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At least 649 records · Page 36Linked to original sources
PubMed1998

Reversible segmental cerebral arterial vasospasm and cerebral infarction: possible association with excessive use of sumatriptan and Midrin.

OBJECTIVE: To describe a patient who developed reversible segmental cerebral arterial vasospasm and cerebral infarction while taking excessive amounts of sumatriptan succinate and a combination drug (Midrin) consisting of isometheptene mucate, 65 mg, dichloralphenazone, 100 mg, and acetaminophen, 325 mg. DESIGN: Case report. SETTING: Tertiary care center. PATIENT: A 43-year-old man who developed a left occipital infarct after taking a total of 23 sumatriptan succinate tablets (25 mg per tablet) and 32 Midrin tablets during a 7-day period and who on digital subtraction angiography was shown to have segmental cerebral arterial narrowing in multiple vessels. An extensive evaluation for other possible risk factors for cerebral infarction was unrevealing. MAIN OUTCOME AND RESULTS: Discontinuation of sumatriptan and Midrin regimens and administration of nicardipine hydrochloride led to nearly total resolution of the angiographic findings, and the patient had no recurrent strokes. CONCLUSIONS: One should consider the diagnosis of drug-induced vasospasm in patients with cerebral infarction and a history of excessive use of sumatriptan and Midrin. The initial angiographic abnormalities may resemble those found in patients with primary angiitis of the central nervous system.

Acetaminophen↗
PubMed1996

Cerebral infarction in patients aged 15 to 40 years.

BACKGROUND AND PURPOSE: Cerebral infarction among young adults has been little studied in Brazil. Most studies adopt a variable upper age limit and often use the term "young" to designate different age ranges. The objective of the present study was to determine possible differences in etiology of cerebral infarction in specific age subpopulations. METHODS: We studied 106 patients aged 15 to 40 years and divided them into two subpopulations by age at time of ictus (ie, 15 to 29 years and 30 to 40 years). On the basis of Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria, we classified the patients into the following five groups: (1) large-artery atherosclerosis, (2) small-vessel occlusion or lacunae, (3) cardioembolism, (4) other determined causes, and (5) undetermined causes. The proportions for each group were compared between the two age ranges to determine whether there was a significant difference in group distribution. RESULTS: The proportions were different between the two age ranges, with a predominance of women and TOAST-criterion group 4 in the 15- to 29-year age range. In the 30- to 40-year age range, there was a predominance of men and of TOAST-criterion group 3. CONCLUSIONS: The proportions of the groups in the two age ranges were significantly different for lacunar infarctions and infarctions of other etiologies. This observation suggests that different age ranges present characteristically different distributions and therefore should be considered separately when investigated. The older age range already presents features that suggest a transition to the spectrum observed among the aged.

Adolescent↗
PubMed1985

Hyponatremia and cerebral infarction in patients with ruptured intracranial aneurysms: is fluid restriction harmful?

We studied retrospectively the relationship between hyponatremia and cerebral infarction in 134 consecutive patients with aneurysmal subarachnoid hemorrhage. In 44 patients sodium levels fell below 135 mmol/L on at least two consecutive days between the second and the tenth day after the hemorrhage. Twenty-five of these patients fulfilled the criteria for the syndrome of inappropriate secretion of antidiuretic hormone. Cerebral infarction developed in 27 of the 44 patients with hyponatremia and in 19 of the 90 patients with normal serum sodium levels (p less than 0.001). Cerebral infarctions were more often fatal in patients with hyponatremia (p less than 0.01). Twenty-six of the 44 patients had been treated with fluid restriction to correct the serum sodium levels, and infarctions developed in 21. Fluid restriction to correct hyponatremia appears to be potentially dangerous in patients with aneurysmal subarachnoid hemorrhage.

Cerebral Infarction↗
PubMed1999

[Abnormal dynamic electrocardiogram in patients with acute cerebral infarction].

