Filipa Raposo Pereira1, Minni T B McMaster2, Nikki Polderman3, Yvon D A T de Vries3, Wim van den Brink2, Guido A van Wingen2. 1. Department of Psychiatry, Academic Medical Center, The University of Amsterdam, AMC (PA.3-220), Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands; Amsterdam Neuroscience, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands; Amsterdam Brain and Cognition, The University of Amsterdam, P.O. Box 19268, 1000 GG, Amsterdam, The Netherlands. Electronic address: f.raposopereira@amc.uva.nl. 2. Department of Psychiatry, Academic Medical Center, The University of Amsterdam, AMC (PA.3-220), Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands; Amsterdam Neuroscience, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands; Amsterdam Brain and Cognition, The University of Amsterdam, P.O. Box 19268, 1000 GG, Amsterdam, The Netherlands. 3. Department of Psychiatry, Academic Medical Center, The University of Amsterdam, AMC (PA.3-220), Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands.
Abstract
BACKGROUND: Gamma-Hydroxybutyric acid (GHB) is a drug of abuse associated with increasing numbers of GHB-dependent patients and emergency attendances often related to GHB-induced coma. Animal studies suggest that GHB induces oxidative stress in the hippocampus, resulting in memory impairments. However, the consequences of chronic GHB use and GHB-induced coma on human brain function and cognition are unknown. METHODS: We recruited 27 GHB users with ≥4 GHB-induced comas (GHB-Coma), 27 GHB users without a coma (GHB-NoComa), and 27 polydrug users who never used GHB (No-GHB). Participants completed verbal and spatial memory tests and an associative memory encoding task during functional magnetic resonance imaging (fMRI) to probe hippocampus functioning. RESULTS: The GHB-Coma group showed a lower premorbid IQ (p = 0.006) and performed worse on the verbal memory test (p = 0.017) compared to the GHB-NoComa group, despite exhibiting similar levels of education. Compared with the other two groups, the GHB-Coma group showed lower left hippocampus (pSVC = 0.044) and left lingual gyrus (pFWE = 0.017) activity, and a trend for lower hippocampal functional connectivity with the left superior temporal cortex during performance of the associative memory encoding task (pFWE = 0.063). No significant differences were observed between the GHB-NoComa group and the No-GHB group. CONCLUSIONS: These results suggest that multiple GHB-induced comas, but not the use of GHB per se, are associated with alterations of memory performance and memory-related brain, although no causal link can be inferred from this cross-sectional study. The results highlight the need for public awareness to minimize the negative health consequences of recreational GHB use, in particular when related with GHB-induced comas.
BACKGROUND:Gamma-Hydroxybutyric acid (GHB) is a drug of abuse associated with increasing numbers of GHB-dependent patients and emergency attendances often related to GHB-induced coma. Animal studies suggest that GHB induces oxidative stress in the hippocampus, resulting in memory impairments. However, the consequences of chronic GHB use and GHB-induced coma on human brain function and cognition are unknown. METHODS: We recruited 27 GHB users with ≥4 GHB-induced comas (GHB-Coma), 27 GHB users without a coma (GHB-NoComa), and 27 polydrug users who never used GHB (No-GHB). Participants completed verbal and spatial memory tests and an associative memory encoding task during functional magnetic resonance imaging (fMRI) to probe hippocampus functioning. RESULTS: The GHB-Coma group showed a lower premorbid IQ (p = 0.006) and performed worse on the verbal memory test (p = 0.017) compared to the GHB-NoComa group, despite exhibiting similar levels of education. Compared with the other two groups, the GHB-Coma group showed lower left hippocampus (pSVC = 0.044) and left lingual gyrus (pFWE = 0.017) activity, and a trend for lower hippocampal functional connectivity with the left superior temporal cortex during performance of the associative memory encoding task (pFWE = 0.063). No significant differences were observed between the GHB-NoComa group and the No-GHB group. CONCLUSIONS: These results suggest that multiple GHB-induced comas, but not the use of GHB per se, are associated with alterations of memory performance and memory-related brain, although no causal link can be inferred from this cross-sectional study. The results highlight the need for public awareness to minimize the negative health consequences of recreational GHB use, in particular when related with GHB-induced comas.
Authors: Filipa Raposo Pereira; Minni T B McMaster; Yvon D A T de Vries; Nikki Polderman; Wim van den Brink; Guido A van Wingen Journal: Eur Addict Res Date: 2019-04-18 Impact factor: 3.015
Authors: R C A Achterbergh; E Hoornenborg; A Boyd; L Coyer; S J A Meuzelaar; A A Hogewoning; U Davidovich; M S van Rooijen; M F Schim van der Loeff; M Prins; H J C de Vries Journal: EClinicalMedicine Date: 2020-08-18
Authors: Filipa Raposo Pereira; Paul Zhutovsky; Minni T B Mcmaster; Nikki Polderman; Yvon D A T de Vries; Wim van den Brink; Guido A van Wingen Journal: Hum Brain Mapp Date: 2019-02-05 Impact factor: 5.038
Authors: Filipa Raposo Pereira; Minni T B McMaster; Arnt Schellekens; Nikki Polderman; Yvon D A T de Vries; Wim van den Brink; Guido A van Wingen Journal: Front Psychiatry Date: 2020-04-02 Impact factor: 4.157
Authors: Filipa Raposo Pereira; Minni T B McMaster; Nikki Polderman; Yvon D A T de Vries; Wim van den Brink; Guido A van Wingen Journal: Neuroimage Clin Date: 2018-09-26 Impact factor: 4.881