assessment of intermittent light stimulation at different frequencies.
Authors: Gomez S M , Gomez C R , Hall I S
Published: June 2011

Seven normal adult volunteers underwent intermittent photic stimulation at frequencies of 5-60 Hz while their posterior cerebral arteries were monitored using transcranial Doppler ultrasound. Baseline measurements were obtained under conditions of total darkness, and sampling was also done during continuous illumination. Overall variation in mean flow velocity between complete darkness and continuous illumination was 9.8%, but the maximal change (expressed as percentage deviation from baseline) occurred consistently when stimulation was undertaken at frequencies of 10 (21%) and 20 (19%) Hz (p = 0.05). Frequencies higher than 20 Hz resulted in mean flow velocity variations that were not significantly different from that found during continuous illumination. The optimal frequency of intermittent visual stimulation required to induce measurable changes in posterior cerebral artery Doppler characteristics appears to be in the range 10-20 Hz.
Cerebrovascular disease in Hong Kong Chinese.
Authors: Huang C Y , Chan F L , Yu Y L , Woo E , Chin D
Published: June 2011

Our prospective study of cerebrovascular disease in Hong Kong confirms a previous clinical impression that stroke in the Chinese has a pattern different from that in Caucasians. We studied 540 patients (aged 20-70 years) with stroke. Computed tomography or autopsy was obtained in 86.1% and showed an increase in the proportion with lacunar infarction, striatocapsular infarction, and parenchymal hemorrhage relative to the frequencies in Caucasians. This increase in the incidence of cerebral hemorrhage occurs not only in semicomatose and comatose patients but also in alert patients (16.9%) and those with a lacunar syndrome (12.5%). Our findings suggest that cerebrovascular disease in the Chinese selectively affects small vessels, causing lacunes and hemorrhages. In future community studies on stroke prevalence, researchers should be cautious about interpreting similar prevalence rates as reflecting similar risk factors or pathologies.
Histamine elicits competing endothelium-dependent constriction and endothelium-independent dilation in vivo in mouse cerebral arterioles.
Authors: Rosenblum W I , Nelson G H , Weinbrecht P
Published: June 2011

We used television microscopy and an image-splitting technique to monitor the changes in diameter produced by histamine applied locally to mouse pial arterioles in vivo. A high dose (50 micrograms/ml, 3 X 10(-4) M) of histamine constricted the arterioles, whereas lower doses (20 and 10 micrograms/ml) relaxed them. Constriction was blocked and dilation occurred when selective injury of the endothelium was produced by light from a helium-neon laser in the presence of intravascular Evans blue. From this we conclude that the constriction was endothelium-dependent and was caused by the release of an endothelium-derived constricting factor. Constriction was also blocked by each of two antagonists of the H1 histamine receptor and by pretreatment of the arterioles with indomethacin. H1 blockade unmasked a dilating action of 1 micrograms/ml histamine, a dose too low to affect the diameter of arterioles not treated with the H1 blocker. An H2 blocker interfered with the relaxation by low-dose (10 micrograms/ml, 6 X 10(-5) M) histamine. These data indicate that for mouse pial arterioles, histamine can interact with H1 receptors on the endothelium to release an endothelium-derived constricting factor that causes constriction of the underlying muscle while simultaneously interacting with H2 receptors in the muscle that mediate relaxation of the vessel.
Are hypertension or cardiac embolism likely causes of lacunar infarction?
Authors: Lodder J , Bamford J M , Sandercock P A , Jones L N , Warlow C P
Published: June 2011

We tested the hypothesis that hypertension is more common and cardiac embolism less common in patients with lacunar infarction than in patients with other types of cerebral infarction. We studied risk factor profiles in a series of 102 consecutive patients with a lacunar infarct and 202 consecutive patients with a carotid artery-distribution infarct involving the cortex registered in the Oxfordshire Community Stroke Project, a community-based study of first-ever stroke. The two groups did not differ in the prevalence of prestroke hypertension (defined in a number of ways) or in the prevalence of markers of sustained hypertension. The presence of atrial fibrillation and a history of myocardial infarction, particularly during the 6 weeks before the stroke, were significantly more common in the group with carotid-distribution infarcts involving the cortex. There was no significant difference in the prevalence of other accepted risk factors for ischemic stroke, including previous transient ischemic attack, cervical bruit, diabetes mellitus, peripheral vascular disease, or cigarette smoking. Our results suggest that hypertension is no more important in the development of lacunar infarction than it is in the development of other types of ischemic stroke that are presumed to be due to atherosclerotic thromboembolism in a major cerebral artery. Our data support the autopsy evidence that cardioembolic occlusion is an unusual cause of lacunar infarction.
Wallerian degeneration of the pyramidal tract in capsular infarction studied by magnetic resonance imaging.
Authors: Pujol J , Martí-Vilalta J L , Junqué C , Vendrell P , Fernández J , Capdevila A
Published: June 2011

