Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:BIOD00035 (CSF)
 30,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Arteriolar diameters and venular erythrocyte velocities in the small pial vessels on the surface of the cat brain were measured by TV methods during induced epileptic seizures through a cranial window. Grand mal seizures maximally dilated arterioles and increased venular erythrocyte velocity up to 400%. High positive correlation existed between changes in CSF hydrogen ion concentration and pial arteriolar diameter, suggesting metabolic regulation of CBF through CSF/interstitial fluid hydrogen ion alterations during the seizure.
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PMID:Brain microvascular hemodynamic responses to induced seizures. 0 70

The diagnosis of brain tumour could not be made in 91 cases at the first investigation in a group of 1155 brain tumours. Slowly growing gliomas causing only epileptic fits and no other symptoms are especially difficult to diagnose. Of 21 personal observations of tumour seizures, in which the diagnosis of the neoplasm was missed at the first investigation in hospital, 9 were oligodendrogliomas, 5 astrocytomas, 3 glioblastomas, 2 spongioblastomas, 1 gangliocytoma and 1 a metastasis. They were all located in the frontal or centroparietal region. In most cases the seizures appeared during the third or fourth decade. The average interval between the first epileptic fit and the tumour diagnosis was 8.2 years in cases of oligodendrogliomas and 2.2 years in astrocytomas. 5 patients had major seizures, 2 had psychomotor attacks and all the others suffered from partial epilepsy. Anticonvulsive therapy was often successfull; either the frequency of the fits diminished or, in 2 cases, the character of the seizures changed. 18 patients had a normal neurostatus at time of the first investigation. Only 3 patients had a slight difference of physiological reflexes, but no other pathological signs. In none of the patients did investigation of the CSF, skull X-rays, brain scanning, pneumencephalography or cerebral angiography first lead to the diagnosis of a brain tumour. The EEG alone showed focal signs corresponding to the location of the tumour in about 50% of the cases.
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PMID:[The problem of early diagnosis of brain tumours causing seizures only (author's transl)]. 5 Oct 77

A patient with a six-year history of seizures and a shorter history of a progressive hemiparesis, had a glioma. A partial frontal lobectomy was performed. The cerebrospinal fluid, 38 days post-operatively, prior to irradiation, had an increase in gamma globulins. Following cranial irradiation the CSF gamma globulin level returned to normal and the hemiparesis disappeared. The significance of these CSF changes is discussed.
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PMID:Elevated CSF gamma globulins with cerebral "glioma.". 7 79

Three single CSF proteins with different molecular size (albumin, immunoglobulin G, and alpha2-macroglobulin) were determined by the method of electroimmunoassay in 61 children with febrile convulsions (FC) in order to evaluate the permeability of the blood-CSF barrier (B-CSF-B). Forty-two children with acute extracerebral infection served as controls. In contrast to a group of 22 children who suffered from acute meningoencephalitis or encephalitis, the CSF values of 48 children with FC were within normal limits. Thus even a very mild form of inflammatory encephalopathy-undetectable with conventional CSF investigation-was excluded in the majority of the children with FC. In 11 patients, however, CSF concentrations of albumin and alpha2-macroglobulin were abnormally raised, indicating a B-CSF-B distrubance. Elevated albumin values were found most frequently. In several children with FC lasting more than 20-30 min, B-CSF-B damage was probably caused by prolonged seizure activity since there is a linear correlation between albumin concentration and duration of convulsions. Several other factors known to raise the children's risk of developing epilepsy in later life were associated with the protein pattern of B-CSF-B disturbance in some of the children. In these cases, the cause of abnormal permeability of B-CSF-B is unknown and the condition might have existed prior to the occurrence of seizures.
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PMID:Febrile convulsions and blood-cerebrospinal fluid barrier. 7 3

