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[Sleep apnea syndrome and cerebral infarction].

OBJECTIVES: To analyze the relationship between snoring and sleep apnea with brain infarction. METHODS: We studied 79 consecutive patients of both sexes with cerebral infarction and 248 age and sex matched controls. We obtained data reflecting arterial hypertension, diabetes mellitus, hypercholesterolemia, smoking and drinking habits, coronary heart disease, cardiopathy, snoring, respiratory pauses during sleep and daytime sleepiness, by using a standard questionnaire to interview every subject and his/her spouse. RESULTS: 53% of patients and 46% of controls snored often or always (p = 0.27). Snoring was significantly more frequent in men. Thirty four percent of patients and 27% of controls were snorers and suffered apnea during sleep (p = 0.19). Nineteen per cent of patients and 11% of controls presented snoring, respiratory pauses during sleep and daytime sleepiness simultaneously, suggesting obstructive sleep apnea syndrome (OSAS) (p = 0.06). However, by separately analyzing people younger than 65 years, the frequency of OSAS was significantly higher in patients (29%) than in controls (7%) (p = 0.006). Finally, 10% of patients and 3% of controls presented snoring, respiratory pauses during sleep and moderate or severe daytime sleepiness simultaneously, suggesting moderate-severe OSAS (p = 0.01). A multiple logistic regression analysis confirmed the independent contribution of moderate-severe OSAS as a risk factor for ischemic stroke, with an adjusted odds ratio of 4.54. In people younger than 65 years, OSAS, regardless of its severity, was also an independent risk factor for ischemic stroke, with an adjusted odds ratio of 5.78. CONCLUSIONS: Clinically diagnosed obstructive sleep apnea syndrome is an independent risk factor for ischemic stroke, especially in people younger than 65 years.

Adult↗

[Therapeutic effectiveness of anticoagulants in the acute phase of cerebral infarction].

500 patients who were admitted to hospitals in acute phases of brain infarctions were treated by intravenous administrations of spasmolytical drugs. 518 patients with similar conditions, besides spasmolytical drugs received anticoagulants (heparin and phenilin). In patients with expressed neurological disorders treated by anticoagulants there was a highly significant improvement, including an increase of the percent of moderate improvement and a drop in the lethality, In those patients with mildly expressed neurological disorders who received anticoagulants an improvement was also marked, but not so distinctly. In cases with slight neurological disorders the different outcomes were not significant. The highest effectivesness of anticoagulants was marked in infarctions, due to thrombosis. The effectiveness indices in patients due to stenosis with angiospasms were not significant.

Acute Disease↗

[Cerebral infarcts as a complication of migraine].

Among 33 young patients suffering from brain infarction we found five with the preceding history of migraine. In four cases the insult coincided with an attack of migraine. The lesions were related to an area supplied by the posterior cerebral artery. The clinical and radiological findings are discussed.

Adult↗

[Antihypertensive drugs in acute stage of atherothrombotic infarction deteriorate the outcome].

To elucidate whether high blood pressure in acute brain infarction should be treated or not, we retrospectively investigated relationship of the use of antihypertensive agents in the acute stage with the area of hypodensity on CT examined one month after onset and functional outcome at discharge. Actual blood pressure value and diurnal fluctuation in the acute stage were also related to the infarct size and outcome. Subjects were compared of 32 atherothrombotic stroke patients with unilateral severe stenotic lesion (> or = 75% stenosis or occlusion) at the extracranial carotid artery or the horizontal portion of the middle cerebral artery confirmed by cerebral angiography. Seven patients (treated group) received antihypertensive drugs within 14 days of onset and the remaining 25 patients (non-treated group) did not. The data of frequent blood pressure measurements were available in five of the treated group and 24 of the non-treated group. There were no significant differences in the daily highest and lowest mean arterial blood pressure (MABP) between the two groups (124.8 +/- 11.8 mmHg vs. 118.5 +/- 13.5 mmHg and 101.9 +/- 10.4 mmHg vs. 104.4 +/- 12.6 mmHg, respectively). However, apparent circadian fluctuation of the MABP (the highest MABP--the lowest MABP > 25 mmHg) was more frequently seen in the treated group (3/5, 60%) than in the non-treated group (0/24, 0%) (chi 2 test, p < 0.01). Large infarcts (> or = 10 cm2) were more commonly found in the treated group (4/7, 57%) than in the non-treated group (1/25, 4%) (chi 2 test, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

[Relation between biochemical indicators of the cerebrospinal fluid and the extent of cerebral infarction].