Using magnetic resonance imaging, we studied 24 patients with ischemic infarction of the internal capsule. Magnetic resonance imaging detected wallerian degeneration of the pyramidal tract below the capsular lesion in 11 patients (45.8%); all 11 had clinical evidence of pyramidal tract damage. In six additional patients magnetic resonance imaging findings, present only on axial slices, were considered to indicate possible wallerian degeneration. When motor deficit was associated with posterior limb lesions, magnetic resonance imaging detected wallerian degeneration of the pyramidal tract in 78.6% (11) of 14 patients.
Prognostic significance of fibrinopeptide A in survivors of cerebral infarction.
Authors: Landi G , Barbarotto R , Morabito A , D'Angelo A , Mannuccio Mannucci P
Published: June 2011

We measured levels of fibrinopeptide A, beta-thromboglobulin, and fibrinogen in the plasma of 27 patients 2 months after their first stroke. Concentrations of fibrinopeptide A, a sensitive index of in vivo hypercoagulability, were significantly higher in the 18 ischemic stroke patients than in 40 age- and sex-matched controls and in the six patients who experienced recurrence within 5 years than in the 12 who remained asymptomatic. On the contrary, fibrinopeptide A levels had no prognostic significance among the nine patients with hemorrhagic stroke. Concentrations of beta-thromboglobulin, an index of platelet activation, were higher in the 27 stroke patients than in the 40 controls, but this index was not associated with stroke recurrence. Fibrinogen levels were not significantly higher in stroke patients than in controls. In a multivariate regression analysis of hemostatic and clinical variables, only fibrinopeptide A levels of greater than 4 ng/ml were significantly related to cerebral infarction. Our results support the role of hypercoagulability in the recurrence of ischemic stroke and may allow identification of subjects at high risk for it. If confirmed in more patients, our results could provide a rationale for clinical trials of anticoagulant therapy in such patients.
Neuropathologic consequences of internal carotid artery occlusion and hemorrhagic hypotension in baboons.
Authors: Graham D I , Mendelow A D , Tuor U , Fitch W
Published: June 2011

We studied eight anesthetized and physiologically monitored adult baboons (Papio cyanocephalus); four were subjected to hemorrhagic hypotension alone and four to hemorrhagic hypotension plus unilateral carotid artery occlusion. Cerebral blood flow was measured using xenon-133, the electroencephalogram was recorded using silver-silver chloride epidural electrodes, and histologic examination was carried out after perfusion-fixation. In the baboons subjected to hypotension alone (mean arterial blood pressure of 28 mm Hg) cerebral blood flow was 28.5 +/- 5.0 ml/100 g/min, whereas in the baboons subjected to hypotension plus unilateral carotid artery occlusion it was 21.8 +/- 1.8 ml/100 g/min at a mean arterial blood pressure of 27 mm Hg. There was no ischemic damage in the former group, but in the latter group there was necrosis in the arterial boundary zones of three baboons and in the distribution of the middle cerebral artery in one. We conclude that, when combined with hypotension, unilateral carotid artery occlusion may lead to hemodynamic ischemia accentuated in the arterial boundary zones of the ipsilateral cerebral hemisphere.
Endogenous platelet activating factor does not modulate blood flow and metabolism in normal rat brain.
Authors: Kochanek P M , Melick J A , Schoettle R J , Magargee M J , Evans R W , Nemoto E M
Published: June 2011

Both platelet activating factor and eicosanoids participate in the cerebrovascular response to ischemia. Eicosanoids also modulate cerebrovascular tone under normal physiologic circumstances, but a similar role for platelet activating factor has not been investigated. Therefore, using 16 rats, we studied the effects of the platelet activating factor receptor blockers BN 52021 (10 mg/kg, n = 4 or 30 mg/kg, n = 2) and WEB 2086 (5 mg/kg, n = 6) on global cerebral blood flow and the cerebral metabolic rate for oxygen and compared them with the effect of indomethacin (10 mg/kg, n = 4). Neither antagonist altered cerebral blood flow (112 +/- 16 and 107 +/- 14 ml/100 g/min at baseline versus 108 +/- 16 and 105 +/- 18 ml/100 g/min after BN 52021 and WEB 2086, respectively). In contrast, indomethacin significantly (p less than 0.05) decreased cerebral blood flow from 106 +/- 8 to 69 +/- 4 ml/100 g/min. No treatment altered the cerebral metabolic rate for oxygen compared with baseline. These data suggest that in normal rat brain, concentrations of platelet activating factor, unlike those of eicosanoids, are subthreshold and do not modulate cerebral blood flow or the cerebral metabolic rate for oxygen.
Cerebral amyloid angiopathy as a cause of subarachnoid hemorrhage.
Authors: Ohshima T , Endo T , Nukui H , Ikeda S , Allsop D , Onaya T
Published: June 2011

