Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glycerol 50 g infused i.v. over 2 to 6 h is widely used to treat cerebral oedema in patients with acute stroke. Its transit through the blood-cerebrospinal fluid barrier in subjects with uninflamed meninges has now been examined. In 7 patients with an external ventriculostomy for occlusive hydrocephalus, each of whom was given 500 ml of a 10% solution IV over 4 h, serum and CSF were repeatedly sampled during and after the infusion and glycerol was measured enzymatically. The highest serum glycerol level of 191-923 mg/l was observed at the end of the infusion. The maximum CSF glycerol of 18.7-110.8 mg/l was attained 0-1 h after the end of the infusion. Elimination both from serum and CSF approximated a single-exponential decay; the elimination half-life from serum was 0.29-0.56 h compared to 1.03-3.68 h from CSF. In six of the seven cases there was a temporary reversal of the serum/CSF concentration gradient during glycerol elimination. The ratios of the AUCs of CSF and serum, which describe the overall penetration of glycerol into CSF, ranged from 0.09-0.31. In conclusion, the serum level of glycerol produced by giving 50 g IV glycerol over 4 h may not be sufficiently high reliably dehydrate to brain tissue in many patients, and the slow elimination of glycerol from the CSF may be related to the so-called rebound phenomenon.
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PMID:Temporary reversal of serum to cerebrospinal fluid glycerol concentration gradient after intravenous infusion of glycerol. 161 50

Gadopentetate dimeglumine was administered prospectively to 50 patients who presented for magnetic resonance (MR) imaging within 2 weeks after a cortical cerebral infarction. Twenty-two patients (44%) were imaged within 3 days after clinical ictus. Abnormalities detected with gadopentetate dimeglumine enhancement were observed in 46 (92%) of 50 patients. Classic parenchymal enhancement was a late finding, observed in all patients (17 of 17) imaged at 7-14 days after infarction. Before this time, three additional phases of contrast material-related abnormalities were observed. Enhancement of vessels supplying the infarct ("intravascular enhancement sign") was the earliest finding, seen in 17 (77%) of 22 infarcts aged 1-3 days. From day 2 to day 6, abnormal enhancement of meninges adjacent to the infarct was frequently noted ("meningeal enhancement sign"). Finally, a transition phase that combined intravascular or meningeal enhancement with early parenchymal enhancement was seen from day 3 to day 6. Gadopentetate dimeglumine-enhanced MR imaging in early stroke reveals evidence of vascular engorgement and sluggish flow, which precede the development of classic parenchymal enhancement.
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PMID:Early cerebral infarction: gadopentetate dimeglumine enhancement. 224 59

Cerebral amyloid angiopathy is a pathologic condition characterized by the deposition of amyloid in the walls of small vessels in the cerebral cortex and meninges. Intracerebral hemorrhage is common in persons with this condition, but pure subarachnoid or subdural hemorrhage is rarely seen. Recently, the existence of two types of amyloid proteins related to cerebral amyloid angiopathy, beta protein and cystatin C, has been reported, and immunohistochemical methods using antisera to these proteins have become available. We describe a patient with fatal subarachnoid hemorrhage presumably caused by beta protein-type cerebral amyloid angiopathy, which was demonstrated immunohistochemically by using a monoclonal antibody to a synthetic peptide corresponding to residues 8-17 of beta protein. We suggest that beta protein-type cerebral amyloid angiopathy is a possible etiologic factor in subarachnoid hemorrhage of unknown cause.
Stroke 1990 Mar
PMID:Cerebral amyloid angiopathy as a cause of subarachnoid hemorrhage. 230 74

We studied the occurrence of tumors of the brain and cranial meninges in a cohort of 34,000 California Seventh-Day Adventists who completed a detailed life-style questionnaire in 1976 and who were followed for cancer incidence until the end of 1982. During the period of follow-up, 31 tumors were diagnosed in the cohort (21 gliomas, 10 meningiomas). Increased risk for glioma was associated with rural residence, history of a positive tuberculosis skin test and consumption of pork products; increased meningioma risk was associated with a positive reaction to a tuberculosis skin test, previous stroke, use of tranquillizers and a vegetarian life-style in childhood.
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PMID:Risk factors for tumors of the brain and cranial meninges in Seventh-Day Adventists. 281 86

