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PubMed2004

Animal protein, animal fat, and cholesterol intakes and risk of cerebral infarction mortality in the adult health study.

BACKGROUND AND PURPOSE: A traditional diet that is poor in animal products is thought to explain the high rate of stroke in Asian populations. The purpose of the present study was to examine the effect of a diet rich in animal protein, animal fat, and cholesterol on the risk of cerebral infarction mortality in a Japanese population. METHODS: A prospective study of 3731 Japanese men and women aged 35 to 89 years was conducted from 1984 to 2001. Nutrient intake was estimated at baseline from the responses to a 24-hour diary. During the follow-up period, cases of cerebral infarction deaths (as entered on death certificates) were monitored. RESULTS: During the follow-up period, 60 deaths were attributed to cerebral infarction. A high intake of animal fat and cholesterol was significantly associated with a reduced risk of cerebral infarction death. The risk was reduced by 62% (CI, 82% to 18%) for those in the third tertile of animal fat intake, compared with those in the first tertile, with a significant linear dose-response relationship (P=0.0073). The risk of death from infarction was reduced by 63% (CI, 82% to 22%) in the high cholesterol consumption group, compared with the low consumption group. A significant linear dose-response relationship was observed. Animal protein was not significantly associated with infarction mortality after adjustment for animal fat and cholesterol. CONCLUSIONS: This study suggests that in Japan, where animal product intake is lower than in Western countries, a high consumption of animal fat and cholesterol was associated with a reduced risk of cerebral infarction death.

Adult↗
PubMed1995

Cerebral infarction in sickle cell disease: transcranial Doppler US versus neurologic examination.

PURPOSE: To evaluate flow velocity measurements in the middle cerebral artery (MCA) and/or neurologic examination for detection of cerebral infarction in sickle cell disease (SCD). MATERIALS AND METHODS: Twenty-four pediatric patients aged 6 1/2-17 years with SCD underwent magnetic resonance (MR) imaging, MR angiography, neurologic examination, and transcranial Doppler ultrasonography (US). Transcranial Doppler studies were evaluated for maximum flow velocity in the right and left MCAs. Combinations of cut-off values were used to determine the sensitivity and specificity of transcranial Doppler US for detection of infarction. RESULTS: Neurologic examination had 58% sensitivity and 92% specificity for cerebral infarction. Maximal flow velocity > 200 cm/sec or < 100 cm/sec (including no flow) helped identify nine of 12 patients with infarcts proved at MR imaging, with only one false-positive result (sensitivity, 75%; specificity 92%). The combination of neurologic examination and transcranial Doppler US produced 92% sensitivity and 83% specificity for cerebral infarction. CONCLUSION: The combination of transcranial Doppler US and neurologic examination has potential as a screening technique for infarction in SCD.

Adolescent↗
PubMed1987

[Secondary prevention of cerebral infarct].

This article reviews current treatment in the secondary prevention of cerebral infarction. Treatment of risk factors, together with treatment of the primary cause of cerebral infarction will significantly lower the recurrence rate. Therefore, it is argued that in patients with ischemic stroke medical history should be taken carefully, thorough physical examination should take place, and proper complementary diagnostic tests should be used when indicated.

Arterial Occlusive Diseases↗
PubMedDate not supplied

Mechanisms and timing of deaths from cerebral infarction.

Clinicopathologic correlations were reviewed in 100 cases of recent cerebral infarctions in the internal carotid artery distribution. The most frequent cause of death was transtentorial herniation, followed in frequency by pneumonia, cardiac causes, and pulmonary embolism. Thirty-six percent of all patients and 47% of those with transtentorial herniation died within 48 hours of cerebral infarction. Of the treatable extracerebral causes of death determined at autopsy, only 34% were recorded premortem in the clinician's death summary.

Brain Edema↗
PubMed2001

[Spontaneous dissection of the anterior cerebral artery presenting subarachnoid hemorrhage and cerebral infarction: a case report].

A case is reported of anterior cerebral artery dissecting aneurysm presenting with subarachnoid hemorrhage and cerebral infarction. A 50-year-old man presented with sudden onset of weakness of the left lower limb was admitted to our hospital. CT scan on admission showed a subarachnoid hemorrhage in the interhemispheric fissure and CT on the 6th day demonstrated a cerebral infarction on the right medial frontal lobe. A carotid angiogram 12 hours after the onset showed no aneurysmal lesion, but, the angiogram repeated 11 days after the onset revealed an aneurysmal dilatation with distal narrowing at the right A2-A3 segment. To prevent rebleeding, we performed a wrapping procedure through the interhemispheric route on the 18th day after onset. The postoperative course was uneventful. We reviewed 27 previously reported cases with symptomatic dissecting aneurysm confined to the anterior cerebral artery.