Cerebral amyloid angiopathy is a pathologic condition characterized by the deposition of amyloid in the walls of small vessels in the cerebral cortex and meninges. Intracerebral hemorrhage is common in persons with this condition, but pure subarachnoid or subdural hemorrhage is rarely seen. Recently, the existence of two types of amyloid proteins related to cerebral amyloid angiopathy, beta protein and cystatin C, has been reported, and immunohistochemical methods using antisera to these proteins have become available. We describe a patient with fatal subarachnoid hemorrhage presumably caused by beta protein-type cerebral amyloid angiopathy, which was demonstrated immunohistochemically by using a monoclonal antibody to a synthetic peptide corresponding to residues 8-17 of beta protein. We suggest that beta protein-type cerebral amyloid angiopathy is a possible etiologic factor in subarachnoid hemorrhage of unknown cause.
Transcranial Doppler ultrasound findings in middle cerebral artery occlusion.
Authors: Kaps M , Damian M S , Teschendorf U , Dorndorf W
Published: June 2011

We evaluated the efficacy of transcranial Doppler ultrasonography in 23 patients suffering from acute middle cerebral artery occlusion. The diagnosis of occlusion was most suggestive when all basal arteries except the affected middle cerebral artery were detectable. Enhanced blood flow velocity in the anterior cerebral artery due to leptomeningeal collateralization was used as a corroborating criterion. With frequent follow-up examinations, we monitored reperfusion of the M1 segment resulting from recanalization or embolus migration in 16 patients. Those patients undergoing recanalization within days after onset of the first symptoms revealed variable clinical courses and lesion patterns on computed tomography, indicating the crucial importance of early and efficient leptomeningeal collateral blood supply. Transcranial Doppler ultrasonography was able to exclude middle cerebral artery occlusion with accuracy, which provides important clinical information. However, distal branch occlusions could not be detected with sufficient exactness.
Prospective study of lacunar infarction using magnetic resonance imaging.
Authors: Hommel M , Besson G , Le Bas J F , Gaio J M , Pollak P , Borgel F , Perret J
Published: June 2011

Using computed tomography and magnetic resonance imaging, we prospectively studied 100 patients hospitalized with a lacunar infarct. Our aim was to evaluate the capabilities of magnetic resonance imaging in the detection and delineation of lacunes in a project of clinicotopographic correlations. Seventy-nine patients had a classic lacunar syndrome; 35 had pure motor stroke, 26 had ataxic hemiparesis, seven had sensorimotor stroke, and 11 had pure sensory stroke. A miscellaneous group of 21 patients had less typical lacunar syndromes, primarily with brainstem signs and symptoms. Among a total of 153 lacunes, magnetic resonance imaging detected at least one lacune appropriate to the symptoms in 89 patients. In 16 patients at least two lesions correlated with the clinical features, and precise clinicotopographic correlations were possible in 68 patients. Magnetic resonance imaging was more effective when it was performed a few days after the stroke. Lesions causing different types of lacunar syndromes had significantly different volumes, suggesting that the size of the lesion may influence clinical features. Magnetic resonance imaging may be the imaging technique of choice in the study of lacunar syndromes.
Platelet thromboxane release after subarachnoid hemorrhage and surgery.
Authors: Juvela S , Kaste M , Hillbom M
Published: June 2011

We studied adenosine diphosphate-induced platelet aggregation and the associated release of thromboxane B2 in platelet-rich plasma from 88 patients with subarachnoid hemorrhage and 26 healthy controls. During the first 3 days after subarachnoid hemorrhage, the patients showed significantly decreased (p less than 0.05) platelet aggregability and thromboxane release relative to the controls, but these effects disappeared in a few days. Platelet count increased for 3 weeks after subarachnoid hemorrhage. Surgery in 67 patients was followed by significant increases in platelet aggregability (p less than 0.05) and thromboxane release (p less than 0.001). Greatest thromboxane release was found in the eight patients showing delayed (postoperative) ischemic deterioration with a permanent neurologic deficit. Although platelet hyperaggregability and increased thromboxane release were particularly prominent in these eight patients, the role of these hematologic parameters in the pathogenesis of delayed ischemic deterioration remains unclear.
Preservation of brain temperature during ischemia in rats.
Authors: Minamisawa H , Mellergård P , Smith M L , Bengtsson F , Theander S , Boris-Möller F , Siesjö B K
Published: June 2011