A virus isolated from the CSF of a patient who had amyotrophic lateral sclerosis for 7 years, and prolonged pleocytosis in the CSF, was adapted to suckling mouse brain by subsequent serial blind passages. This Schu virus belongs to the tick-borne encephalitis complex of the genus Flavivirus (Togaviridae). Suckling mouse brain homogenate of the 13th passage was used for transmission experiments in various species of laboratory animals. Golden hamsters infected subcutaneously fell ill after a number of months, lost weight, and had paresis of the legs. Histologically they had petechial hemorrhages in different parts of the CNS and inflammatory changes in the gray substance of the spinal cord. Pilot studies with repeated inoculations of small doses of different flavivirus strains suggest a course of the disease in experimental animals which resembles slow-virus infections insofar as no encephalitis is produced and degenerative changes of the anterior horn cells prevail over inflammatory signs in the spinal cord. After intracerebral application of Schu virus, cynomolgus monkeys developed the typical lesions of togavirus panencephalitis with epileptic seizures, ataxia, and paresis. After subcutaneous application, the virus seems to spread along peripheral nerves to anterior spinal roots and spinal cord, where mainly motor neurons of the anterior horn are damaged, and from there to the brain. The histological findings are such that one may assume the disease of the patient was due to the infection with the virus isolated from his CSF. Therefore, the hypothesis may be advanced that at least some of the cases diagnosed as amyotrophic lateral sclerosis are due to a togavirus infection.
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PMID:Attempts to reproduce amyotrophic lateral sclerosis in laboratory animals by inoculation of Schu virus isolated from a patient with apparent amyotrophic lateral sclerosis. 8 63

A mildly dyslexic boy of 11 years, with no neurological deficit or history of epileptic seizures, had marked hypersomnia for 2 years, which was most pronounced in the morning hours. Repeated EEG studies and power spectral analysis revealed simultaneous posterior alpha rhythm and sleep patterns (spindles, vertex waves, K complexes) over vertex and frontocentral regions, while the patient was behaviorally awake. Bilateral synchronous anterior spikes were frequently noted in association with sleep patterns. A polysomnogram over 24 h confirmed excessive sleep, night and day (especially morning hours) and there was evidence of a large REM sleep percentage (on EMG and EOG basis) while the EEG had predominantly non-REM sleep patterns. Special neurotransmitter studies were performed in view of a presumed disturbance affecting the neurobiochemical sleep regulation. These studies were based on CSF metabolite levels and provided evidence for a high serotonin metabolite (5HIAA) level. It is tempting to hypothesize that the biochemical disturbance has led to encroachment of non-REM sleep patterns on both wakefulness and REM sleep. Further discussion deals with the bilateral-synchronous spike activity and its relationship to arousal patterns in sleep.
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PMID:Hypersomnia with simultaneous waking and sleep patterns in the electroencephalogram. A case report with neurotransmitter studies. 9 32

Authors report 49 patients bacteriologicallyly diagnosed of acute meningococcal infection collected during a 12 months period out of a series of 76 cases diagnosed on clinical grounds. "N. meningitidis" was found in 18 blood and 43 CSF cultures. 31 cases were of the B-group, one was A-group and 17 were not typed. All of them were sulphamide resistant. Hyperthermia with vomiting, cephalea, arthralgia and seizures were the initial symptoms. All patients showed pettechiae, purpura and/or ecchymoses. Endotoxic shock was diagnosed in 26,5% of the cases. In them systolic blood pressures were under p-5. Overall mortality was 14%, and that of endotoxic patients 53%. Therapeutic routines and chemoprophylaxis are reviewed.
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PMID:[Acute meningococcal infection (author's transl)]. 11 89

Clinical, electrical and biochemical studies in an eight years old boy with movement-induced seizures were reported. The attack was usually triggered by sudden initiation of movement, but rarely occurred without any apparent movement. Repeated jumping provoked attacks constantly, which was recorded cinematographically. No abnormality was found either in ictal or interictal EEGs. Haloperidol aggravated the condition, but 1-DOPA had no effect, while DPH (100 mg/day) controlled attacks perfectly with the serum DPH concentration of just 2.0 ug/dl. In overnight sleep analysis, sleep rhythms and characters of REM sleep were not differed significantly from the standard. After DPH therapy, stabilization of sleep in general was noticed; that is, total sleep time prolonged, number of sleep stages decreased and interrupting awakening disappeared. Probenecid loading test revealed that 5-HIAA was normal, HVA high, and large amount of octopamine was detected in CSF.
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PMID:Overnight sleep EEG and cerebrospinal fluid monoamines in seizures induced by movement. 22 8

