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)

Lumbar CSF HVA and 5-HIAA levels were assayed in 3 groups each of 10 subjects, which were respectively deprived of sleep for 30 h, deprived of REM sleep and disturbed with several awakenings during SW sleep for two consecutive nights. HVA levels after total sleep (39 +/- 20 ng/ml) or REM (35 +/- 11 ng/ml) deprivation as well as after SW sleep awakenings (32 +/- 26 ng/ml) were not different from controls (42 +/- 14 ng/ml). 5-HIAA levels after REM deprivation (32 +/- 15 ng/ml) appeared increased when compared with controls (21 +/- 7 ng/ml), total sleep-deprived subjects (21 +/- 10 ng/ml) or subjects with SW sleep awakenings (27 +/- 13 ng/ml). Possible increase in 5-HT turnover after REM deprivation and possible 5-HT role in REM sleep regulation in humans are discussed.
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PMID:Homovanillic acid and 5-hydroxyindoleacetic acid in lumbar cerebrospinal fluid after total and REM sleep deprivation in humans. 21 22

Patients with tardive dyskinesia showed no significant difference in CSF HVA when compared with groups of schizophrenic or depressives. CSF cAMP in the tardive dyskinesia group was significantly lower when compared to schizophrenics but not depressives. These results do not support a dopamine-receptor supersensitivity hypothesis in permanent tardive dyskinesia.
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PMID:Tardive dyskinesia: a clinical test of the supersensitivity hypothesis. 22 Jun 54

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

Central nervous system metabolism in six children and one adult with the syndrome of chronic multiple tics was studied by measuring the accumulation of acid metabolites of dopamine and serotonin (homovanillic acid [HVA] and 5-hydroxyindole-acetic acid [5-HIAA], respectively) in the CSF following probenecid administration. The accumulation of 5-HIAA was reduced in patients with multiple tics in contrast with other pediatric patients (N = 27). The degree of reduction in 5-HIAA relative to HVA appeared to be associated with the severity of the tic disorder. With dextroamphetamine, tic symptoms worsened, CSF HVA level decreased, and CSF 5-HIAA concentration increased. These findings suggest an association in Gilles de la Tourette's disease of reduced functioning of inhibitory serotonergic mechanisms and functional dopaminergic overactivity.
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PMID:Chronic, multiple tics of Gilles de la Tourette's disease. CSF acid monoamine metabolites after probenecid administration. 27 37

MHPG concentration in CSF, urinary excretion of NA and A as well as activity of serum DBH were significantly elevated during alcohol delirium as compared to the recovery period. Urinary DA and HVA in CSF did not show any constant change. One single dosage of clozapine (100 mg orally) induces higher urinary NA and A excretion. There is a time course of clozapine action. MHPG in rat brain a single dosage (50 mg/kg) is elevated; after repeated administration (11 days) a decrease is observed. After 10 days of treatment with clozapine (300 mg/day) a decrease of MHPG in CSF can be seen. It is hypothesized that there is a relationship between delirious states and increases central NA turnover.
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PMID:Pathophysiology of delirious states. 29 Jul 37

Biogenic amine metabolism in the central nervous system of 9 children with Tourette syndrome was evaluated by quantitation of their metabolites in cerebrospinal fluid by a gas chromatographic/mass spectrometric method. Homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylethylene glycol (MHPG) were measured in CSF before and after oral administration of probenecid. Dopamine metabolism appeared defective, as both baseline and accumulated levels of HVA after probenecid were decreased. Serotonin metabolism also appeared defective in some patients with low baseline and low accumulated levels of 5-HIAA after probenecid. Taken together with other clinical features of this disease, the results suggest an underlying disorder of dopamine and serotonin metabolism in Tourette syndrome.
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PMID:Biogenic amine metabolism in Tourette syndrome. 29 54