Our objectives were to study the loss of heat from ischemic brain and to devise a method of maintaining brain temperature. Reversible forebrain ischemia was induced by carotid clamping and exsanguination in 30 anesthetized and artificially ventilated rats. Rectal, skull, and brain temperatures were measured, confirming previous findings that brain temperature falls by 4-5 degrees C during 15 minutes of ischemia unless measures are taken to maintain head temperature by external heating. Temperature gradients developed within the ischemic brain, superficial tissues being cooler than deep ones. These temperature gradients were reversed when skull temperature was maintained at core body (rectal) temperature by external heating. With rectal and skull temperatures maintained at 38 degrees, 37 degrees, 35 degrees, or 33 degrees C, brain temperatures nonetheless decreased by approximately 1 degree C during ischemia. This decrease in brain temperature could be prevented by placing the rat in a Plexiglas box with circulating air at temperatures close to that of the body core and a relative humidity of approximately 100%. We also found that, unless special precautions are taken, a temperature gradient develops between the brain and body core during recirculation.
Analysis of cerebrovascular sympathetic nerve density in relation to stroke development in spontaneously hypertensive rats.
Authors: Smeda J S
Published: June 2011

Previous studies have shown that elevating the K+ levels from 0.75% to 2.11% in the diet of stroke-prone spontaneously hypertensive rats significantly retards the development of stroke and increases their lifespan. On the other hand, stroke-resistant spontaneously hypertensive rats fail to develop stroke even if they are fed the low-K+ version of this diet. Since sympathetic nerves surrounding the cerebral vasculature play an important role in protecting the brain from stroke during hypertension, I studied whether changes in sympathetic nerve density accounted for the differing incidences of stroke in stroke-prone spontaneously hypertensive rats fed high- and low-K+ diets and in stroke-resistant and stroke-prone spontaneously hypertensive rats fed a low-K+ diet. At 14 weeks of age, all 11 stroke-prone rats fed the low-K+ diet had evidence of cerebral hemorrhage while such lesions were virtually absent in the 11 littermates fed the high-K+ diet and totally absent in the eight stroke-resistant rats fed the low-K+ diet. Stroke-prone (regardless of diet) but not stroke-resistant rats exhibited greater sympathetic nerve densities in the left hemisphere than in the right. When stroke-prone rats were compared, in some areas of the cerebrovasculature, rats fed the high-K+ diet had greater mean sympathetic nerve densities than those fed the low-K+ diet. On the other hand, stroke-resistant and stroke-prone rats fed the low-K+ diet exhibited comparable sympathetic nerve densities in most cerebral arteries studied.(ABSTRACT TRUNCATED AT 250 WORDS)
Cerebral thrombosis in beta-thalassemia/hemoglobin E disease.
Authors: Wong V , Yu Y L , Liang R H , Tso W K , Li A M , Chan T K
Published: June 2011

We describe two Chinese patients with beta-thalassemia/hemoglobin E disease who developed cerebral infarction due to occlusion or stenosis of their extracranial carotid arteries. The roles of platelet abnormalities and other factors in this condition are discussed.
Functional image of dynamic computed tomography for the evaluation of cerebral hemodynamics.
Authors: Nagata K , Asano T
Published: June 2011

We report the usefulness of functional image of dynamic computed tomography as a technique for evaluating cerebral hemodynamics. Although the technique itself has been reported, the advance of computer technology has made it possible to obtain high-resolution functional images within only a few minutes. We conducted 70 examinations on 57 patients with cerebral ischemia and correlated the findings with clinical outcome. Those patients whose abnormalities were detected on all corrected mean transit time, time to peak, and peak value images developed massive cortical infarcts. On the other hand, patients with abnormalities detected only on the corrected mean transit time image had only partial low-density lesions on follow-up computed tomograms. Patients with abnormalities detected only on the time to peak image suffered repeated transient ischemic attacks, but follow-up computed tomograms showed no low-density lesion in most cases. Single-photon emission computed tomography with N-isopropyl-p-(123I)iodoamphetamine performed at the time of functional image of dynamic computed tomography showed a high concordance of the findings in many cases, especially those with hyperacute-stage cerebral ischemia, in which the concordance rate was 90.5% (19 of 21). Comparing images constructed from different parameters, functional image of dynamic computed tomography can delineate other than hemodynamic factors, such as extent of the vascular bed or the degree of collateral circulation. Thus, functional image of dynamic computed tomography is a potentially important and useful technique for the further analysis of cerebral hemodynamics.
Prosthetic valve endocarditis 1976-1987. Antibiotics, anticoagulation, and stroke.
Authors: Davenport J , Hart R G
Published: June 2011