Radiographic quality as well as adverse effects of intrathecal metrizamide instillation was prospectively investigated in thirty-three clinical cases admitted to the department of neurosurgery, University of Tokyo Hospital, and Kantoh Teishin Hospital. Metrizamide CT cisternography was performed in fifteen cases using in most cases 10 ml of 170 mg I/ml solution through lumbar route. Eleven cases exhibited "normal" pattern CSF circulation and the remaining four, "delayed" pattern. Eight cases (53%) experienced headache, nausea, and/or vomiting several hours after the instillation. All of these belong to the "normal" pattern group. Four cases of "normal" pattern received electroencephalographic examinations before and after metrizamide instillation. Three revealed appearance of negative spike and slow wave burst or sharp waves one to twenty-four hours after the instillation, along with penetration of metrizamide into brain parenchyma. Diagnostic quality was interpreted as "good" in eleven cases. Small acoustic neurinoma, pituitary adenoma, arachnoid cyst, and subdural hygroma were diagnosed among others. Metrizamide ventriculography was done in four cases. No untoward effect of significance was attributed to metrizamide per se. Cervical myelograpy and/or CT myelography was done in fourteen cases using, in most cases, 10 ml of metrizamide 170 mgI/ml. Polytome tomography with metrizamide instillation through lateral cervical puncture was highly diagnostic, whereas, ordinary X-ray with lumbar instillation yielded less satisfactory results. CT myelography in cases of subarachnoid block required good consideration on instillation site and positioning of the patient. Six cases (50%) among twelve cases where metrizamide had run into the cranial cavity experienced headache, nausea, and/or vomiting to a lesser degree than those of cisterno graphy. Metrizamide is the first contrast agent ever made which can be safely introduced into human subarachnoid space, if administered judiciously, nervous. However, metrizamide is weakly toxic to central system and provokes minor untoward effects as well as electroencephalographic abnormalities and, sometimes, clinical convulsive seizure. It would be wiser to restrict the dosage of metrizamide in cisternographic study, expecially in cases of "normal" pattern CSF circulation, to 1.2 gI or 7 ml of 170 mg I/ml solution. Routine use of X-ray cisternography should thus be discouraged because it needs higher concentration of metrizamide in the intracranial cisterns.
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PMID:[Usefulness and adverse effects of intrathecal metrizamide instillation (author's transl)]. 31 37

Nowadays, in severe infections during the neonatal period new bacteria--group B streptococci--have to be taken into account, since in some clinics they already predominate over gramnegative rods. Septicemia and meningitis may be caused by group B streptococci. The septicemia which especially threatents prematures starts with apnoeic spells in the very first hours after birth and may be easily misdiagnosed as an idiopathic respiratory distress syndrome. The mortality is very high (about 60%). Meningitis starts later, normally during the 3rd to 4th week. Seizures are typical at the onset. Group B streptococci may be identified in the CSF by counterimmunoelectrophoresis within one hour. The prognosis is more favourable in meningitis than in septicemia (mortality about 20%). Survivors have little neurological sequelae. Penicillin G or ampicillin combination with an aminoglycoside is recommended as chemotherapy. Exchange transfusion should be considered early. Group B streptococci causing the septic form may be transfered during labour since up to 25% of pregnant women are colonized. Nosocomial transmission of group B streptococci may be the reason for meningitis. Prophylactic penicillin does not seem to help in preventing the disease, but it is possible, that meningitis of the newborn may be prevented by immunizing the mother during pregnancy.
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PMID:[Group B streptococcus infections during the neonatal period (author's transl)]. 35 54


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