[A case of brain stem infarction complicated with Castleman's disease].
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Adult↗
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Protective effect of vitamin E in a rat model of focal cerebral ischemia.
Under certain pathological conditions such as cerebral ischemia and reperfusion the occurrence of free radicals is remarkably increased. However, only very little information is available on their quantitative relevance for the pathophysiology and final outcome of diseases. The aim of the present study was to evaluate the contribution of oxygen radicals in the pathogenesis of a stroke. For this purpose a rat model for stroke was used. Two of three vitamin E deficient groups were repleted with different dosages of DL-alpha-tocopherylacetate. No signs of vitamin E deficiency could be observed. However, the weight gain during repletion was increased in the vitamin E repleted groups. Brain infarction was created by occlusion of the right middle cerebral artery (MCAO) for two hours. After 24 hours the measurements of infarct volumes were taken. The infarct volume of the group with the highest repletion dosage was significantly reduced by 81%. This was also expressed in a higher rate of gait disturbances after MCAO of the deficient animals. The control of vitamin E status exhibited a similar repletion-dependent level in plasma and brain. These results strongly support the hypothesis that the generation of oxygen radicals occurring during reperfusion is an important aspect of the pathophysiological mechanism in brain infarction.
Animals↗
Neuroprotective effects of tanshinones in transient focal cerebral ischemia in mice.
Tanshinones are the major lipid soluble pharmacological constituents of Danshen, the dried roots of Salvia miltiorrhiza Bunge (Labiatae), a well known traditional Chinese medicine used for the treatment of cerebrovascular diseases including stroke. Potential neuroprotective effects of tanshinones IIA (TsIIA) and IIB (TsIIB) were examined in adult mice subjected to transient focal cerebral ischemia caused by middle cerebral artery occlusion (MCAo). Our results revealed that TsIIA (16 mg/kg) readily penetrated the blood brain barrier reaching a peak concentration of 0.41 nmol/g brain wet weight 60 minutes after intraperitoneal injection and decreased slowly over several hours. Twenty-four hours after middle cerebral artery occlusion, brain infarct volume was reduced by 30% and 37% following treatment with TsIIA and TsIIB, respectively. The reduction in brain infarct volume was accompanied by a significant decrease in the observed neurological deficit. Tanshinones or other structurally related compounds may have potential for further development as neuroprotective drugs.
Abietanes↗
[Eales' disease with bilateral brain strokes and jaw-closing dystonia].
Eales' disease is an idiopathic occlusive vasculopathy of the retina, which is characterized by extensive peripheral non-perfusion, perivascular sheathing, and neovascularization. It is associated with recurrent vitreous hemorrhages. Both eyes are affected consecutively in 80% to 90% of the patients. In spite of the multiple theories that have been proposed, it continues to have unknown origin and its diagnosis relies on exclusion of other causes of retinal vasculopathy. In some occasions, these patients develop complications of the central nervous system, above all brain infarcts. We present the case of a 38 year old woman with Eales' disease who developed bilateral brain infarcts associated with occlusion or stenosis of the middle cerebral arteries. The cerebral angiography showed beading of the Silvian arteries, suggestive of an underlying inflammatory disorder. Early corticosteroid therapy could avoid contralateral retinal involvement and neurological complications. The patient also presented delayed jaw closing dystonia secondary to basal ganglia infarct which followed a benign course with spontaneous resolution in a few days.
Adult↗
Alpha-adducin polymorphism, atherosclerosis, and cardiovascular and cerebrovascular risk.
