Abstract
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Proceedings of the National Academy of Science of the United States of America |
| Vol/bind | 91 |
| Udgave nummer | 24 |
| Sider (fra-til) | 11651-4 |
| Antal sider | 3 |
| ISSN | 0027-8424 |
| Status | Udgivet - 1994 |
| Udgivet eksternt | Ja |
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Elevated dopa decarboxylase activity in living brain of patients with psychosis. / Reith, J; Benkelfat, C; Sherwin, A; Yasuhara, Y; Kuwabara, H; Andermann, F; Bachneff, S; Cumming, P; Diksic, M; Dyve, S E; Etienne, P; Evans, A C; Lal, S; Shevell, M; Savard, G; Wong, D F; Chouinard, G; Gjedde, A.
I: Proceedings of the National Academy of Science of the United States of America, Bind 91, Nr. 24, 1994, s. 11651-4.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › peer review
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TY - JOUR
T1 - Elevated dopa decarboxylase activity in living brain of patients with psychosis.
AU - Reith, J
AU - Benkelfat, C
AU - Sherwin, A
AU - Yasuhara, Y
AU - Kuwabara, H
AU - Andermann, F
AU - Bachneff, S
AU - Cumming, P
AU - Diksic, M
AU - Dyve, S E
AU - Etienne, P
AU - Evans, A C
AU - Lal, S
AU - Shevell, M
AU - Savard, G
AU - Wong, D F
AU - Chouinard, G
AU - Gjedde, A
PY - 1994
Y1 - 1994
N2 - The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.
AB - The hypofrontality theory of the pathogenesis of schizophrenia predicts that cortical lesions cause psychosis. During a search for abnormalities of catecholaminergic neurotransmission in patients with complex partial seizures of the mesial temporal lobe, we discovered an increase of the rate of metabolism of an exogenous dopa tracer (6-[18F]fluoro-L-dopa) in the neostriatum of a subgroup of patients with a history of psychosis. When specifically assayed for this abnormality, patients with schizophrenia revealed the same significant increase of the rate of metabolism in the striatum. The finding is consistent with the theory that a state of psychosis arises when episodic dopamine excess is superimposed on a trait of basic dopamine deficiency in the striatum. The finding is explained by the hypothesis that cortical insufficiency, a proposed pathogenetic mechanism of both disorders, causes an up-regulation of the enzymes responsible for dopa turnover in the neostriatum as well as the receptors mediating dopaminergic neurotransmission.
M3 - Journal article
C2 - 7972118
VL - 91
SP - 11651
EP - 11654
JO - Proceedings of the National Academy of Sciences of the United States of America
JF - Proceedings of the National Academy of Sciences of the United States of America
SN - 0027-8424
IS - 24
ER -