OBJECTIVE: To assess the effect of lesions of insular cortex on cardiac damages in patients with cerebral infarction. METHODS: 24-hour dynamic electrocardiogram recordings was measured were performed in 74 patients with hemispheric cerebral infarction in the acute phase and in 39 control subjects. RESULTS: Supraventricular arrhythmias were significantly increased in groups of right insular infarction as compared with groups of lesions in other regions and with the control. A significantly increased rate of ST segment abnormality was found in groups of left insular infarction as compared with groups of lesions in other regions and with the controls. CONCLUSION: The effect of hemispheric cerebral infarction on heart function are mainly correlated with destruction of insular or regions adjacent to the insular. Increased rate of supraventricular arrhythmias is associated with right insular infarction. While increased rate of ST segment abnormality is associated with left insular infarction.

Aged↗
PubMed2000

[A case of intravascular malignant lymphomatosis presenting as cerebral infarction].

A case of intravascular malignant lymphomatosis (IML) presenting as progressive cerebral infarction is reported. A 62-year-old previously healthy male developed progressive dementia. MRI of the brain at the nearest hospital revealed multiple infarcts with unknown etiology. His level of consciousness deteriorated rapidly, and then he was transferred to our hospital for further evaluation. High grade fever, raised serum C reactive protein (CRP), and raised lymphoma markers (serum LDH and soluble IL-2 receptor (sIL-2R)) were observed. Repeated brain MRI disclosed progression of multifocal cerebral infarctions. We considered IML most likely, and we performed muscle biopsy. However muscle biopsy didn't demonstrate any proliferation of neoplastic cells of lymphoid origin within small vessels. Thereafter IML was diagnosed by brain biopsy. The patient underwent chemotherapy, but died of pneumonia due to severe myelosuppression. IML is a rare disease but most commonly shows neurological symptomatology as its clinical manifestation. Dementia is the most common neurological symptom, and progressive multiple infarction is the most common of the MRI findings. Rapidly progressive dementia associated with multiple infarction, when elevated CRP, LDH and sIL-2R are observed in the laboratory data, is suggestive of IML.

Biomarkers, Tumor↗
PubMed2006

Expression of cytoskeleton and apoptosis related genes after cerebral infarction.

OBJECTIVE: The aim of the study was to investigate the expression and regulation of cytoskeleton and apoptosis related genes in several brain areas after cerebral infarction. METHODS: Tissues were collected from ten autopsy brains from cerebral infarction patients. Using immunohistochemistry, several cytoskeleton and apoptosis related genes were examined in these tissues. The genes included microtubule-associated protein (MAP), glial fibrillary acidic protein (GFAP), neurofilament protein (NF-200), apoptosis gene bc1-2 and factor VIII related antigen (F-VIII). Based on morphological changes in the damaged areas after infarction, the focus and the surrounding areas of injured brain were divided into four areas. RESULTS: In area 0, there was almost no cell survival after infraction, and all markers mentioned above were negative in this area. In addition, both MAP-2 and NF200 like immunoreactivities were dramatically down-regulated in area 1. However, in area 2 and area 3, MAP-2 and NF-200 expressed at normal level. GFAP- and F-VIII immunoreactive cells could hardly found in areas 0 and 1. In the short phase of ischemia, both GFAP and F-immmunoreactive cells could be seen in areas 2 and 3, and the number of GFAP and F (positive cells) was strongly increased in the long phase of ischemia. Bcl-2 immunoreactive cells were only seen in area 2. CONCLUSION: Cerebral infarction causes cell death and physipathological changes of cytoskeleton and apoptosis related genes.

Aged↗
PubMed2000

Fulminant cerebral infarction in a patient with nephrotic syndrome.

Fulminant cerebral infarction secondary to arterial thrombosis in adults with nephrotic syndrome is rare. We report a 42 year old male with fulminant right anterior cerebral and middle cerebral artery infarction. Minimal change disease of the kidney was documented by renal biopsy. The possible pathogenesis is discussed and pertinent literature reviewed.

Adult↗
PubMed1994

[Prevalence and prognostic value of transient ischemic complication preceding cerebral infarction].