The authors assessed liquor biochemical indices, mainly enzymes, on day 1-3 of hemispheric ischemic stroke in correlation with brain infarction size in 90 relevant male patients (mean age 70 +/- 6 years). The brain damage was verified by computed tomography with measuring the infarction lesion. The latter in view, the patients were assigned in three groups: with ischemic lesion less than 5.0 cm3, less than 30 cm3 and greater than 30.0 cm3 or/and multiple lesions. The results were compared with those in patients who had suffered hemispheric ischemic stroke followed by discirculatory encephalopathy.

Aged↗

Evaluation of the roles of the Leiden V mutation and ACE I/D polymorphism in subtypes of ischaemic stroke.

OBJECTIVE: The Leiden V mutation, which causes activated protein C resistance and thrombophilia, has been found to be a risk factor for venous thrombosis. The angiotensin converting enzyme (ACE) D allele indirectly exerts an unfavourable effect on the vasoregulatory system. In this study, the frequency of these mutations was analysed in different subtypes of ischaemic stroke. METHOD AND MATERIAL: According to the clinical and radiological features 664 Hungarian patients who had suffered acute ischaemic stroke were divided into 3 subtypes: small and large vessel infarcts and a mixed type. In all 664 patients, the Leiden V mutation and ACE I/D polymorphism were examined by means of the PCR technique. The frequencies of the different genotypes for the Leiden V mutation and ACE I/D polymorphism in the 3 subgroups of stroke were compared with 199 stroke-free control subjects whose MRI findings were normal. RESULTS: No significant associations were found between the overall group of cerebral infarctions and the Leiden V, ACE I/D and ACE D/D genotypes. The ACE D/D genotype was significantly more common in the patients with small deep infarcts (40.3%; p < 0.0005; OR 2.31, 95% CI 1.49-3.57) than in the control group (22.6%). The Leiden V mutation was significantly more common in patients with large infarcts (13.6%; p < 0.025; OR 2.25, CI 1.16-4.34) than in the stroke-free control subjects (6.5%). CONCLUSIONS: The ACE D/D genotype possibly contributes to the occurrence of small-vessel infarcts rather than large vessel infarcts. The Leiden V mutation might predispose to large brain infarcts. Neither the Leiden V factor nor the ACE D/D genotype has been proved to be a risk factor for ischaemic stroke as a whole.

Adult↗

Acidic fibroblast growth factor-like immunoreactivity in rat brain following cerebral infarction.

Expression of acidic fibroblast growth factor (aFGF) was studied by immunocytochemistry in the rat brain with or without cerebral infarction. In a model of infarction produced by occlusion of the middle cerebral artery, aFGF-positive staining that was not seen in controls appeared in both neurons and macrophages. Positive neurons were distributed mainly in the periventricular region of the hypothalamus. The neuronal aFGF began to be detectable about 24 h after the occlusion. The staining intensity for such neuronal aFGF increased until about 14 days after the surgery, but decreased gradually and was undetectable after more than 30 days. Positive macrophages first appeared on the 3rd day after the occlusion and were persistently seen up to the 7th day, but were no longer visible after 14 days. The present results suggest that aFGF may be involved in the repair processes following brain infarction.

Animals↗

Lactate quantitation in a gerbil brain stroke model by GSLIM of multiple-quantum-filtered signals. Generalized spectral localization by imaging.

Quantitative magnetic resonance imaging of lactate using a zero-quantum/double-quantum filter and generalized spectral localization by imaging (GSLIM) was applied to a model of unilateral stroke in gerbil brain. GSLIM lactate images at 4T clearly reveal elevated concentrations of lactate in the ischemic compared with the normal hemisphere 100-175 minutes after unilateral carotid ligation. These results indicate that the technique is capable of studies of brain infarcts, and that application to human ischemic pathology in brain and other tissues may be possible.

