Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with uraemic encephalopathy were previously found to have low total tryptophan (bound plus free), but high free tryptophan concentrations in the plasma and high CSF tryptophan concentrations. The 5-hydroxytryptamine metabolite 5-hydroxyindoleacetic acid was also raised in the CSF. A study of the effect of dialysis treatment on these substances in chronic uraemic patients with and without dialysis dementia is described. After an episode of dialysis the patients without dialysis dementia showed increased plasma total tryptophan and decreased free tryptophan. These changes were associated with a decrease of plasma free fatty acid. The patients with dialysis dementia did not show changes in tryptophan, but plasma free fatty acid rose. CSF concentrations of 5-hydroxyindoleacetic acid fell moderately in both groups of patients on dialysis.
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PMID:Effect of dialysis on plasma and CSF tryptophan and CSF 5-hydroxyindoleacetic acid in advanced renal disease. 615 56

A 58 year-old man developed a progressive encephalopathy four years after Whipple's disease onset with digestive, lymph node, and multiple joint lesions, treated over a period of two years. The diagnosis of neurological manifestations of Whipple's disease was based on clinical findings and the presence of PAS+ inclusion bodies in CSF cells. The outcome was fatal in spite of antibiotic therapy. Diagnostic features of this rare neurological affection are discussed. Preventive treatment and surveillance of patients with Whipple's disease are necessary even after well-conducted therapy.
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PMID:[Whipple's disease with encephalopathy. A case report with review of the literature]. 619 73

The Central Nervous System has often been classified as a "drug sanctuary" as most anticancer drugs do not achieve effective penetration of the blood-brain barrier. With more effective systemic chemotherapy programs (especially in acute leukemia in children), the incidence of meningeal tumor involvement has increased. Even though a number of systemically administered agents might be used in treating the CNS, only three have been used intrathecally with good clinical results: the antimetabolites methotrexate (MTX) and cytosine arabinoside (Ara-C) and the alkylating derivative thiophosphoramide (thio-TEPA). Drug distribution in the CSF which is injected by lumbar puncture does not generally allow for delivery of effective quantities of drug to the cisternae nor the ventricles. Thus direct intraventricular injection via a subcutaneously implanted (Ommaya) reservoir is necessary to achieve adequate drug levels in the higher CNS cavities. The peak ventricular concentration of MTX, which was administered by Ommaya reservoir, at a dose of 15mg/m2, was 2.5 +/- 0.9 X 10(-4)M, and remained as a level of 10(-6)M for 72 hours with a half-life of 10.5 hours. During an intravenous 6 hour-infusion at a dose of 750-3,000mg/m2, MTX concentration in CSF reached 8.2 X 10(-7)M to 2.7 X 10(-6)M. The drug content in CSF had a linear concentration related to the drug level in plasma. Intrathecal MTX and Ara-C frequently cause symptoms of meningeal irritation. Occasionally cases of weakness and paralysis and rare instances of severe encephalopathy may occur. The best established causes of these symptoms is high concentration of these drugs in the CSF, or prolonged exposure of the brain to low CSF concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Pharmacokinetics of intrathecal chemotherapy and clinical problems]. 643 96

Hyperammonemic associated encephalopathy developed in an adult receiving essential amino acids. Evidence that her encephalopathy was related to her hyperammonemia included (1) elevated CSF glutamine and serum ammonia levels, (2) the absence of any other drug or metabolic cause of encephalopathy, and (3) resolution of her encephalopathy and abnormal ammonia levels with discontinuation of the hyperalimentation. The serum ammonia levels of patients receiving essential amino acid fluid should be monitored. If the levels remain elevated or if toxicity develops, consideration should be given to switching to an alternate fluid.
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PMID:Hyperammonemic encephalopathy due to essential amino acid hyperalimentation. 643 58

Levels of gamma-aminobutyric acid (GABA) in CSF were measured by the ion exchange-fluorometric method in 136 patients who underwent evaluation for neurologic disorders. In 19 patients with no organic neurologic or mental disorders who acted as normal controls, the mean (+/-SD) GABA level in CSF was 239 +/- 76 picomoles/mL. Patients with acute hypoxic encephalopathy showed a mean GABA level in CSF higher than that of the controls, a difference that was statistically significant. In all the other disorders studied, the mean GABA level in CSF was either equal to or lower than that found in the controls. Statistically significant reductions of the GABA level in CSF were seen in patients with Huntington's disease, dementias, cerebellar cortical atrophy, multiple sclerosis, epilepsy, and Parkinson's disease.
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PMID:Levels of gamma-aminobutyric acid in cerebrospinal fluid in various neurologic disorders. 644 78

Over a five-year period we identified 22 term newborns with intracranial hemorrhage by computed tomography in an intensive care unit for newborns. Primary subarachnoid hemorrhage (diffuse or focal) was the most common type of hemorrhage. Diffuse subarachnoid hemorrhage was caused either by traumatic delivery or severe hypoxic-ischemic encephalopathy and caused seizures on the first day. Focal subarachnoid hemorrhage was associated with cerebral infarction. Intraventricular hemorrhage was always accompanied by bloody CSF. Somewhat more than half the newborns with intraventricular hemorrhage had a history of traumatic delivery. In the remainder there were no associated risk factors for the hemorrhage. Hemorrhage into the cerebral hemispheres occurred without any identifiable risk factors. Hemorrhage into the cerebellum was associated with traumatic delivery.
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PMID:Intracranial hemorrhage in the term newborn. 668 84