Aortic Dissection↗
PubMed2005

The apolipoprotein E epsilon4 allele increases the odds of chronic cerebral infarction [corrected] detected at autopsy in older persons.

BACKGROUND AND PURPOSE: Studies investigating the relation of the apolipoprotein E (apoE) epsilon4 allele to clinical stroke and to vascular changes on magnetic resonance imaging have been conflicting. Little data are available regarding the relation of apoE epsilon4 to cerebral infarctions documented on postmortem examination. METHODS: We studied the apoE epsilon4 allele in 214 deceased members of the Religious Orders Study, a longitudinal clinical-pathologic study of aging and Alzheimer disease. The apoE genotype was determined using DNA from lymphocytes. Brains were removed a median of 5 hours (interquartile range, 5.5) after death. At postmortem examination, age, location, and size of macroscopic chronic cerebral infarctions were recorded from 1-cm coronal slabs after paraformaldehyde fixation. We also examined 20-microm paraffin-embedded sections of midfrontal and calcarine cortex for amyloid angiopathy on a scale of 1 to 4. RESULTS: Subjects included 96 males and 118 females with a mean age at death of 86 years (SD, 7). Sixty-five subjects (30.4%) had at least 1 apoE epsilon4 allele and 76 (35.5%) exhibited cerebral infarctions. More than 74% of the subjects exhibited amyloid angiopathy with a mean score of 1.4+/-1.2. After controlling for age and sex, apoE epsilon4 increased the odds of cerebral infarction by 2.3-fold (95% CI, 1.2 to 4.2). apoE epsilon4 increased the odds of cortical 3.2-fold (95% CI, 1.3 to 7.7) and subcortical infarctions 2.3-fold (95% CI, 1.2 to 4.5). The effect was unchanged after accounting for amyloid angiopathy. CONCLUSIONS: apoE epsilon4 increases the odds of chronic cerebral infarction detected at autopsy in older persons.

Aged↗
PubMed1993

[Morphological study on acupuncture in interfering experimental cerebral infarction in rat. I. Compensation of cerebral PIA mater artery in cerebral surface].

Occluding unilateral middle cerebral artery (MCAo) of rat, the compensatory blood vessels (CBV) within ischemic area in cerebral surface shown by cerebral perfusion and effect of acupuncture were observed dynamically. Perfusing immediately after MCAo, there was no any blood vessel in the ischemic area. In acupuncture group, the CBV had extended a lot from anastomotic network of cerebral pia mater (ACA-MCA, PCA-MCA) located in marginal zone of ischemic area 3 hs after MCAo. 6.24 and 48 hs after MCAo, the CBV increased much more than control group (non-acupuncture) P < 0.01. The experiment pointed out that there existed a serious vasospasm in the MCA system in initial stage of MCAo, which led up to decompensation in the ischemic area. The acupuncture can remit the vasospasm, and reverse the deteriorated process in early.

Acupuncture Therapy↗
PubMed1987

Concealment of neonatal cerebral infarction on MRI by normal brain water.

Magnetic resonance imaging (MRI) is highly sensitive in detecting cerebral infarction in adults, both in the acute and chronic stages. Cytotoxic and vasogenic edema produce an increase in the water content of acutely ischemic brain, resulting in good tissue contrast from adjacent normal brain on spin density, T1 and T2 weighted MR images. Gliosis and other chronic brain changes are well seen in later stages. We recently encountered a case of remote cerebral infarction in an infant, however, which was not evident on the initial MR examination at 7 weeks of age but which was clearly seen on a follow-up scan at 9 1/2 months. Our contention is that the infarct was masked by the known increased water content of the neonatal brain, which results in lengthened spin density and relaxation times; edema and gliosis may thus be obscured. This age-related concealment of ischemic brain changes on MR has not to our knowledge been reported, and we present this case as a caveat in the detection of cerebral infarction in neonates.

Body Water↗
PubMed1990

Cerebral infarcts and seizures in the neonate.