To evaluate the prevalence, the aetiological profile and the neurological consequences at day 15 of a transient ischaemic attack (TIA) before a cerebral infarction, we undertook survey from 1985 to 1991, on 1,149 cases with cerebral infarction observed on the population of Dijon. On 1,149 cases, 275 (24%) were preceded by a TIA. Fifty seven cases were lacunar infarcts (20.7%) and 218 were cortical infarcts (79.3%). On the aetiological point of view, the group with 275 infarctions preceded by a TIA was statistically different from the group of 874 infarctions without any TIA, with higher blood pressure, cardiac arrhythmia, tobacco abuse and ischaemic cardiac disease history. Only 65 out of 275 infarctions preceded by one TIA (23.6%) had a perfect territorial relationship between the 2 attacks, and 210 out of 275 (76.4%) had no territorial relationship. While the Barthel score at day 15 was similar within the 2 groups, inversely, pseudo-bulbar syndrome was significantly more frequent in the first group. Former TIA does not increase the general handicap resulting from a cerebral infarct, nevertheless it gives rise to a pseudo-bulbar syndrome.

Aged↗
PubMed1987

Cerebral infarction as a result of tumor emboli.

Autopsy records at Mayo Clinic were reviewed to determine the pattern of cerebral infarction occurring as a consequence of nonmyxomatous tumor emboli. Between 1951 and 1984, there were seven adult patients who fulfilled the criteria: focal or multifocal neurologic disease of abrupt onset; systemic cancer; and pathologic demonstration of tumor emboli in appropriate vessels. Tumors originated from the lung in four patients and from the colon and hypopharynx in one each; in one patient the primary source was unknown. Five patients had carotid and two had vertebrobasilar system strokes. Two patients had at least one antecedent transient ischemic attack (TIA). Three patients presented with cerebral infarction as the initial manifestation of their cancer. In two patients, it occurred immediately after pneumonectomy. In four patients, cerebral infarction occurred in a setting of widespread systemic, including pulmonary, metastases. At postmortem examination, one patient had a single large basilar artery tumor embolus. The others had multiple large and small vessel tumor embolic occlusions. The anterior circulation was affected in three patients, the posterior circulation in two, and both circulations were affected in two. Four patients had additional brain parenchymal metastases including one with diffuse leptomeningeal spread.

Aged↗
PubMed2004

[Asymptomatic cerebral infarction and depression--the concept of vascular depression].

At 1997, Alexopoulos and Krishnan coined the term "vascular depression" to describe depression associated with cerebrovascular disease. Vascular depression included both post-stroke depression, depression occurring after a stroke, and MRI-defined vascular depression in which cerebral infarction is detected by magnetic resonance imaging findings. Post-stroke depression is well known as showing cerebral infarction on imaging modalities as well as clinical symptoms such as localized neurological symptoms related to infarcts. MRI-defined vascular depression demonstrates cerebral infarction on imaging modalities, but there are no clinical symptoms such as localized neurological symptoms or stroke. MRI-defined vascular depression is equivalent to the term "depression with silent cerebral infarction", a condition we studied in the past decade. When the accumulation of infarct lesions induces obstruction in the neuron network related to mood and will exceeds a certain threshold, the patient becomes predisposed to vascular depression. Neurological factors are more prominent than genetic factors or psychosocial stressors in patients with vascular depression due to an accumulation of infarct lesions. Anti-cholinergic drugs and anti-dopaminergic drugs easily induce adverse central nervous system reactions in patients with vascular depression demonstrating prominent neurological factors. Research on vascular depression has contributed to clarifying the onset mechanism of endogenous depression.

Cerebrovascular Disorders↗
PubMed2000

Cerebral infarction and transient ischemic attacks. Efficient evaluation is essential to beneficial intervention.

Rapid but precise evaluation of patients presenting with cerebral infarction is essential to determine immediate intervention. Initial assessment should include history taking, physical examination, routine laboratory testing, electrocardiography, chest radiology, and noncontrast head CT. Localizing the event to the appropriate arterial circulation (anterior versus posterior) and determining topography (subcortical versus cortical) guide sequential testing to ascertain the mechanism of cerebral infarction. Diagnostic testing focuses on selectively identifying potential cardiac, large-vessel, small-vessel, or hematologic causes. Although diagnostic tools are evolving, 15% of cerebral infarctions still have an unknown cause or multiple potential sources.

Cerebral Infarction↗
PubMedDate not supplied

[Cerebral infarct in systemic lupus erythematosus].