We retrospectively reviewed the clinical characteristics and outcomes of 61 patients with 62 episodes of prosthetic valve endocarditis, paying particular attention to neurologic complications (stroke). Atypical features of the group included a benign outcome of early postoperative infection (18% mortality) and a high stroke morbidity and mortality rate with Staphylococcus epidermidis infections. Eleven patients (18%) suffered an embolic stroke, most less than or equal to 3 days after diagnosis and before the initiation of antimicrobial therapy; the rate of embolic stroke recurrence was low (9%). The risk of embolic stroke was lower with bioprosthetic than with mechanical valves. No protective effect of anticoagulation therapy with warfarin was observed. Six patients (8%) suffered brain hemorrhage due to septic arteritis, brain infarction, or undetermined causes; no specific risk of hemorrhagic stroke was evident with anticoagulation therapy. Antibiotic treatment appears to be more important than anticoagulation to prevent neurologic complications in patients with prosthetic valve endocarditis.
Acute toxicity of a nuclear magnetic resonance cerebral blood flow indicator in cats.
Authors: Branch C A , Ewing J R , Fagan S C , Goldberg D A , Welch K M
Published: June 2011

We studied trifluoromethane as a potential gaseous indicator in nuclear magnetic resonance measurements of cerebral blood flow. We considered the effects of trifluoromethane on cerebral blood flow in 17 cats and on the electroencephalogram and electrocardiogram in nine cats and compared these with the effects of the more toxic compound chlorodifluoromethane in five cats. Inhaled at 60%, trifluoromethane had no effect on cerebral blood flow, the cerebral metabolic rate for oxygen, or oxyhemoglobin content. At 70%, trifluoromethane sensitized the cats' hearts to epinephrine, but to a much lesser degree than 40% chlorodifluoromethane, and produced only moderate changes in cerebral electrical activity as measured by the electroencephalogram. We found trifluoromethane to be suitable for use in animals, but its toxicity needs to be studied further before it can be used in humans for the measurement of cerebral blood flow.
Blood-brain barrier integrity during cardiopulmonary resuscitation in dogs.
Authors: Schleien C L , Koehler R C , Shaffner D H , Traystman R J
Published: June 2011

Blood-brain barrier integrity during cardiopulmonary resuscitation may be important because of the potential effects of adrenergic agonists administered during arrest on cerebral metabolism and the cerebral vasculature. As an index of blood-brain barrier permeability to small molecules, we measured the brain uptake of [14C]alpha-aminoisobutyric acid during a 10-minute period in 25 anesthetized dogs. To correct for the amount of carbon-14 label in the plasma space, we administered [3H] inulin 2 minutes before death. The mean transfer coefficient in 14 brain regions of five control dogs ranged from 0.002 to 0.007 ml/g/min. After 8 (n = 15) or 15 (n = 5) minutes of cardiac arrest, external chest compression was instituted to maintain aortic blood pressure above 60 mm Hg. The transfer coefficient was not elevated during chest compression (n = 10), immediately following defibrillation (n = 5), or 4 hours after resuscitation (n = 5); in some brain regions the transfer coefficient decreased. However, the decrease in the transfer coefficient was proportional to the decrease in the cerebral plasma volume as measured by the ratio of the [3H]inulin concentration in the tissue to that in the plasma. Thus, it is unlikely that a decrease in capillary surface area masked an increase in blood-brain barrier permeability. Therefore, we found no evidence of blood-brain barrier disruption during or after cardiopulmonary resuscitation in dogs. Despite the large phasic increases in sagittal sinus pressure associated with external chest compression, concurrent increases in cerebrospinal fluid pressure apparently protect the microcirculation from increased transmural pressure.
Effect of nimodipine on platelet function in patients with subarachnoid hemorrhage.
Authors: Juvela S , Kaste M , Hillbom M
Published: June 2011

