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Neuropsychopharmacology (1995) 12 123-132.
Depression of Thalamic Metabolism by Lorazepam Is Associated with Sleepiness
Nora D Volkow MD 1, Gene-Jack Wang MD 1, Robert Hitzemann Ph.D 2, Joanna S Fowler Ph.D 1, Naome Pappas MS 1, Patricia Lowrimore MD 4, Gail Burr BSN 3, Katherine Pascani BSN 3, John Overall Ph.D 5 and Alfred P Wolf Ph.D 1 |
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1From the Brookhaven Natiional Laboratory, Upton, New York
2Department of Psychiatry, State University of New York at Stony Brook
3Veterans Administration Hospital, Northport, New York
4Beth Israel Medical Center, New York
5University of Texas in Houston
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ABSTRACT
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Though it is well recognized that the pharmacological actions of benzodiazepines are mediated by facilitation of GABAergic neurotransmission, the consequences of these changes in regional brain function are not well understood. This study measured regional brain glucose metabolism using Positron Emission Tomography and 2-deoxy-2[18F]fluoro-D-glucose in normal controls (n = 21) investigated with and without lorazepam (30  g/kg IV) and with flumazenil given after lorazepam (n = 9). Lorazepam markedly decreased metabolism in thalamus (23± 8%) and occipital cortex (19± 8%), and flumazenil partially reversed these changes. Changes in metabolic activity in thalamus were significantly correlated with lorazepam-induced sleepiness (r = .69, df 20, p < .0005) and there was a trend of an association between the reversal by flumazenil of lorazepam-induced change in thalamus and in sleepiness (r = .63, df 8,p = .07). Benzodiazepine-induced changes in thalamic activity may account for their sedative properties.
Keywords: Benzodiazepines; Positron emission tomography; Brain glucose metabolism; Sedation; Thalamus |
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