The presented material comprised 17 cases observed in four Warsaw hospitals in a period of 20 years. Nine patients with the pseudotumour syndrome were diagnosed correctly and referred to neurosurgical services. The remaining eight cases died in neurological hospital departments with the following clinical diagnoses: cerebral stroke 3, subarachnoid haemorrhage 1, comatose state preceded by dementia 1, chronic meningoencephalitis 1, status epilepticus 2 cases postmortem investigations demonstrated cerebral cysticercosis in all cases. In four patients with predominant symptoms of cerebrovascular disease lesions were found of the type of residual vasculitis cysticercosa, the sequelae of which might have caused secondary complications independent of concomitant arteriosclerosis. Dementia appeared in a patient with huge hydrocephalus consequent to numerous cysticerci. The patient with the diagnosis of meningoencephalitis had an inflammatory reaction of the ependyma and meninges caused by a cysticercus floating in the IV ventricle. Of the patients dying in status epilepticus attention is called to a 6-year-old girl with a solitary cysticercus localised subcortically in the motor area. The authors suggest that the possibility of cysticercosis should be kept in mind, despite its rarity, in cases with a not completely clear clinical manifestations of cerebrovascular disease, chronic meningoencephalitis and epilepsy or dementia.
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PMID:[Neuropathologic analysis of 8 undiagnosed cases of cerebral cysticercosis]. 344 11

Clonidine-displacing substance (CDS) is a novel endogenous ligand for clonidine receptors previously detected in bovine brain and human serum. We examined for the first time whether CDS can be detected and measured in human cerebrospinal fluid (CSF). Using the [3H]clonidine displacement assay, we found that CDS could be identified and quantified in each of the CSF samples obtained from 81 patients with various neurological disorders. Mean level of CDS in CSF was 4.66 units/ml. Exceedingly high levels were observed in the CSF of patients with neoplastic meningitis (mean, 36.75 units/ml) and stroke (mean, 19.5 units/ml) (P < 0.0001). No correlation was found between CDS levels in CSF and age, gender, CSF protein or number of cells. CDS levels in CSF were higher than those in the serum (P < 0.01). We conclude that CDS is present and can be measured in human CSF. High CDS levels in CSF from patients with leptomeningeal metastases may serve as a tumor marker for malignant infiltration of the meninges. Additional studies in stroke patients will determine whether this endogenous ligand plays a role in the pathogenesis of cerebral ischemia.
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PMID:Detection and measurement of an endogenous clonidine-displacing substance in human cerebrospinal fluid. 843 81

We report a unique case of histologically confirmed meningeal fibrosis in a child who had progressive ischemic neurologic symptoms before the delayed diagnosis of an intracranial primitive neuroectodermal tumor (PNET) was made > 1 year after initial presentation. This pathology has previously been described after neurosurgical procedures, subarachnoid hemorrhage, cranial irradiation, and with no known etiology, but has never been reported in association with a central nervous system neoplasm. In a 6-year-old boy with headaches of several months' duration MRI demonstrated hydrocephalus, a right cerebellopontine angle cyst, and dural enhancement. Biopsies of the thickened meninges taken when the cyst was surgically fenestrated demonstrated only fibrosis with no evidence of infection, hemorrhage, or neoplasm. In the next 6 months, the child had two acute stroke-like episodes with alternating hemiparesis that gradually improved. There were ischemic changes in the diencephalon on MRI. Repeat dural biopsies were unchanged. One year after the initial operation, a left hemiparesis recurred and MRI demonstrated multiple intracranial masses in the cerebral cortex, cerebellum, suprasellar area, and cauda equina. After surgical resection, the cortical mass was found to be a PNET. All the lesions regressed after treatment with radiation and chemotherapy. We hypothesize that the meningeal fibrosis represented a "desmoplastic" reaction to an occult PNET, similar to the fibrous proliferation with cerebellar desmoplastic medulloblastoma except for the extent of the meningeal involvement and the long undetected parenchymal tumor. The mechanism of the ischemic brain injury was most likely vascular involvement by the fibrotic process, either directly or by predisposition to vasoconstriction.
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PMID:Leptomeningeal fibrosis and the delayed diagnosis of a central nervous system neoplasm (primitive neuroectodermal tumor). 904 9