We studied platelet function in 41 patients with subarachnoid hemorrhage who were randomized to receive either nimodipine or placebo in a double-blind fashion. Nimodipine was given to 21 patients, intravenously for 7-10 days and then orally until 21 days after the subarachnoid hemorrhage. The other 20 patients received placebo in a similar manner. Nimodipine did not significantly influence platelet aggregability. For the first 1-5 days after the subarachnoid hemorrhage, nimodipine treatment did not have any notable effect on adenosine diphosphate-induced platelet thromboxane B2 release, but a significant (p less than 0.05) inhibitory effect was observed thereafter. During intravenous administration, nimodipine prevented the increase in thromboxane release otherwise observed after subarachnoid hemorrhage. Concomitant with the decrease in thromboxane release, nimodipine increased the platelet count both before and after surgery so that the capacity for thromboxane formation per liter of blood decreased less than expected on the basis of thromboxane release per 10(7) platelets. Our study suggests that nimodipine might diminish the chance of cerebral ischemia by inhibiting platelet thromboxane release.
Arterial pathology in cerebellar infarction.
Authors: Amarenco P , Hauw J J , Gautier J C
Published: June 2011

We reviewed 88 pathologically proven cerebellar infarcts, examining the entire thoracocervical arterial system (including the spinal part of the vertebral artery, the intracranial arteries, and the heart) in all cases. For 50 infarcts, we found an arterial occlusion. The intracranial part of the vertebral artery was involved in 38 infarcts (76%), the basilar artery in 20 infarcts (40%), and a cerebellar artery in 12 infarcts (24%). Eight infarcts were due to bilateral distal vertebral artery occlusions. For the 50 infarcts, the cause of the occlusion was atherosclerosis in 28 (56%) and a cardiac embolism in 12 (24%). For the remaining 38 infarcts, we found no arterial occlusions on postmortem examination. Of these 38 infarcts, 26 (68%) were associated with a cardiac source of emboli. For the entire group of 88 infarcts, atherosclerosis was the cause in 31 (35%), while a cardiac embolism was proven or presumed in 38 (43%). Dissecting aneurysms, atherosclerotic artery-to-artery embolism, or hemodynamic mechanisms could have been responsible for a few infarcts. We conclude that cerebellar infarcts often arise from cardiogenic embolism.
Magnetic resonance imaging in lateral sinus hypoplasia and thrombosis.
Authors: Mas J L , Meder J F , Meary E , Bousser M G
Published: June 2011

Lateral sinus thrombosis may be difficult to differentiate angiographically from lateral sinus hypoplasia, which mainly affects its proximal transverse portion. Using magnetic resonance imaging, we evaluated six patients who demonstrated poor filling or lack of filling of one or both lateral sinuses at angiography. In each patient, magnetic resonance imaging unambiguously demonstrated either lateral sinus thrombosis or lateral sinus hypoplasia. The latter was characterized by a frank asymmetry in size (surface of section) of the transverse portion of the lateral sinuses on parasagittal images without any abnormal signal in the course of the sinus. Lateral sinus thrombosis was indicated by increased intraluminal signal on all planes and with all pulse sequences. By virtue of its freedom from bone-related artifact, its multiplanar imaging capability, and its sensitivity to both blood flow and thrombus formation, magnetic resonance imaging is an excellent tool for the evaluation of lateral sinus thrombosis or hypoplasia.
Responses of rat basilar artery to acetylcholine and platelet products in vivo.
Authors: Faraci F M , Mayhan W G , Heistad D D
Published: June 2011

Studies in vitro suggest that the basilar artery has distinctive responses to endothelium-dependent stimuli. Our first goal was to examine the effects of acetylcholine on diameter of the basilar artery in vivo. Because aggregating platelets may have important effects on cerebral arteries, our second goal was to examine the effects on the basilar artery of products that are released by platelets (thromboxane, serotonin, and adenosine 5'-diphosphate). Diameter of the basilar artery was measured through a cranial window in anesthetized rats (n = 25). Baseline diameter of the basilar artery was 247 +/- 10 microns mean +/- SEM. Topical application of acetylcholine at 10(-6) and 10(-5) M dilated the basilar artery by 13 +/- 2% and 19 +/- 2%, respectively. The thromboxane analogue U46619 at 10(-8) and 10(-7) M reduced the diameter of the basilar artery by 18 +/- 5% and 29 +/- 4%, respectively. At 10(-8) and 10(-7) M, serotonin had little effect on pial arterioles on the cerebrum but constricted the basilar artery by 18 +/- 2% and 29 +/- 4%, respectively. At 10(-6) and 10(-5) M, adenosine 5'-diphosphate produced marked dilatation of pial arterioles on the cerebrum (9 +/- 2% and 20 +/- 3%, respectively) but had little effect on the basilar artery (increased diameter by 4 +/- 2% and 6 +/- 2%, respectively). Thus, in contrast to some studies of the basilar artery in vitro, acetylcholine produces dilatation of the basilar artery in vivo. Potent constrictor responses to thromboxane and serotonin, in combination with the minimal dilator effect of adenosine 5'-diphosphate, suggest that release of these products during platelet aggregation would favor constriction of the basilar artery.
Lithium ion does not protect brain against transient ischemia in gerbils.
Authors: Yoshida S , Kirino T , Tamura A , Basugi N , Sano K
Published: June 2011

