Homovanillic Acid and Prolactin in Plasma and CSF of Medicated Epileptic Patients

Kalfakis, Nikolaos; Markianos, Manolis

doi:10.1111/j.1528-1157.1987.tb03639.x

Cited by 4 publications

(2 citation statements)

References 13 publications

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“…First, in the study of Habel et al (1981), some children received phenothiazines, antihistamines, or AEDs. The possible role of these medications on CSF monoamine metabolites is difficult to establish and has led to conflicting reports (Reynolds et al, 1975; Shaywitz et al, 1975; Chadwick et al, 1977; Kalfakis and Markianos, 1987). Second, the delay between the convulsion and the lumbar puncture was apparently more important in the study of Habel et al (1981) (within 2 8 h) than in the present study (mean time 2 h), which can lead to attenuation of the metabolite changes.…”

Section: Discussionmentioning

confidence: 57%

5‐Hydroxyindoleacetic Acid and Homovanillic Acid in Cerebrospinal Fluid of Children with Febrile Convulsions

Giroud¹,

Dumas²,

Dauvergne

et al. 1990

Epilepsia

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5-Hydroxyindoleacetic acid (5-HIAA) and homovanillic acid (HVA) were measured by high-performance liquid chromatography (HPLC) in lumbar cerebrospinal fluid (CSF) obtained from febrile children subdivided according to the presence or absence of convulsions. Lumbar puncture was made either early (mean time 2 h) or late (3-6 days) after the febrile convulsion. The level of 5-HIAA was significantly decreased in children early and late after the febrile convulsion as compared with the convulsion-free group, but the HVA level was reduced only early after the febrile convulsion. These results support the hypothesis that a decrease in CSF 5-HIAA may be a biologic marker of susceptibility to convulsions and indicate that the transient decrease in HVA is a secondary phenomenon related to occurrence of convulsions.

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Section: Discussionmentioning

confidence: 57%

5‐Hydroxyindoleacetic Acid and Homovanillic Acid in Cerebrospinal Fluid of Children with Febrile Convulsions

Giroud¹,

Dumas²,

Dauvergne

et al. 1990

Epilepsia

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show abstract

“…Other body fluids have been sampled, with Rao et al (1989) finding no change in the plasma dopamine levels of 12 patients either during or 2 h after seizure activity verified by a combination of video and EEG recording. Markianos and Kalfakis (1991) remarked that urinary HYA was normal in a group of 38 idiopathic epileptics who had been receiving either carbamazepine or phenytoin, confirming their earlier finding of an insignificant rise in plasma HVA following anticonvulsant medication (Kalfakis and Markianos, 1987). It should be noted that the latter results are at variance with those obtained by Reynolds et al (1975).…”

Section: Dopamine: the Common Denominator Inmentioning

confidence: 61%

The role of dopamine in epilepsy

Starr

1996

Synapse

241

157

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The clinical benefits of dopamine agonists in the management of epilepsy can be traced back over a century, whilst the introduction of neuroleptics into psychiatry practice 40 years ago witnessed the emergence of fits as a side effect of dopamine receptor blockade. Epidemiologists noticed a reciprocal relationship between the supposed dopaminergic overactivity syndrome of schizophrenia and epilepsy, which came to be regarded as a dopamine underactivity condition. Early pharmacological studies of epilepsy employed nonselective drugs, that often did not permit dopamine's antiepileptic action to be clearly dissociated from that of other monoamines. Likewise, the biochemical search for genetic abnormalities in brain dopamine function, as predeterminants of spontaneous epilepsy, proved largely inconclusive. The discovery of multiple dopamine receptor families (D1 and D2), mediating opposing influences on neuronal excitability, heralded a new era of dopamine‐epilepsy research. The traditional anticonvulsant action of dopamine was attributed to D2 receptor stimulation in the forebrain, while the advent of selective D1 agonists with proconvulsant properties revealed for the first time that dopamine could also lower the seizure threshold from the midbrain. Whilst there is no immediate prospect of developing D2 agonists or D1 antagonists as clinically useful antiepileptics, there is a growing awareness that seizures might be precipitated as a consequence of treating other neurological disorders with D2 antagonists (schizophrenia) or D1 agonists (parkinsonism). © 1996 Wiley‐Liss, Inc.

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Cerebrospinal fluid examinations in cryptogenic West and Lennox-Gastaut syndrome before and after intravenous immunoglobulin administration

et al. 1994

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Homovanillic Acid and Prolactin in Plasma and CSF of Medicated Epileptic Patients

Cited by 4 publications

References 13 publications

5‐Hydroxyindoleacetic Acid and Homovanillic Acid in Cerebrospinal Fluid of Children with Febrile Convulsions

5‐Hydroxyindoleacetic Acid and Homovanillic Acid in Cerebrospinal Fluid of Children with Febrile Convulsions

The role of dopamine in epilepsy

Cerebrospinal fluid examinations in cryptogenic West and Lennox-Gastaut syndrome before and after intravenous immunoglobulin administration

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