BACKGROUND AND PURPOSE: Carriers of the 460Trp allele of the alpha-adducin gene (ADD1) show higher rates of sodium reabsorption compared with homozygous carriers of the Gly460 allele and were found to have an increased risk of hypertension and cardiovascular disease. We studied the association between the Gly460Trp polymorphism and atherosclerosis, cardiovascular disease, and cerebrovascular disease. METHODS: Intima-media thickness of the common carotid artery, as well as incident stroke and myocardial infarction, were studied within 6471 subjects of the Rotterdam Study. Within 1018 subjects of the Rotterdam Scan Study, prevalent silent brain infarcts and cerebral white matter lesions were studied. Subjects were grouped into 460Trp carriers (variant carriers) and homozygous carriers of the Gly460 allele (reference). RESULTS: Intima-media thickness of the common carotid artery was 0.80 mm in variant carriers compared with 0.79 mm in the reference group (P=0.04). Variant carriers had an increased risk of any stroke (hazard ratio [HR], 1.22; 95% CI, 1.02 to 1.45), ischemic stroke (HR, 1.29; 95% CI, 1.02 to 1.63), hemorrhagic stroke (HR, 1.07; 95% CI, 0.59 to 1.92), and of myocardial infarction (HR, 1.33; 95% CI, 1.05 to 1.69). For any ischemic stroke, there was a significant interaction between the Gly460Trp polymorphism and hypertension. Variant carriers more often had a silent brain infarct (odds ratio, 1.36; 95% CI, 0.98 to 1.88) and had more subcortical white matter lesions than the reference group (1.45 vs1.24 mL; P=0.22). CONCLUSIONS: The Gly460Trp polymorphism is associated with atherosclerosis, cardiovascular disease, and cerebrovascular disease, especially in hypertensive subjects.
Aged↗
Oxyresveratrol (trans-2,3',4,5'-tetrahydroxystilbene) is neuroprotective and inhibits the apoptotic cell death in transient cerebral ischemia.
Oxidative stress is one of the major pathological factors in the cascade that leads to cell death in cerebral ischemia. Here, we investigated the neuroprotective effect of a naturally occurring antioxidant, oxyresveratrol, to reduce brain injury after cerebral stroke. We used the transient rat middle cerebral artery occlusion (MCAO) model of brain ischemia to induce a defined brain infarction. Oxyresveratrol was given twice intraperitoneally: immediately after occlusion and at the time of reperfusion. Oxyresveratrol (10 or 20 mg/kg) significantly reduced the brain infarct volume by approximately 54% and 63%, respectively, when compared to vehicle-treated MCAO rats. Also, the neurological deficits as assessed by different scoring methods improved in oxyresveratrol-treated MCAO rats. Histological analysis of apoptotic markers in the ischemic brain area revealed that oxyresveratrol treatment diminished cytochrome c release and decreased caspase-3 activation in MCAO rats. Also, staining for apoptotic DNA showed that the number of apoptotic nuclei in ischemic brain was reduced after oxyresveratrol treatment as compared to the vehicle-treated MCAO rats. This dose-dependent neuroprotective effect of oxyresveratrol in an in vivo stroke model demonstrates that this drug may prove to be beneficial for a therapeutic strategy to limit brain injury in acute brain ischemia.
Analysis of Variance↗
Proton MR spectroscopy in acute middle cerebral artery stroke.
PURPOSE: To investigate the feasibility of performing multisection proton MR spectroscopy in patients with acute stroke, and to determine whether this imaging technique can depict ischemic or infarcted brain regions. METHODS: Multisection proton MR spectroscopy, MR imaging, and MR angiography were performed within 24 hours of stroke onset (mean, 12 hours) in 12 patients who had had a stroke of the middle cerebral artery. Spectra were analyzed from brain regions containing T2 hyperintensity abnormalities on MR images, from regions immediately adjacent to these abnormalities, and from anatomically similar contralateral regions. Areas of brain containing lactate were compared with areas of T2 hyperintensities on MR images. RESULTS: One data set was discarded because of excessive artifacts from patient motion. Regions of T2 hyperintensities on MR images were found to contain elevated lactate (all 11 cases) and reduced N-acetyl-aspartate (10 of 11 cases) relative to contralateral measurements. Lactate levels in regions adjacent to T2 hyperintensities were not significantly different from those of infarcted brain. On the other hand, N-acetyl-aspartate was significantly lower in regions of infarction compared with periinfarct tissue. Areas of brain containing elevated lactate significantly exceeded those of T2 abnormality. CONCLUSIONS: Proton MR spectroscopy is feasible for imaging patients with acute stroke. In the early stages of stroke, tissue containing elevated lactate but no other spectroscopic or MR imaging abnormality can be identified. Such regions may represent an ischemic zone at risk of infarction.
Acute Disease↗
Isolated inferior oblique paresis from brain-stem infarction. Perspective on oculomotor fascicular organization in the ventral midbrain tegmentum.
We present the case of an isolated inferior oblique muscle paresis from ventral midbrain infarction involving the oculomotor fascicular fibers. Based on this case and a review of the literature, the anatomic organization of the oculomotor nerve fascicles and of the pupillary fibers in the ventral midbrain tegmentum is proposed.