Animals↗

Prevention of stroke and dementia with statins: Effects beyond lipid lowering.

Stroke is a major cause of mortality and morbidity. The epidemiologic association between elevated serum cholesterol and stroke risk is controversial. However, recent secondary prevention studies with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have demonstrated a significant reduction in ischemic stroke without an increase in hemorrhagic stroke. Statins probably reduce stroke by a variety of mechanisms, including modulation of precerebral atherothrombosis in the aorta and the carotid artery, thus preventing plaque disruption and artery-to-artery thromboembolism. Statins also improve endothelial homeostasis by increasing the bioavailability of nitric oxide, which orchestrates the paracrine antiatherosclerotic functions of the endothelium. Studies in experimental models of ischemic stroke show that statin therapy reduces brain infarct size and improves neurologic outcome by directly upregulating brain endothelial nitric oxide synthase. Putative anti-inflammatory actions of statins may also contribute to neuroprotection and stroke prevention. Although the clinical benefit of statins largely depends on lowering low-density lipoprotein cholesterol, accumulating data indicate that many of the pleiotropic effects of statins are attributable to the cellular consequences of depletion of intermediates in the cholesterol biosynthetic pathway (isoprenoids). These molecules play fundamental roles in cell growth, signal transduction, and mitogenesis. In addition to reducing stroke risk, emerging data suggest that statins may reduce dementia. Further studies are needed to fully address the role of statins in the prevention of stroke in patients without established vascular disease and the role of cholesterol modulation in the treatment of dementia.

Anticholesteremic Agents↗

Timing of autopsy-confirmed hemorrhagic infarction with reference to cardioembolic stroke.

We studied the temporal profile of hemorrhagic transformation in 34 cases with autopsy-confirmed hemorrhagic infarction who died within 15 days following a supratentorial brain infarct, provided they had undergone computed tomography. It appeared that within 4 days, at least 76% (95% confidence interval 39-100%) of 21 cardioembolic strokes had become hemorrhagic. We conclude that if anticoagulation is considered in cardioembolic stroke, such treatment should not be started sooner than at least 4 days after the onset of stroke, provided that computed tomography at that time shows no hemorrhagic infarction.

Aged↗

Cerebellar infarction. Clinical and neuroimaging analysis in 293 patients. The Tohoku Cerebellar Infarction Study Group.

BACKGROUND AND PURPOSE: We performed this multicenter study to explore the full spectrum of the clinical characteristics and neuroimaging findings of cerebellar infarction, including patients with mild to severe illnesses. METHODS: We studied 293 consecutive patients with cerebellar infarction diagnosed by computed tomography and/or magnetic resonance imaging who were admitted to 36 hospitals during 5 years. RESULTS: Cerebellar infarcts constituted 2.3% of the total patients with acute brain infarction. The backgrounds and risk factors were similar to those in patients with infarctions of the cerebral hemispheres. At least 24% were embolic, and the diagnosis of embolism could not be ruled out in 27%. Infarcts involving the superior cerebellar artery (SCA) region (52%) and the posterior inferior cerebellar artery (PICA) region (49%) were far more frequent than those involving the anterior inferior cerebellar artery (AICA) region (20%). Patients with SCA infarcts exhibited obtunded consciousness and ataxia more frequently than those with PICA infarcts (P < .05). Infarcts in the PICA regions were associated with abnormalities of the PICA (64%) or the vertebral arteries (57%), whereas infarcts in the SCA and AICA regions were associated with abnormalities in the SCA or AICA, respectively, in approximately 30% of patients, in the basilar artery in approximately 16%, and in the vertebral artery in more than 60% of patients. Outcomes were poorer with SCA infarcts than with AICA and PICA infarcts. CONCLUSIONS: These data indicate similar frequencies of SCA and PICA infarcts and illustrate the difference in clinical presentation and outcomes between SCA and PICA infarcts. They also indicate that not only in situ thrombosis but also cardiogenic or artery-to-artery embolism and the insufficiency of collateral circulation play important roles in the pathogenesis of cerebellar infarction.