Nine children treated for acute leukemia or lymphosarcoma developed subacute encephalopathy starting with listlessness, depression and impairment of speech. Walking difficulties, ataxia, spasticity and sphincter disorders developed later. Transient intracranial hypertension and abnormal movements respectively developed in two patients. EEG frontal slow waves, raised CSF protein, abnormal white matter radioisotope uptake and CT scan hypodensity with patchy contrast enhancement were evident at the onset. Later, dilated ventricles and calcification appeared in the younger patients. Post-mortem neuropathological studies of three patients disclosed predominantly perivascular myelin loss in areas of white matter necrosis, abnormalities of small vessels and numerous axonal swellings. The spinal cord showed secondary degeneration of the corticospinal tracts. Analysis of the aetiological factors in this series points to the prevailing danger of cranial radiotherapy, probably increased by the young age of patients and by associated drug administration.
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PMID:Necrotising leukoencephalopathy complicating treatment of childhood leukaemia. 669 15

Seventy six patients with neuroparalytic accidents due to antirabies vaccination (ARV) with BPL vaccine were studied. The mean age of incidence was 26.9 +/- 15.7 years. The suspected source of infection was by the bite of a dog in 72 (97.3%) out of 74. The mean duration of interval between the first dose of ARV and onset of neurological deficits was 12.2 +/- 8.4 days. The number of doses was 7 or less in 49 (65.3%) cases and more than 7 in 26 (34.7%) cases. With regard to neurological deficits, 6 (7.9%) had encephalopathy, 23 (30.3%) had encephalomyeloradiculopathy, 7 (9.2%) had myelopathy, 21 (27.6%) had myeloradiculopathy, 18 (23.7%) had polyradiculopathy and one had bilateral 7th cranial nerve palsies. Lumbar CSF analysis was done in 67 patients and was abnormal in 47 (70.1%) patients in the form of pleocytosis or raised protein or both. EEG, done in 30 patients, was abnormal in 13 (43.3%) and the abnormalities were not related to clinical features in 6. Electroneuromyography (ENMG) was done in 25 and was abnormal in 21 cases. Visual evoked potentials (VEP) was done in 11 cases and was abnormal in two. Sixty eight patients received steroids and 17 patients received cyclophosphamide in addition to steroids, 14 during the first admission and 3 during follow up when the recovery with steroids was not satisfactory. The therapeutic results were better in those who received cyclophosphamide and was statistically significant. Fourteen (18.4%) patients died and 6 were autopsied. The pathological features were essentially myeloradiculopathies, with variable degree of encephalic involvement. Two showed distinct necrotising myelopathy of immune type.
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PMID:Neurological complications due to beta-propiolactone (BPL)-inactivated antirabies vaccination. Clinical, electrophysiological and therapeutic aspects. 669 51

To evaluate the role of catecholamines in Reye's syndrome, a specific and sensitive radioenzymatic assay was used to study plasma and CSF concentration of dopamine, norepinephrine, and epinephrine in 14 patients with liver-biopsy-proven Reye's syndrome. The results (median and range) revealed significant (P less than .04, P less than .0024, and P less than .030, respectively) elevation in plasma dopamine (131, 0 to 1,193 pg/mL), norepinephrine (1,455, 20 to 5,271 pg/mL), and epinephrine (345, 7.6 to 2,504 pg/mL) at the onset of the disease when compared with the level of these neurotransmitters in a group of hospitalized patients without hepatic disorders. There was a positive correlation between plasma catecholamines and stage of coma on admission (r = .54 to .86; P less than .001 to .024). Furthermore, the concentration of dopamine, norepinephrine, and epinephrine in the CSF increased significantly during the development of cerebral edema in all patients with Reye's syndrome as compared with concentrations in a control population. Hypercatecholaminemia may contribute to the encephalopathy of Reye's syndrome.
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PMID:Hypercatecholaminemia in Reye's syndrome. 670 27

The concentration of creatine kinase BB isoenzyme (CK BB) was measured by radioimmunoassay in CSF from 306 patients with various neurologic disorders. Levels above 2.0 ng/mL were not found in patients without neurologic disease. Whereas mean CSF CK BB level was less than 2.0 ng/mL in groups of patients with systemic malignant neoplasms, latent syphilis, peripheral neuropathy, disk disease, polyradiculopathy, myelopathy, multiple sclerosis, neurodegenerative disease, encephalopathy, and hydrocephalus, it was elevated in groups of patients with convulsive disorder, CNS neoplasm, cerebrovascular disease, vasculitis, and meningoencephalitis.
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PMID:Creatine kinase BB isoenzyme in CSF in neurologic diseases. Measurement by radioimmunoassay. 683 Apr 58


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