Aged↗
Hyperthermia in ischemic stroke.
Hyperthermia following ischemic stroke is a common but undesirable event whose pathophysiology and clinical importance are not fully recognized. Hyperthermia in ischemic stroke may result from the brain infarct itself; however, the progress of biochemical and inflammatory mechanisms associated with cerebral ischemia is also relevant. Consequently, the presence of hyperthermia accentuates ischemic mechanisms within the penumbra, an area of reversibly impaired neuronal function surrounding the infarct, contributing to conversion of the penumbra into an irreversible lesion. Therefore, hyperthermia following ischemic stroke seems to be an event both induced by and inducing brain infarct progression. Both clinical and experimental studies show hyperthermia-dependent exacerbation of ischemic brain damage and stroke outcome. The detrimental effects of hyperthermia in human stroke are associated in particular with increased body temperature within the first 24 hours of the disease. The common occurrence of superimposed infections in stroke patients may be an important peripheral cause of poststroke hyperthermia. Pharmacological antipyretic medication is recommended in every case of hyperthermia following ischaemic stroke, regardless of its cause, as any hyperthermia may worsen stroke outcome. There is currently no evidence from randomized trials to support the routine use of chemical or physical cooling therapy in acute stroke Further understanding of the mechanisms inducing hyperthermia and its contribution to an increase in the degree of injury during stroke may lead to new and important therapeutic approaches.
Animals↗
[Posttraumatic ischemic stroke in childhood].
Children with brain infarction due to traumatic dissection of the carotid artery (14 cases) and vertebral artery (4 cases) were observed. In all the cases of brain infarction due to carotid dissection, history of trauma, immediate typical headache after the accident, development of infarction 24 hours after the accident and the presence of the Gorner's syndrome ipsilateral to infarction allowed definite clinical diagnosis. Clinical diagnosis of infarction due to vertebral artery dissection was more difficult and the diagnosis was established only after neuro visualization. In all the cases, outcomes were favorable. Posttraumatic sinovenous occlusion was observed in 17 children. Clinical features failed to meet a diagnosis of thrombosis, which was confirmed only after neurovisualization. Sinovenous thrombosis was often accompanied with cortical venous infarction and, in some cases, thrombosis spread to the deep cerebral veins. In acute period, fundus haemorrhagies and subdural haematomas developed frequently. There were poor outcomes in cases of venous infarctions, especially in deep cerebral ones.
Adolescent↗
Isoenzymes of creatine phosphokinase in some muscular diseases, myocardial infarction and brain neoplasms.
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Brain Neoplasms↗
Silent cerebral lesions on magnetic resonance imaging in subjects with coronary artery disease.
MRI of subjects with silent intracranial damages may provide more evidence than CT. Our objectives were to determine the prevalence of silent MRI lesions in patients with coronary artery disease. The study included 72 consecutive patients with angiographically proven coronary artery disease and 26 age and sex matched controls with normal coronary angiography. All subjects were evaluated for coronary atherosclerosis (Gensini and coronary angiography scores), the number of silent cerebral lesions detected by MRI, carotid stenosis and the risk factors for stroke. Thirty one of 72 (43.0%) patients had silent brain lesions on MRI while 8 of 26 (30.7%) control subjects showed silent brain infarction. The main finding on T2-weighted MRI was white matter hyperintensities (WMH) which were seen in all patients with silent brain lesions. The mean age of the patients with coronary artery disease and with silent cerebral lesions was significantly higher than that of patients without silent brain lesions. The Gensini score, coronary angiography score and prevalence of carotid stenosis are significantly higher in patients with silent cerebral lesions than that of patients without silent cerebral lesions. There was no significant difference between silent cerebral lesions and the other risk factors for stroke. Silent brain lesions are a common complication in patients with coronary artery disease. In patients with coronary artery disease, carotid artery stenosis and age were important risk factors for the development of silent brain infarction.
Adult↗
Significance of the perfusion-diffusion mismatch in chronic cerebral ischemia.