INTRODUCTION AND OBJECTIVE: Systemic lupus erythematosus is a syndrome of variable clinical and immunological expression, which may affect any organ. Stroke is an uncommon complication of systemic lupus erythematosus, attributed to many different etiopathogenic mechanisms such as early atherosclerosis, coagulopathy, vasculitis, cardiogenic embolism, etc. Our objectives were to analyze the incidence, clinical and immunological characteristics of this condition and to evaluate the therapeutic approach and evolution. CLINICAL CASES: We present the cases of six patients with cerebral infarcts who also had systemic lupus erythematosus. The frequency of cerebral infarct in our series of systemic lupus erythematosus was 6%. The average age was 45 years (range 13-67). All the cerebral infarcts occurred whilst the systemic lupus erythematosus was active. There were positive antiphospholipid antibodies in three of the patients and two patients had potentially embologenic cardiopathy (33%). Fifty percent of the patients required treatment with cyclophosphamide for their severe systemic disease and 66% received anticoagulants for an antiphospholipid syndrome and/or suspected thromboembolism. The clinical course was satisfactory in all cases but the one who died. CONCLUSIONS: The incidence of cerebral infarct in relation to systemic lupus erythematosus is low, and generally appears during advanced, active phases of the disease. The many etiopathogenic mechanisms involved generally act together so that it is difficult to say which is the main cause, especially in elderly patients. Amongst these mechanisms is the presence of antiphospholipid antibodies, detection of which is essential in this condition, and cardiogenic embolism. The evolution depends mainly on the multi-organ involvement and how early immunosuppressive and/or anticoagulant treatment is started.

Adolescent↗
PubMed1988

Calcification in a recent cerebral infarct--radiologic and pathologic correlation.

This 60 year old male developed a right hemiplegia and aphasia. A C.T. head scan showed a cerebral infarct which appeared hyperdense on a subsequent scan done 18 days after presentation. This was interpreted as indicating a hemorrhagic transformation resulting in discontinuation of anticoagulation therapy. At autopsy, the area of infarction in the left frontoparietal hemisphere appeared intensely green due to breakdown of the blood-brain barrier in the presence of jaundice. A striking finding on microscopy was the presence of calcium salts throughout the area of infarction but most prominent in the grey matter at the periphery of the infarct corresponding to the areas which appeared hyperdense on the CT head scan and stained intensely with bilirubin. There was no evidence of recent hemorrhage. This case illustrates that calcification can occur within weeks after the onset of a recent cerebral infarct and should be considered when interpreting the development of C.T. scan hyperdensity in recent cerebral infarcts.

Brain Diseases↗
PubMed1983

Relationship between regional pertechnetate cerebral circulation time and EEG in patients with cerebral infarction.

The qualitative and regional correlations between the EEG and the cerebral circulation time (CCT), obtained by using intravenously injected pertechnetate and a multidetector device, were studied in 75 patients with supratentorial cerebral infarction. Because bolus dispersion and changes in systemic circulation may distort absolute CCT values when intravenous injection of the isotope is used, the inter- and intrahemispheric relative CCT values were used as indices of CCT. Overall good correlations could be demonstrated between both inter- and intrahemispheric CCT abnormalities and the EEG, though not in all patients. The number of patients with pathological CCT findings showed a tendency to increase with increasing severity of the EEG abnormality. The number of abnormal CCT areas per patient (indicating the size of the circulation disturbance) also increased significantly with increasing severity of the EEG disturbance. Interestingly, relative 'hypervelocity' areas occurred in fewer patients with normal or clearly disturbed EEGs than in patients with mildly disturbed EEGs, perhaps due to differences in autoregulatory capacity and collateral circulation. Within the EEG focus the relative number of CCT abnormalities was greater than outside it. In spite of this fairly good overall correlation between the EEG focus and the CCT abnormality, more than 10% of the patients with an EEG focus showed no CCT abnormalities, thus indicating the complementary roles of these methods. The present study on cerebral infarction, though using intravenously injected pertechnetate for the CCT measurement, showed a reasonable correspondence with earlier reports on the relationship between the EEG and either the CBF or the CCT (obtained by intra-arterially injected isotope). This would seem to suggest that the used non-invasive method for regional CCT measurement has potential for evaluation of cerebral haemodynamics.