Aged↗

Inhibition of NF-kappaB activation by 5-lipoxygenase inhibitors protects brain against injury in a rat model of focal cerebral ischemia.

BACKGROUND: Stroke is one of the leading causes of death worldwide and a major cause of morbidity and mortality in the United States of America. Brain ischemia-reperfusion (IR) triggers a complex series of biochemical events including inflammation. Leukotrienes derived from 5-lipoxygenase (5-LOX) cause inflammation and are thus involved in the pathobiology of stroke injury. METHODS: To test the neuroprotective efficacy of 5-LOX inhibition in a rat model of focal cerebral IR, ischemic animals were either pre- or post-treated with a potent selective 5-LOX inhibitor, (N- [3-[3-(-fluorophenoxy) phenyl]-1-methyl-2-propenyl]-N-hydroxyurea (BW-B 70C). They were evaluated at 24 h after reperfusion for brain infarction, neurological deficit score, and the expression of 5-LOX. Furthermore, the mechanism and the anti-inflammatory potential of BW-B 70C in the regulation of nuclear factor kappa B (NF-kappaB) and inflammatory inducible nitric oxide synthase (iNOS) were investigated both in vivo and in vitro. RESULTS AND DISCUSSION: Both pre- and post-treatment with BW-B 70C reduced infarctions and improved neurological deficit scores. Immunohistochemical study of brain sections showed IR-mediated increased expression of 5-LOX in the neurons and microglia. BW-B 70C down-regulated 5-LOX and inhibited iNOS expression by preventing NF-kappaB activation. Two other structurally different 5-LOX inhibitors were also administered post IR: caffeic acid and 2,3,5-trimethyl-6-[12-hydroxy-5,10-dodecadiynyl]-1,4-benzoquinone (AA-861). As with BW-B 70C, they provided remarkable neuroprotection. Furthermore, in vitro, BW-B 70C inhibited lipopolysaccharide (LPS) mediated nitric oxide production, iNOS induction and NF-kappaB activation in the BV2 microglial cell line. Treating rat primary microglia with BW-B70C confirmed blockage of LPS-mediated translocation of the p65 subunit of NF-kappaB from cytosol to nucleus. CONCLUSION: The study demonstrates the neuroprotective potential of 5-LOX inhibition through down-regulation of NF-kappaB in a rat model of experimental stroke.

Journal Article↗

Persistent neurologic sequelae of migraine: a case report.

Multiple cerebral infarctions occurred in a 32-year-old man with both basilar artery and hemiplegic migraine. One event was associated with decrement of propranolol dosage. Platelet aggregation, coagulation studies, and other laboratory studies were normal. Computerized tomography revealed several areas of both old and new infarction. The relationship of the migraine attacks to the brain infarcts remains circumstantial, but migraine was the only identifiable cause of the infarcts in this patient.

Adult↗

[Multivisceral infarcts are complication of invasive aspergillosis].

Aspergillus fumigatus is one of the species of Aspergillus that causes aspergillosis. The clinical picture of invasive-disseminated aspergillosis is generally characterized by fever and respiratory distress that usually follows a fatal course. This form of intensive aspergillosis is suffered by severely immunossuppressed patients. There is another clinical form of severe aspergillosis, aortic aspergillosis, that appears after cardiac surgery. We present two cases of invasive aspergillosis complicated by multiple visceral infarcts involving the liver, spleen, kidneys, pancreas, thiroid and brain. Infarcts were confirmed in necropsy and appeared to be caused by an overwhelming amount of intravascular hiphae, which were observed in the infarcted areas acting forming septic embolus. We believe that multi-visceral infarcts are an underestimated complication of invasive aspergillosis. Given the progressive increase in the population of immunossuppressed patients, clinicians have to aware of all the possible presentations of invasive aspergillosis.

Aged↗

[Evaluation of pontine visualization with single photon emission computed tomography using N-isopropyl-p-(I-123)iodoamphetamine in normal and pathological cases].

