[Causes of cerebral infarction--from the standpoint of cerebral angiography].
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Adult↗
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Effect of nimodipine on memory after cerebral infarction.
OBJECTIVES: Epidemiological studies indicate widespread memory impairment in patients with stroke in the early post-ictal stage. Nimodipine may have psychopharmacological properties and may improve memory. We conducted a single-blind randomized controlled trial to determine whether nimodipine given 7-14 days after cerebral infarction improved memory. MATERIAL AND METHODS: One hundred patients with acute cerebral infarction were consecutively enrolled between D7 to D14. After stratification, patients were randomized to receive oral nimodipine 90 mg daily for 12 weeks, or no drug. Independent assessors administered Mini-Mental State Examination (MMSE) and Fuld Object-Memory Evaluation (FOME) at baseline, 6 weeks, and 12 weeks. RESULTS: Patients receiving nimodipine showed greater improvement in FOME mean scores at 12 weeks (P=0.0334), and also in FOME score change across time (P=0.0283). Patients with severe disability who received nimodipine also showed greater MMSE score change across time (P=0.0495). CONCLUSION: Nimodipine given 7-14 days after cerebral infarction for 3 months results in memory improvement.
Aged↗
[Predictable risk of cerebral infarction following a transient ischaemic attack].
To date most studies that have addressed prognostic factors in patients who have had a transient ischaemic attack (TIA) have determined the risk of cerebral infarction during the first 3 years following TIA. Two recent studies have investigated the very long-term and very short-term risks. The long-term study found that the risk unexpectedly increased after 3 years. The short-term study found the very early risk of cerebral infarct (< 7 days) to be substantial at 10%. The proposed ABCD score enables the physician to easily identify patients at particularly high risk: (A) 1 point for age > or =6o years, (B) 1 for systolic blood pressure >140 mmHg and/or diastolic pressure >90 mmHg, (C) 2 points for unilateral weakness, 1 for speech disturbance without weakness, (D) 2 points for an attack lasting > or =1 h and 1 point for an attack lasting 10-59 min. A patient with a total score of 5 has a risk of 12.1% of developing a cerebral infarct within 7 days. In a patient with a score of 6 this risk is 31.4%.
Cerebral Infarction↗
Magnetic resonance imaging of human cerebral infarction: enhancement with Gd-DTPA.
Five patients (1 female and 4 males) with cerebral infarction of 4 h to 27 months duration were studied 9 times with magnetic resonance (MR) using Gd-DTPA. Spin-echo (SE) MR images (MRI) were obtained before and after the administration of Gd-DTPA, and correlative CT scans were performed on the same day. In 2 cases, 4 h and 27 months after the ictus, there was no enhancement with Gd-DTPA. There was faint enhancement in 2 cases with cerebral infarction of about 24 h duration and obvious enhancement in all cases in the subacute stage. Compared with enhanced CT, MR using Gd-DTPA demonstrated more obvious enhancement of infarcted areas. MR enhancement using Gd-DTPA showed a gradual increase and the accumulated Gd-DTPA in infarcted areas slowly diffused to the periphery. MR enhancement with Gd-DTPA is similar to that of enhanced CT, but may be more sensitive in the detection of blood brain barrier breakdown.
Adult↗
[Asymptomatic cerebral infarction associated with a patent foramen ovale and atrial septal aneurysm].
We reported two young adults (a 42-year-old female and a 45-year-old male) with tension type headache who had a patent foramen ovale and atrial septal aneurysm demonstrated by transesophageal echocardiography, associated with asymptomatic cerebral infarctions. There were multiple subcortical infarctions in the frontal and parietal lobes in case 1, and cerebral infarctions in the right corona radiata, head and body of the caudate nucleus, and putamen in case 2. The two cases did not have hypertension, diabetes mellitus, hyperlipidemia, cardiac diseases detected by electrocardiography and transthoracic echocardiography, and abnormality of intracranial and extracranial arteries by ultrasound sonography and cerebral angiography. Transeosophageal echocardiography revealed atrial septal aneurysm, and showed right-to-left shunt (patent foramen ovale) by Valsalva maneuver. Two cases were diagnosed as paradoxical cerebral embolism associated with a patent foramen ovale. If asymptomatic cerebral infarctions are cryptogenic stroke, a patent foramen ovale and atrial septal aneurysm should be examined by transesophageal echocardiography with Valsalva maneuver.