Adult↗
PubMed2004

Differential regulation by Seogak Jihwang-Tang on cytokines production in peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness.

Seogak Jihwang-Tang (SJT) has been widely used to treat patients suffering from cerebral infarction. However, very little scientific investigation has been carried out. We investigated the effect of SJT on the production of various cytokines using peripheral blood mononuclear cells from the cerebral infarction patients presenting with altered consciousness. The cytokines production was determined by enzyme-linked immunosorbent assay. The amount of IL-4, IL-10 and TGF-beta1 in culture supernatant significantly increased in the SJT, lipopolysaccharide (LPS) or PHA-treated cells compared to unstimulated cells (P < 0.05). We also showed that increased IL-4 and IL-10 levels by LPS or phytohaemagglutinin (PHA) were significantly inhibited by SJT in a dose-dependent manner. Maximal inhibition rate of IL-4 and IL-10 production by SJT was 45.6 +/- 3.3% and 61 +/- 4.7% for LPS-stimulated cells and 27.3 +/- 1.2% and 83.6 +/- 2% for PHA-stimulated cells, respectively (P < 0.05). On the other hand, SJT significantly increased the LPS or PHA-induced TGF-beta1 production (P < 0.05). These data suggest that SJT has a regulatory effect on the cytokines production, which might explain its beneficial effect in the treatment of cerebral infarction.

Cells, Cultured↗
PubMed1993

Longitudinal changes in proton magnetic resonance spectroscopy in cerebral infarction.

BACKGROUND AND PURPOSE: Proton magnetic resonance spectroscopy has revealed changes in lactate and N-acetyl-aspartate in acute cerebral infarction. However, the details of these drastic changes and subsequent chronic changes have not been clarified. The purpose of this study was to disclose longitudinal changes in spectra seen in proton magnetic resonance spectroscopy. METHODS: Six patients with completed cerebral infarction were examined longitudinally with localized proton magnetic resonance spectroscopy. RESULTS: (1) In the acute stage (within 2 days after onset), two drastic changes were observed: N-acetyl-aspartate decreased rapidly and severely within 2 days after onset, and lactate increased immediately and reached a high level in the acute stage after onset. (2) In the chronic stage (more than 1 month after onset), two features were observed: lactate, which had increased in the acute stage, remained high for more than 1 month, and other signals such as those of N-acetyl-aspartate, choline, and phosphocreatine/creatine decreased dramatically. CONCLUSIONS: These results suggest that N-acetyl-aspartate and lactate as revealed by proton magnetic resonance spectroscopy can be useful indicators of the ischemic damage to the brain in clinical cases of cerebral infarction.

Adult↗
PubMed1999

Acute cerebral infarction: quantification of spin-density and T2 shine-through phenomena on diffusion-weighted MR images.

PURPOSE: To quantify the relative contributions of spin density and T2 effects ("shine through") on diffusion-weighted (DW) magnetic resonance (MR) images of acute and subacute cerebral infarction. MATERIALS AND METHODS: In 30 patients, 1.5-T imaging was performed within the first 7 days after onset of cerebral infarction. Estimates of T2, spin density, and apparent diffusion coefficient (ADC) in the region of stroke and contralateral normal brain were computed by means of standard regression techniques after quadruple-echo conventional MR imaging and single-shot echo-planar DW imaging with a maximum b value of 1,000 sec/mm2. Expected signal intensity (S) enhancement ratios resulting from independent changes in T2, spin density, and ADC were then calculated for the DW sequence. RESULTS: The overall SI of cerebral infarction on DW images was significantly higher than that of normal brain throughout the 1st week after stroke (mean relative SI enhancement ratio, 2.29; P < .001). During the first 2 days after stroke, decreased ADC within the stroke region made the dominant contribution to increased SI on DW images. By day 3, increased T2 values in the stroke region became equally important, and, from days 3-7, the contribution to SI from T2 effects became dominant. A slight increase of spin density in the stroke region made a relatively small and constant contribution to DW SI over the 1st week. CONCLUSION: The increased SI of subacute cerebral infarction on DW images reflects not only a shortening of ADC but a prolongation of T2 and spin-density values.

Acute Disease↗