Nocardiosis is an opportunistic infection caused by gram-positive, weakly acid-fast filamentous aerobic organisms. Three species cause infection in man: N. asteroides, N. brasiliensis, and N. caviae, the first one being the most common. With increased use of immunosuppressive therapy for various autoimmune diseases, opportunistic infection by Nocardia has increasingly been reported. N. asteroides infections manifest in various ways; the lungs, skin, and brain are the organs most frequently involved. We describe a patient with Evans' syndrome, a disease requiring long-term immunosuppression, who acquired systemic nocardiosis. The infection was primarily pulmonary, misdiagnosed as tuberculosis, with subsequent hematogenous dissemination to the skin and central nervous system. The diagnosis of cerebral involvement was difficult to prove, as the patient presented with stroke-like episodes. After a positive blood culture was obtained, antibiotic therapy was introduced. The patient's condition deteriorated and the brain with infiltration of the meninges, lungs, skin, and kidneys. Nocardia is an important but often overlooked opportunistic infectious agent in immunocompromised hosts, causing diagnostic and therapeutic problems. As the mortality of cerebral nocardiosis is greater than 80%, early diagnosis and appropriate therapy are crucial.
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PMID:Disseminated nocardiosis as a complication of Evans' syndrome. 1046 Mar 54

Most frequently, chronic granulomatous meningitis (CGM) is caused by infectious agents. However, in some cases the cause of CGM remains undetermined. It is unclear whether antimicrobial agents, including antituberculous drugs, are helpful in such cases. We describe a 61-year-old man who had multiple cranial nerve lesions, epilepsy, sinus thrombosis, stroke, and hydrocephalus attributable to CGM. Repeated extensive search for a causative agent in the cerebrospinal fluid (CSF) and the meninges remained negative. Only a single culture of the sputum revealed growth of Mycobacterium tuberculosis, which prompted antituberculous therapy with isoniazid, rifampicin, and ethambutol. After 6 months of therapy, neurologic abnormalities were slightly improved. We conclude that antimicrobial/ antituberculous agents have only a minor short-term effect in long-lasting CGM of undetermined cause.
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PMID:Chronic granulomatous meningitis with multiple cranial nerve lesions hydrocephalus, stroke, sinus thrombosis, and epilepsy. 1109 65

Cavernous malformations are vascular anomalies that can cause severe neurological deficits, seizures and hemorrhagic stroke if these lesions are located in the brain. In patients with cavernomas, constitutional mutations of the KRIT1 gene have been identified. The pathogenetic mechanisms leading to cerebral cavernous malformations (CCM) development are poorly understood. CCM development might be induced in utero owing to the underlying KRIT1 defect, and is triggered by environmental factors. Another model suggests that CCM develop according to the two-hit model of tumorigenesis associated with biallelic inactivation of KRIT1. So far, CCM specimens themselves have not been subjected to mutation analysis. We identified two somatic mutations in the cavernoma of a sporadic case, suggesting that pathogenesis is associated with somatic KRIT1 alterations. To gain a better understanding of the role of KRIT1 during morphogenesis, the main goal of this study was to provide a detailed description of the spatio-temporal expression pattern of Krit1 and its interaction partner Rap1A during mouse embryogenesis. We did not observe enhanced expression of either gene in the heart or large vessels; however, their expression in the developing small vessels or capillaries could not be assessed by the methods applied. At early embryonic stages, Krit1 and, to a lesser extent, Rap1A are expressed in the developing nervous system. During later phases of fetal development, specific expression of both genes is observed in regions of ossification, the dermis, tendons and in the meninges. These findings provide evidence of differential Krit1 and Rap1A expression during mouse ontogenesis and suggest a more widespread functional significance of Krit1, not restricted to vascular endothelial cells.
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PMID:Mutation and expression analysis of the KRIT1 gene associated with cerebral cavernous malformations (CCM1). 1217 8


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