Adult↗
[Effect of mailuoning on C-Fos protein expression in rats with cerebral infarction].
OBJECTIVE: To investigate the protective effect of mailuoning (MLN) on nerve cells after cerebral infarction induced by photochemistry. METHODS: Eighty SD rats were divided into three groups, the control group (n = 20), the model group (n = 30) and the MLN group (n = 30). Focal cerebro-ischemia induced by photothrombosis in adult rat was used as a model. Changes of C-Fos protein expression before and after MLN treatment were observed using immunohistochemistry, computerized imaging technique and transmission electron microscopy (TEM). RESULTS: C-Fos positive cells located in the transitional zone between the necrotic core and normal cortex. C-Fos protein expression began to show 3 hrs after cerebral infarction, peaked at 6 hrs. As compared with the model group, C-Fos expression was significantly reduced in the MLN group (P<0.01). CONCLUSION: MLN could markedly reduce the injury of nerve cell in the transitional zone, the protection may be related with its inhibition on C-Fos protein expression.
Animals↗
Neuroprotective effect of geranylgeranylacetone, a noninvasive heat shock protein inducer, on cerebral infarction in rats.
The present study evaluated the neuroprotective effect of geranylgeranylacetone (GGA), which is known as an antiulcer agent and more recently as a heat shock protein (HSP) inducer, against cerebral infarction induced by permanent left middle cerebral artery (MCA) occlusion. GGA was given orally in various regimens prior to MCA occlusion in rats. Pretreatment with a single oral GGA dose (800 mg/kg) 48 h before ischemia significantly attenuated cerebral infarction volume (81.7+/-18.4 mm3 versus 369.1+/-70.2 mm3; P<.01). A significant increase in HSP70 immunoreactivity was found in the neocortex in GGA-treated animals with or without ischemia. Pretreatment with a single oral dose of GGA provides an important tool for exploring the mechanisms of neuroprotection against cerebral ischemic neuronal damage.
Animals↗
Brain atrophy and cerebral infarction.
The subjects of the study (109 males, 48 females) were all diagnosed to have cerebral infarction by computerized tomography (CT). The cerebrospinal fluid (CSF) space volume and cranial cavity volume in the normal hemisphere of the patients were estimated using CT at the time from 1 to 3 weeks after the attack of cerebral infarction. The percentage of the CSF space volume to the cranial cavity volume was calculated as an indicator for brain atrophy and called brain atrophy index (BAI): BAI (%) = 100(%) X (CSF space volume/cranial cavity volume). The BAI immediately after the attack of infarction (6.6 +/- 2.2, n = 15), during which no detectable change occurred on CT examination, was the same as the BAI at the time from 1 to 332 days after the attack (6.6 +/- 2.4, n = 20). Therefore we compared the BAI in patients without infarction with the BAI in patients with infarction irrespective of secondary atrophy of the brain after the attack. The BAIs in males with infarction were significantly greater than the BAIs in males without infarction in the age of fifties, sixties and seventies. The BAIs in females with infarction were significantly greater than in females without infarction in the age of fifties, sixties and eighties.
Adult↗
Multiple cerebral infarctions and dementia associated with anticardiolipin antibodies.
Antibodies to negatively charged phospholipids including cardiolipin have been recognized in the sera of patients with systemic lupus erythematosus and other disorders. We report 4 patients who experienced cerebral infarctions and dementia in association with anticardiolipin antibodies. These patients did not have the characteristic lupus anticoagulant or systemic lupus erythematosus. The occurrence of anticardiolipin antibodies in patients with multiple cerebral infarctions who do not have evidence of a systemic vasculitis or inflammatory condition suggests that this association may be more common than previously recognized. It may be useful to test for the presence of anticardiolipin antibodies in patients who have unexplained cerebral infarctions.