PURPOSE: To determine whether the perfusion deficit could predict brain infarction in patients with chronic cerebral ischemia who experienced recurring episodes of neurological symptoms and showed a perfusion-diffusion mismatch on magnetic resonance (MR) images. MATERIALS AND METHODS: In 53 consecutive patients (38 males and 15 females, 62+/-13 years old) with ischemia in the middle cerebral artery (MCA) territory, lesion volumetry was performed on parametric maps of the time-to-peak, the cerebral blood volume, and diffusion-weighted (DW) images. The infarct lesions were assessed on follow-up T2-weighted (T2W) MR images after eight days. Cerebrovascular changes were determined by time-of-flight (TOF) MR angiography (MRA). Inferential and correlation statistics were used. RESULTS: Patients with chronic ischemic brain disease (N=39) who presented with a severe perfusion-diffusion mismatch in the presence of a normal cerebral blood volume had no or small brain infarctions as found on follow-up T2W images. MRA revealed widespread abnormalities of the basal cerebral arteries compatible with brain perfusion abnormalities. In contrast, in acute stroke patients (N=14) the deficit of cerebral perfusion predicted the infarct lesion in the T2W images. CONCLUSION: Our results suggest that in chronic cerebral ischemia the normal blood volume was maintained despite the depression of cerebral perfusion and recurring minor insults.
Adult↗
Neuroprotective effects of a dihydropyridine derivative, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarbox ylic acid methyl 6-(5-phenyl-3-pyrazolyloxy)hexyl ester (CV-159), on rat ischemic brain injury.
CV-159, 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridinedicarboxylic++ + acid methyl 6-(5-phenyl-3-pyrazolyloxy)hexyl ester, is a dihydropyridine derivative that blocks the L-type Ca2+ channel and inhibits the calmodulin (CaM)-dependent pathway. In this study, we examined the effects of CV-159 on rat ischemic brain injury. CV-159 (5 and 10 mg/kg, p.o.) gave significant protection against delayed neuronal death in the hippocampal CA1 region after 15-min transient forebrain ischemia. In contrast, the Ca2+ antagonists nicardipine (1 and 10 mg/kg, p.o.) and nifedipine (1 mg/kg, i.p.) and the CaM antagonist N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7, 500 ng, i.c.v.) had no effect on this hippocampal neuronal death. CV-159 also diminished the size of the brain infarct after permanent middle cerebral artery (MCA) occlusion, although physiological variables, including regional cerebral blood flow, were not affected. The increase in the water content of the infarcted cortex induced by MCA occlusion was significantly reduced by CV-159. On the other hand, neither nicardipine nor nifedipine affected the brain infarct size, volume or increased water content induced by MCA occlusion, as previously reported (A. Sauter and M. Rudin, Am. J. Hypertens. 4 121S-127S, 1991). These findings indicate that Ca2+ antagonists, such as nicardipine and nifedipine, and W-7 have no effect on rat ischemic brain injury. The results suggest that CV-159 protects against ischemic brain injury. This might be mediated by both blocking the L-type Ca2+ channel and inhibiting CaM-dependent function via Ca2+/CaM binding at a different binding site from that of W-7 to CaM (H. Umekawa, K. Yamakawa, K. Nunoki, N. Taira, T. Tanaka, and H. Hidaka, Biochem. Pharmacol. 37 3377-3381, 1988).
Animals↗
Universal dissociated anesthesia due to bilateral brain-stem infarcts.
A 59-year-old man had loss of pin-prick and temperature sensation over his head, face, neck, trunk, and all extremities while light touch, vibration, joint position sense, and deep pain were preserved. This was the cumulative result of infarctions in the territories of the right superior cerebellar and left posterior inferior cerebellar arteries that occurred three years apart. To our knowledge, a syndrome of bilateral discrete interruption of spinothalamic tracts and of the spinal tracts of the trigeminal system in the brain stem has not been reported. Dissociated sensory loss enveloping the entire body accompanied by truncal and limb ataxia without weakness demonstrated a striking clinical picture. The preservation of deep somatic and visceral pain when cutaneous pain sensation was lost was another notable feature. We review the causes of widespread dissociated sensory loss and discuss the implications of the dissociation of deep from superficial pain.
Brain Stem↗
Subclinical brain magnetic resonance imaging abnormalities predict physical functional decline in high-functioning older adults.