A retrospective analysis was performed on 54 infants who suffered perinatal hypoxic-ischemic insults and came to autopsy, in an attempt to assess the association of cerebral infarcts with seizures. Fifty infants had several types of cerebrovascular lesions, including intraventricular hemorrhage (32 cases), periventricular leukomalacia (24), ischemic neuronal necrosis (18), pontosubicular necrosis (12), cerebral infarct (9), and cerebellar hemorrhage (7). Of these infants, nine had electroencephalographic seizures. Among a variety of cerebrovascular lesions, cerebral infarcts represented the single lesion most highly correlated with seizures. The incidence of seizures in infants with cerebral infarcts (44%) was significantly higher than with other types of vascular lesions.

Asphyxia Neonatorum↗
PubMed1997

[A case of successful surgical treatment for active endocarditis 2 days after the onset of cerebral infarction].

We performed double valve replacement for a patient with active endocarditis 2 days after the onset of cerebral infarction because of intractable cardiac failure. The use of heparin and the hypotension brought by cardiopulmonary bypass can lead exacerbation of the cerebral symptoms after open heart surgery which is performed during acute phase of cerebral infarction. Perfusion pressure was maintained over 70 mmHg during cardiopulmonary bypass and activated clotting time was kept about 400 seconds to prevent aggravation of cerebral complications in this case. The patients recovered from surgery uneventfully. We described a case who was received double valve replacement 2 days after the onset of cerebral infarction successfully.

Aortic Valve↗
PubMed1996

Surgical treatment of infective endocarditis complicated by annular infection and cerebral infarction.

The surgical treatment of nine patients with infective endocarditis (IE) complicated by annular infection and five with IE complicated by cerebral infarction is described herein. In those with annular infection, after thorough débridement of the infected tissues, valve replacement was performed at the original position in five, at the supraannular position in three, and one underwent a translocation procedure. Aortic valve replacement was able to be performed at the original position in two patients by closing the defect at the aortic annulus with a patch after through débridement. The five patients who underwent original valve position replacement recovered well. Of the three who underwent supraannular position replacement, two died of septicemia after a redo operation, and one received pacemaker implantation. The patient undergoing the translocation procedure died of intestinal infarction. In the five patients who suffered cerebral infarction due to embolus of the vegetation, valve replacement was performed between 40 h and 5 months after its onset. Although one patient died of the rapid progression of brain damage, the other four are alive and well, including two who developed mycotic cerebral aneurysm in the infarcted areas. In conclusion, early surgery for IE is mandatory irrespective of active infection, due to the high mortality and morbidity associated with serious sequelae such as annular abscess or cerebral infarction.

Abscess↗
PubMed2003

Vitamin E isoforms alpha-tocotrienol and gamma-tocopherol prevent cerebral infarction in mice.

Alpha-tocopherol and its derivatives have been shown to be effective in reducing cerebral ischemia-induced brain damage. However, the effects of other vitamin E isoforms have not been characterized. In the present study, we investigated the effects of six different isoforms of vitamin E on the ischemic brain damage in the mice middle cerebral artery (MCA) occlusion model. All vitamin E isoforms were injected i.v., twice, immediately before and 3 h after the occlusion. Alpha-tocopherol (2 mM), alpha-tocotrienol (0.2 and 2 mM) and gamma-tocopherol (0.2 and 2 mM) significantly decreased the size of the cerebral infarcts 1 day after the MCA occlusion, while gamma-tocotrienol, delta-tocopherol and delta-tocotrienol showed no effect on the cerebral infarcts. These results suggest that alpha-tocotrienol and gamma-tocopherol are potent and effective agents for preventing cerebral infarction induced by MCA occlusion.

Animals↗
PubMed1987

Course of blood pressure after cerebral infarction and transient ischemic attack.

In 63 patients, admitted for cerebral infarction or transient ischemic attack (TIA), the blood pressure course was studied. The blood pressure before the event was studied retrospectively; 32 patients were normotensive, in 31 patients existed hypertension, with antihypertensive treatment in 15 of these cases. The blood pressure after the event was studied prospectively, and turned out to be risen in 67% of the patients on the day of admission. It fell in the first day after infarction or TIA, mainly on the second day, to a plateau level reached on the fifth day. Only 3 patients (5%) remained hypertensive until discharge from the hospital. In 48 patients blood pressure values were available as measured two to six months after discharge, without a change in antihypertensive medication. Blood pressure was increased compared to the value measured before discharge. In 14 patients (29%) hypertensive blood pressure figures were measured at that time. It is concluded that blood pressure is elevated in the acute phase of cerebral infarction and TIA, but falls spontaneously in the first days to normotensive levels in most patients; because blood pressure may increase again, measurements of blood pressure within the first months after discharge are needed.

Aged↗