Adult↗
A preliminary double-blind cross-over trial of lipo-PGI2, a prostacyclin derivative incorporated in lipid microspheres, in cerebral infarction.
Lipo-PGI2 is a drug preparation of a PGI2 analogue (isocarbacyclin methylester) which is incorporated into lipid microspheres with a diameter of 0.2 mu. Lipo-PGI2 has been shown to accumulate at the vascular wall, particularly those of arteriosclerotic lesions, and it has a much stronger inhibitory activity on platelet aggregation than free isocarbacyclin. In this study, a preliminary double-blind cross over trial of lipo-PGI2 in cerebral infarction was carried out. Seventeen patients with chronic cerebral infarction received 2 micrograms of lipo-PGI2 and placebo daily for one week each in a cross-over double blind test. A significant improvement was noted for lipo-PGI2 compared with placebo in the overall improvement in neurological and mental symptoms (p less than 0.01). The patient's preference also indicated the effectiveness of lipo-PGI2 (p less than 0.05). Adverse reactions were noted in 3 patients receiving placebo, but not in any receiving lipo-PGI2. These results show that lipo-PGI2 at a very low dose would be beneficial as a treatment for relieving the clinical symptoms of chronic cerebral infarction and that lipid microspheres are a useful drug carrier for PGI2 analogue therapy.
Adult↗
Prevalence and clinical importance of sleep apnea in the first night after cerebral infarction.
OBJECTIVE: To determine the prevalence of sleep apnea (SA) during the first night after hemispheric ischemic stroke and its influence on clinical presentation, course, and functional outcome at 6 months. METHODS: The first night after cerebral infarction onset, 50 patients underwent polysomnography (PSG) followed by oximetry during the next 24 hours. Neurologic severity and early worsening were assessed by the Scandinavian Stroke Scale and outcome by the Barthel Index. Patients were evaluated on admission, on the third day, at discharge, and at 1, 3, and 6 months. RESULTS: There were 30 males and 20 females with a mean age of 66.8 +/- 9.5 years. Latency between stroke onset and PSG was 11.6 +/- 5.3 hours. Thirty-one (62%) subjects had SA (apnea-hypopnea index [AHI] > or = 10). Of these, 23 (46%) had an AHI > or =20 and 21 (42%) an AHI > or =25. Sleep-related stroke onset occurred in 24 (48%) patients and was predicted only by an AHI > or =25 on logistic regression analysis. SA was related to early neurologic worsening and oxyhemoglobin desaturations but not to sleep history before stroke onset, infarct topography and size, neurologic severity, or functional outcome. Early neurologic worsening was found in 15 (30%) patients, and logistic regression analysis identified SA and serum glucose as its independent predictors. CONCLUSIONS: SA is frequent during the first night after cerebral infarction (62%) and is associated with early neurologic worsening but not with functional outcome at 6 months. Cerebral infarction onset during sleep is associated with the presence of moderate to severe SA (AHI > or = 25).
Aged↗
Prognosis for patients following a transient ischemic attack with and without a cerebral infarction on brain CT. North American Symptomatic Carotid Endarterectomy Trial (NASCET) Group.