It has been proposed that lithium ion desensitizes neuronal receptors that function via the inositol phospholipid signaling mechanism. We examined the effects of lithium chloride on the morphologic outcome after 5 minutes of cerebral ischemia induced in gerbils by occluding both common carotid arteries under brief halothane anesthesia. In three treated groups of 10 gerbils each, 5 meq/kg i.p. lithium chloride was given 2 days, 1 day, and 2 hours before ischemia; 2 hours before ischemia; or immediately after the end of ischemia. Corresponding control groups of nine or 10 gerbils each received equivalent volumes of saline injected at comparable times. All gerbils were perfusion-fixed 1 week later, and neuronal density of the hippocampal CA1 pyramidal cells was determined. Lithium induced very mild intraischemic systemic hypothermia, but postischemic hyperthermia developed in both treated and control groups. Neuronal densities were equal in corresponding groups. The results indicate that our regimen of lithium administration provides no benefit in survival of hippocampal neurons, and intraischemic hypothermia of less than 0.8 degrees C is not protective. Other strategies to inactivate the signal transduction system that is specific for excitatory neurotransmission should be evaluated.
Computed tomographic evaluation of bleeding sites in primary pontine hemorrhages.
Authors: Komiyama M , Yasui T , Yagura H , Fu Y
Published: June 2011

With the aim of identifying common bleeding sites and probable parent vessels in "small" primary pontine hemorrhages, we reviewed computerized tomographic scans of 20 patients with hematomas less than 2.5 cm in diameter.

We used scans depicting the upper and lower pons and plotted the centers of the hematomas, assuming them to be a probable source of bleeding. No predilection sites were found on the axial plane.

Both the paramedian and the long and short circumferential arteries were probable sources of hemorrhage in the present series.
Cardioembolic stroke revealed by increased hemostatic markers associated with intracardiac thrombus.
Authors: Yasaka M , Yamaguchi T
Published: June 2011

The presence of hemocoagulative disorders in acute ischemic stroke has been reported occasionally. However, the cause of the hemostatic derangement has not been fully elucidated.

A 66-year-old woman with a history of hypertension and myocardial infarction developed pure motor hemiparesis. On admission, she was thought to have a lacunar infarction. However, computed tomography of the brain with contrast medium revealed a small infarct in the cortex of the frontal lobe. Conventional angiography showed no stenotic or occlusive lesions. Sensitive hemocoagulative tests revealed hypercoagulative and hyperfibrinolytic states. Ultrafast computed tomography of the heart with contrast enhancement demonstrated a large left ventricular mural thrombus. There were no further abnormal findings suggestive of other systemic diseases that affect blood coagulability. As a result, the patient was diagnosed as having suffered a cardioembolic stroke.

An intracardiac thrombus could be one of the causes of the hemostatic disorders of acute cardioembolic stroke.
Evidence of somatotopic organization of the sensory thalamus based on infarction in the nucleus ventralis posterior.
Authors: Combarros O , Polo J M , Pascual J , Berciano J
Published: June 2011

This is to describe a restricted sensory syndrome of unique distribution due to thalamic infarct.

We report a case of pure sensory disturbance involving the left intraoral and perioral regions and the tips of the thumb and forefinger of the left hand. Magnetic resonance imaging revealed a small infarct in the contralateral thalamus, presumably affecting the nucleus ventralis posterior.

This patient provides an excellent correlation between clinical findings and thalamic representation of body surface as established during stereotactic procedures.
The anterior choroidal artery does not supply the corona radiata and lateral ventricular wall.
Authors: Mohr J P , Steinke W , Timsit S G , Sacco R L , Tatemichi T K
Published: June 2011

We sought first to characterize the clinical syndromes of patients found to have angiographic, computed tomographic, or magnetic resonance imaging scan indexes of anterior choroidal artery territory infarction and then to determine the frequency of involvement of the periventricular corona radiata in such patients.

Sixteen patients were selected based on angiographically, or surgically, documented occlusion of the anterior choroidal artery or based on infarcts whose minimal lesions included the anterior choroidal territory as defined by Kolisko and Beevor. We mapped the lesions using the templates of the Matsui and Hirano atlas and entered them into a computer using a program allowing overlapping diagrams of the cases.

The anatomic distributions were fairly uniform, all involving the lower portion of the posterior limb of the internal capsule, the medial pallidum (75% of cases), cerebral peduncle in 44%, thalamus in 37%, and the medial temporal lobe in 38%. None extended outside these areas to include the upper corona radiata. The clinical picture corresponded to the well-established neurological syndrome featuring motor deficits with varying degrees of visual field and sensory impairments. Only two showed hypesthetic ataxic hemiparesis.