Pontine visualization with single photon emission computed tomography (SPECT) using N-isopropyl-p-[I-123]iodoamphetamine (I-123 IMP) was evaluated in 99 cases including 46 cases of brain infarction, 25 of other cerebrovascular disorders and 28 of brain tumor and in 19 normal subjects. In each case, SPECT using a rotating gamma camera was started at 30 minutes after intravenous administration of 111 MBq of I-123 IMP. Transverse images were reconstructed parallel to the cantho-meatal line and displayed on films. Pontine visualization was visually classified into three grades: high radioactive accumulation confined to the pons with clear contour (Grade 3), faint accumulation with indistinct contour in the pontine region (Grade 1), the pontine accumulation was identified but its activity was less significant (Grade 2). The results showed that grade of the pontine accumulation was lower in pathological cases compared to normal subjects. Six cases with brain stem lesion demonstrated pontine accumulation of grade 1 in 4 case and of grade 2 in 2 cases. Lower grade was also revealed in 29 cases with crossed cerebellar diaschisis (CCD). No significant correlation was observed between classified grade of pontine accumulation and maximum counts of reconstructed images. We concluded that SPECT could detect brain stem lesions and that lower accumulation in pons with CCD positive cases was thought to partially reflect the reduced blood flow and metabolism in the pontine nuclei.

Adolescent↗

[Free serum amino acids in the acute period of cerebral stroke].

A comparative study of free aminoacid content in the blood of 27 patients will brain hemorrhages and 32 patients with brain infarctions was conducted during the first 12 hours of brain stroke. A comparison of the data obtained with the results of a study of 16 normals and 24 patients with atherosclerosis and hypertensive disease demonstrated changes in the aminoacids spectrum which is characteristic for a hemorrhagical and ischemic stroke. The differences in the content of 10 aminoacids are shown. The achieved results are discussed in the light of their differential diagnostic significance.

Acute Disease↗

[A case of bilateral necrosis of the basal ganglia after hypotensive shocks].

We reported a case with bilateral necrosis of the basal ganglia after hypotensive shocks. The patient was a 69-year-old woman, who fell into a hypotensive shock (B.P. below 40 mmHg) of unknown origin during examination of her bladder cancer and was admitted into CCU. After admission, hypotensive shocks were repeated four times (B.P. below 50 mmHg each time). Neurological examination revealed a left spastic hemiplegia. Brain CT on 10th day showed bilaterally low density areas around the basal ganglia and a diagnosis of brain infarction was made. She gradually presented quadriplegia and symptomatic changes from pyramidal to extrapyramidal signs. Brain CT on 24th day showed bilateral hemorrhagic infarction of the basal ganglia with enhanced effect. On 79th day, she again fell into shock and died. Neuropathological examination of the brain was as follows. 1) laminar necrosis of the deep layers of the cerebral cortex, 2) bilateral necrosis of the hippocampal Sommer sector, 3) bilateral necrosis of the caudate nucleus, putamen and pallidum with neuronal loss and infiltration of fat granule cells, 4) sparing of the internal capsules, 5) bilateral necrosis of the reticular zone of the substantia nigra, 6) foci of fresh necrosis and loss of Purkinje cells in the cerebellum. These lesions are consistent with those of selective vulnerability in hypoxia as described by Scholz et al. An extensive distribution of cerebral as well as basal ganglia necrosis in this case was caused by repeated shocks.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Vascular reactivity to carbon dioxide in the acute stage of cerebral infarction in rats].

The effect of CO2 on the cerebral circulation was assessed 24 hours after induction of unilateral brain infarction performed in the rat by injecting radioactive calibrated 50 microns microspheres into the internal carotid artery. The intracerebral distribution of microspheres and regional cerebral blood flow were measured bilaterally in 8 brain regions. In control rats, increase in arterial pCO2 to about 80 mm Hg resulted in 30 to 100% increase in flow according to the area. Cerebral blood flow was also enhanced in the embolized rats, the basal values being multiplied by a factor 1.7 in the embolized hemisphere and by a factor 1.8 in the contralateral hemisphere. These results do not provide evidence for the existence of a "steal" phenomenon between the non infarcted and infarcted hemispheres.

Animals↗