BACKGROUND: Although cerebral infarctions are commonly observed on brain CTs of patients with TIAs, their prognostic importance is unknown. METHOD: The association between appropriately sited brain infarctions (ie, lesions located in the anterior circulation of the brain and ipsilateral to the symptomatic stenosed carotid artery) visualized on CT and the risk of subsequent stroke was assessed by Cox proportional hazards regression in 164 patients presenting with TIA (and no history of previous stroke) and severe angiographically defined carotid stenosis (70 to 99%) from the North American Symptomatic Carotid Endarterectomy Trial. RESULTS: Patients with a TIA and CT-verified brain lesions were older and were more likely to have higher degrees of carotid stenosis and carotid plaque ulceration, a longer duration of symptoms, and a history of hypertension. With regard to prognosis, after adjusting for all known risk factors (patient characteristics) in a regression analysis, the presence of ischemic lesions observed on CT was not associated with an increased risk of ipsilateral stroke at 2 years (adjusted hazard ratio = 1.00; 95% CI: 0.39 to 2.58; p value = 0.99). CONCLUSION: Considered in combination with other patient characteristics, the mere presence of an appropriately sited cerebral infarction on CT does not alter the prognosis (risk of ipsilateral strokes) of severely stenosed patients with TIA. Therefore, there is no clinical rationale in differentiating patients with TIA on the basis of CT findings alone.
Aged↗
Cerebral infarction: time course of signal intensity changes on diffusion-weighted MR images.
OBJECTIVE: The objective of this study was to determine the time course of signal intensity changes on diffusion-weighted MR images after cerebral infarction. MATERIALS AND METHODS: Echoplanar diffusion-weighted MR images were obtained at 1.5 T in 212 patients referred for suspected cerebral infarction over a 6-month period. Of those patients, 85 met strict criteria for inclusion in this study: final clinical diagnosis of stroke, reliable timing of clinical ictus by history, and neurologic symptoms persisting longer than 48 hr after onset. Using adjacent or contralateral normal brain for comparison, diffusion-weighted images were visually analyzed retrospectively to evaluate for abnormalities in signal intensity. Because three patients were scanned on two occasions and five patients had two anatomically separable infarctions, 93 reliably dated brain lesions were analyzed. RESULTS: Diffusion-weighted images showed abnormal findings in 13 (100%) of 13 lesions less than 1 day old, 46 (96%) of 48 lesions 1-4 days old, 16 (94%) of 17 lesions 5-9 days old, three (60%) of five lesions 10-14 days old, and zero (0%) of 10 lesions more than 14 days old. CONCLUSION: Abnormal signal intensity was present on all diffusion-weighted MR studies obtained in patients within 24 hr of acute cerebral infarction and in up to 94% of patients scanned during the first 2 weeks after ictus. The percentage of abnormal diffusion studies declined with time, and no signal intensity abnormality was seen in stroke patients scanned more than 2 weeks after symptom onset.
Aged↗
Cerebral infarction following pituitary apoplexy--case report.
A 29-year-old man presented with lethargy, headache, high fever, and visual disturbance. Neurological examination showed mydriatic pupil, ptosis, diminished light reflex, and ophthalmoplegia on the left. Magnetic resonance (MR) imaging showed the typical findings of pituitary apoplexy, and cerebral angiography disclosed mild narrowing of the A1 segment of the left anterior cerebral artery (ACA). Transsphenoidal tumor resection was performed. Transient severe right hemiparesis occurred directly after the operation. Computed tomography demonstrated cerebral infarction in the territory of the left Heubner's and medial lenticulostriate arteries. Pituitary apoplexy followed by cerebral infarction is very rare. Vasospasm of the perforating arteries of the ACA probably caused the cerebral infarction. Subarachnoid blood or vasoactive agents released from the tumor were the most likely cause of the vasospasm. MR imaging findings of contrast enhancement around the vessels may indicate reactive processes around the vessels.
Adult↗
Early carotid endarterectomy after cerebral infarction.