Our findings indicate that the syndrome of anterior choroidal artery infarction is fairly uniform; ataxic hemiparesis occurs infrequently; and lesions in the lateral ventricular wall and the corona radiata are not part of the territory supplied by the anterior choroidal artery.
Lacunar infarction as an embolic complication of cardiac and arch angiography.
Authors: Cacciatore A , Russo L S
Published: June 2011

Lacunar infarcts are small, deep cerebral infarcts resulting from occlusion of small, penetrating cerebral arteries. They are most commonly associated with hypertension. Cardiac sources of embolization are sometimes present in patients with lacunes, but direct proof of a causal relationship is lacking. This report attempts to support the contention that emboli can cause lacunar syndromes and lacunar infarction.

We report two cases of pure motor hemiplegia, each of which developed while the patient was undergoing cardiac or aortic arch angiography. Neither patient had a history of previous transient ischemic attack or stroke. Initial computed tomography of the brain was normal in each. Repeat computed tomography in one confirmed a small, low-density lesion in the posterior limb of the internal capsule on the side appropriate to the patient's symptoms and remained normal in the second patient.

These two cases offer evidence that the classic lacunar stroke syndrome of pure motor hemiplegia can occur on an embolic basis.
Effects of dextromethorphan on rat brain during ischemia and reperfusion assessed by magnetic resonance spectroscopy.
Authors: van Rijen P C , Verheul H B , van Echteld C J , Balázs R , Lewis P , Nasim M M , Tulleken C A
Published: June 2011

Using proton and phosphorus magnetic resonance spectroscopy, we evaluated the metabolic effects of preischemic administration of the N-methyl-D-aspartate antagonist dextromethorphan (50 mg/kg i.p.) during global forebrain ischemia and subsequent reperfusion in rats. Dextromethorphan-treated animals (n = 10) showed less lactate formation during ischemia than untreated animals (n = 11, p less than 0.001). During reperfusion, the lactate level in the treated group was reduced (p less than 0.05). Tissue pH declined less in the treated group during ischemia (p less than 0.01). There was no difference in the phosphocreatine/inorganic phosphate peak height ratio between groups. During ischemia, the N-acetylaspartate resonance peaks decreased in both groups. Histologic damage assessed in the hippocampal CA1 region 7 days after the ischemic insult was more severe in the untreated group (p less than 0.05). There was a significant correlation between end-ischemic tissue pH and hippocampal damage (r = -0.73, p less than 0.05). In the dextromethorphan-treated animals, 90% of the rats survived compared with 47% of the untreated animals (p less than 0.05). These results support findings in previous studies that dextromethorphan attenuates ischemic damage.
Postischemic (S)-emopamil therapy ameliorates focal ischemic brain injury in rats.
Authors: Morikawa E , Ginsberg M D , Dietrich W D , Duncan R C , Busto R
Published: June 2011

(S)-Emopamil is a calcium channel blocker of the phenylalkylamine class, having potent serotonin S2 antagonistic properties and high blood-brain barrier penetrability. Previous studies have documented cerebroprotective effect in animal models of both focal and global ischemia. The present study was undertaken to define the postischemic "window" of therapeutic efficacy for this agent. Sprague-Dawley rats were subjected to permanent proximal middle cerebral artery occlusion, combined with an initial 30-minute period of halothane-induced hypotension (50 mm Hg). (S)-Emopamil (20 mg/kg) was administered intraperitoneally either 20-30 minutes prior to middle cerebral artery occlusion or 1 hour, 2 hours, or 3 hours following occlusion. Treated groups received a second similar dose 2.5 hours later and twice daily for 2 days thereafter. Brains were perfusion-fixed on the third day. Planimetric analysis of hemotoxylin and eosin-stained coronal brain sections documented a cortical infarct averaging 72.9 +/- 33.3 mm3 (mean +/- SD) in untreated rats. Cortical infarct volume was reduced by 48% (to 37.6 +/- 27.6 mm3) when therapy was initiated 1 hour postischemia (p less than 0.05). When treatment was deferred to 2 hours postichemia, mean cortical infarct volume was reduced by 34%, but this difference did not attain statistical significance. Infarct volume in rats with treatment initiated at 3 hours postischemia was indistinguishable from that in controls. Striatal infarct volume was similar in all groups. These results document a postischemic therapeutic window of cerebroprotection for (S)-emopamil lying between 1 and 2 hours after middle cerebral artery occlusion.