Fifteen patients with a variety of myoclonic syndromes were studied clinically, pharmacologically, and physiologically. CSF tryptophan, 5HIAA, and HVA were also measured. Of these patients, 8 were improved to varying degrees by therapy with 5HTP, tryptophan in combination with MAOI (but not tryptophan alone), and clonazepam. This group included 6 cases of post-anoxic myoclonus, one case of post-traumatic myoclonus and one undiagnosed case of non-progressive focal myoclonus and epilepsy. In this group low levels of CSF 5HIAA were found compared to non-responsive cases and controls. Two cases of dysynergia cerebellaris myoclonica, 2 cases of undiagnosed aetiology, 2 cases of essential myoclonus, and one case of palatal myoclonus failed to respond to drug therapy. However, even amongst the responsive group the improvement varied. The most dramatic responses were seen in those patients in whom physiological study suggested that myoclonus was mediated by brain-stem structures. Less dramatic responses were seen in patients in whom the myoclonus appeared to originate from cortical structures. The neurochemical basis of myoclonus responding to 5HT precursors and clonazepam is discussed. It is suggested that such myoclonus arises from a relative hypoactivity of the 5HT neuronal system which results in a release of abnormal responses to sensory stimuli which characterize this type of myoclonus.
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PMID:Clinical, biochemical, and physiological features distinguishing myoclonus responsive to 5-hydroxytryptophan, tryptophan with a monoamine oxidase inhibitor, and clonazepam. 41 60

Transient hyperkinesia was observed in a 16-year-old epileptic and mentally retarded patient after a single intravenous perfusion of diphenylhydantoin (DPH). No clinical signs of DPH intoxication were associated with the movement disorder. Repeated plasma anticonvulsant level determinations never showed toxic concentrations of DPH. Since a few spontaneous episodes of hyperkinesia had been observed before, the DPH intravenous perfusion could have unmasked a preexisting latent movement disorder in our patient. However, neuroradiological investigations failed to demonstrate the existence of any anatomical damage of the basal ganglia, and HVA as well as 5-HIAA levels measured in the CSF with the probenecid technique were within the normal range 2 months after cessation of hyperkinesia. HVA and 5-HIAA levels have also been measured in the CSF during the period with hyperkinesia; the results are discussed with reference to previously published data concerning cerebral monoamine metabolism in drug-treated epileptic patients.
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PMID:Transient hyperkinesia after a single intravenous perfusion of diphenylhydantoin. Report of a case associated with nontoxic plasma levels of diphenylhydantoin. 45 89

Research thus far indicates that CSF 5HIAA and HVA may be correlated with state components of psychotic syndromes. HVA may be positively correlated with a component of arousal or activity. The negative correlation between 5HIAA and state variables of activity or agitation in one study suggests an inhibitory deficit in some acute psychoses or a circulating psychotomimetic substance acting on 5HT receptors. Low CSF HVA values in some psychotic patients could be a manifestation of DA receptor supersensitivity which may antedate and promote the occurrence of acute psychosis. The low CSF HVA is also consistent with a Type B monoamine oxidase deficiency in chronic patients. Such a deficiency could theoretically play a role in either (or both) state or trait behavioral components of psychotic illnesses. Decreased CSF HVA could also be related to trait behaviors in psychoses as a possible reflection of MBD. An increasingly important aspect of biological research in psychotic states in the recognition that biological studies should relate to the component behaviors which make up particular psychotic disorders.
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PMID:CSF acid monoamine metabolites in psychotic syndromes: what might they signify? 66 35

An in vivo electrochemical system which continuously records the concentration of metabolites of biogenic amines in small animal CSF is described. A small electrode, immersed in lateral ventricle CSF through a guide cannula, measures the amine metabolites by voltammetric oxidation. The detailed results of HVA release following electrical stimulation of the nigrostriatal pathway in rats are presented and compared with previous perfusion data. All the electrochemical results are verified by independent liquid chromatographic (chemical) analysis.
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PMID:In vivo voltammetry: monitoring of dopamine metabolites in CSF following release by electrical stimulation. 72 1


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