The objective of the study was to review our recent experience with carotid endarterectomy performed within 30 days of completed cerebral infarction and to evaluate the role of computed tomographic (CT) scanning in the decision-making process. Twenty-seven of 302 operations (9%) were carried out during the 30-day time period. The mean interval between cerebral infarction and surgery was 14 days. Angiography revealed severe stenosis (greater than 75%) of the internal carotid artery in 19 patients. Severe stenosis with deep ulceration found in 6 patients and moderate stenosis (i.e., 50-75%) with deep ulceration was found in 2 patients. CT scans showed recent infarction in 4 patients and an old subcortical lacune in 2 patients. Twenty-two patients were neurologically stable with mild deficits and showed normal results on a CT scan performed 24 hours or more after the ischemic event. These patients underwent early cerebral angiography and carotid endarterectomy without permanent morbidity or mortality. Two patients with moderate stable neurological deficits and findings of recent infarction on CT scans had uneventful postoperative courses. Five patients who were neurologically unstable underwent surgery. The 2 patients with repeated transient ischemic attacks and normal findings on CT scans had uneventful postoperative courses. Two of the three patients with progressive neurological deficits and CT findings of recent cerebral infarction experienced extension of their infarcts after surgery. One of these patients died. Our personal experience, together with a review of previous reports, indicated that patients who have minimal residual neurological deficits and whose CT scans show normal findings are at low surgical risk, perhaps approaching that of patients with transient ischemic attacks.(ABSTRACT TRUNCATED AT 250 WORDS)
Brain Ischemia↗
Factor V (His 1299 Arg) in young Turkish patients with cerebral infarct.
Inherited gene defects related to the coagulation system have been reported as risk factors for stroke. Recently, a genetic component in the factor V (FV) gene that contributes to activated protein C resistance both in the presence and absence of FV 1691 G-->A was reported. This highly conserved FV gene haplotype was marked as R2 polymorphism, an A to G alteration at position 4070 in exon 13 that predicts the His 1299 Arg substitutions. The aim of this study was to evaluate the role of this mutation in Turkish children with ischemic infarct. The case-control study included 48 patients with cerebral infarction; all were 18 years of age or younger (range: 10 months to 18 years). Ten (20.8%) of the 48 patients were found to carry the FV 1299 His-->Arg mutation, one being homozygous. One patient who had a combination of FV 1691 G-->A and protein C deficiency also carried the FV 4070A mutation. A homozygous FV 1299A patient had a prothrombin (PT) 20210A mutation in the heterozygous state. The cerebral infarct risk for FV 1299 was found to be 2.4 (95% confidence interval 0.9-6.8) for all groups. When underlying conditions were excluded, the incidence of FV 1299 was found to be 8/35 (22.8%), but the risk was almost the same. When two other common thrombophilic mutations (i.e. FV 1691 G-->A and PT 20210 G-->A) were excluded, the incidence of FV 4070 mutation increased to 7/21 (33.3%). The risk also increased to 3.9 (95% confidence interval 1.2-12.3).
Adolescent↗
[The experimental study on material basis of motor skill plasticity after acute cerebral infarction].
OBJECTIVE: To investigate the structure basis of motor skill plasticity and the recovery mechanism after acute cerebral infarction. METHODS: After MCAO, the motor skill of rats was examined via beam walking test; and the neuron, synapse and the distribution of neurofilament (NF), microtubule associated protein 2 (MAP2), growth associated protein 43 (GAP43) and synaptophysin (SYP) were observed by electron scope and immunohistology staining. RESULTS: All rats had paralysis after MCAO. The motor skill began to recover significantly at the end of 3 weeks, and kept to improve. The number of injured neuron decreased to normal level at week 9 after an increase resulted from MCAO(1st week: 74.6 +/- 8.8/200 field, 9th week: 2.6 +/- 2.5/200 field); the number and structure of synapse regained to normal level gradually, at last outstripped the control group (number of synapse, 1st week: 8.8 +/- 1.7/8,000 field, 9th week: 15.3 +/- 2.4/8,000 field; normal control: 12.3 +/- 2.0/8,000 field); So did SYP, NF and MAP2. The GAP43 increased only at week 1. CONCLUSION: With the reduction of apoptosis cell, the relevant changes in the number, function and structure of synapse form the material basis of motor skill's plasticity together after cerebral infarction. The regeneration of neuron dose not play important role in motor skill recovery.
Acute Disease↗
[Cerebral infarction in systemic lupus erythematosus].
The case-history of a man aged 31 years with systemic lupus erythematosus and cerebral infarction is presented. Although patients with active disease are young, cerebral infarcts are strikingly frequent among them.
Adult↗