OBJECTIVES: To determine whether severity of subclinical brain magnetic resonance imaging (MRI) abnormalities predicts incident self-reported physical impairment or rate of decline in motor performance. DESIGN: Longitudinal analysis, average follow-up time: 4.0 years. SETTING: Cardiovascular Health Study (CHS). PARTICIPANTS: CHS participants with modified Mini-Mental State Examination (3MS) score of 80 or greater, no self-reported disability, no history of stroke, and at least one assessment of mobility (n=2,450, mean age=74.4). MEASUREMENTS: Brain MRI abnormalities (ventricular enlargement, white matter hyperintensities, subcortical and basal ganglia small brain infarcts), self-reported physical impairment (difficulty walking half a mile or with one or more activities of daily living), and motor performance (gait speed, timed chair stand). RESULTS: After adjusting for demographics, cardiovascular risk factors, and diseases, risk of incident self-reported physical impairment was 35% greater for those with severe ventricular enlargement than for those with minimal ventricular enlargement, 22% greater for those with moderate white matter hyperintensities than for those with minimal white matter hyperintensities, and 26% greater for participants with at least one brain infarct than for those with no infarcts. Those with moderate to severe brain abnormalities experienced faster gait speed decline (0.02 m/s per year) than those with no MRI abnormalities (0.01 m/s per year). Further adjustment for incident stroke, incident dementia, and 3MS score did not substantially attenuate hazard ratios for incident self-reported physical impairment or coefficients for decline in gait speed. CONCLUSION: Subclinical structural brain abnormalities in high-functioning older adults can increase the risk of developing physical disabilities and declining in motor performance.
Activities of Daily Living↗
Basilar artery diameter and 5-year mortality in patients with stroke.
BACKGROUND AND PURPOSE: Few and conflicting data exist on the case fatality rate in stroke patients with basilar artery dolichoectasia. We analyzed basilar artery characteristics (diameter, height of bifurcation, transverse position) and 5-year mortality (all-cause, nonstroke vascular, and stroke) in patients with brain infarction. METHODS: The basilar artery diameter was measured with a 16-diopter lens in 466 consecutively recruited patients with brain infarction confirmed by magnetic resonance imaging. The height of the bifurcation and the transverse position of the basilar artery were assessed on semiquantitative scales. Patients were followed up for a median of 5.3 years (range, 1.5 to 6.6) and were classified as having had stroke, nonstroke vascular, and nonvascular death according to the French national registry of death certificates. RESULTS: Of the 157 deaths, 88 were vascular (including 54 stroke deaths). Basilar artery diameter was associated with an increased 5-year stroke mortality rate but not with all-cause or nonstroke vascular mortality. The adjusted hazard ratio (HR) of stroke mortality per 1-mm increase in basilar artery diameter was 1.23 (95% confidence interval [CI], 1.07 to 1.41). A higher risk of stroke death was associated with basilar artery diameter at the 95th percentile (diameter >4.3 mm; adjusted HR 3.69; 95% CI, 1.63 to 8.38) and the height of bifurcation (adjusted HR for score >1, 2.08; 95% CI, 0.93 to 4.68) but not with transverse position. CONCLUSIONS: Basilar artery diameter was independently associated with cerebrovascular mortality. A diameter >4.3 mm may be a marker for a high risk of fatal stroke.
Aged↗
Regional metabolic disturbances and cerebrovascular anatomy after permanent middle cerebral artery occlusion in C57black/6 and SV129 mice.
C57Black/6 and SV129 mice are widely used for the production of transgenic mutants in molecular stroke research but the ischemic susceptibility of these strains is influenced by differences in vascular anatomy and the responsiveness to excitotoxins and vasodilatory stimuli. To differentiate between these opposing effects on infarct size, the vascular territory of the two strains was correlated with the hemodynamic, metabolic, and morphological consequences of permanent middle cerebral artery (MCA) occlusion. The vascular anatomy was studied by latex infusion, brain infarction by vital staining, the size of the ischemic penumbra by imaging of ATP and protein synthesis, and blood flow by laser-Doppler flowmetry. In C57Black/6 mice the MCA-supplied vascular territory and the size of brain infarcts were significantly larger than in SV129 mice but the size of the penumbra and the residual blood flow in the center of the MCA-supplying territory were similar in both strains. These findings suggest that differences in infarct size in C57Black/6 and SV129 mice are determined mainly by the vascular anatomy and not by differences in collateral vascular responsiveness or excitotoxicity.
Adenosine Triphosphate↗