Depression of thalamic metabolism by lorazepam is associated with sleepiness

Nora D. Volkow, Gene Jack Wang, Robert Hitzemann, Joanna S. Fowler, Naome Pappas, Patricia Lowrimore, Gail Burr, Katherine Pascani, John Overall, Alfred P. Wolf

Research output: Contribution to journalArticlepeer-review

76 Scopus citations


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 pg/kg IV) and with flumazenil given after lorazepam fn = 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.

Original languageEnglish
Pages (from-to)123-132
Number of pages10
Issue number2
StatePublished - Apr 1995
Externally publishedYes


  • Benzodiazepines
  • Brain glucose metabolism
  • Positron emission tomography
  • Sedation
  • Thalamus


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