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A 1H-MRS and Neurocognitive Analysis of Psychotic Symptoms in Stimulant Dependence Open Access


Other title
Type of item
Degree grantor
University of Alberta
Author or creator
Lakusta, Bonnie J
Supervisor and department
Tibbo, Phil (Psychiatry)
Examining committee member and department
Purdon, Scot (Psychiatry)
Wild, Cam (Public Health)
Baker, Glen (Psychiatry)
Lepage, Martin (Psychiatry)
Tibbo, Phil (Psychiatry)
Department of Psychiatry

Date accepted
Graduation date
Doctor of Philosophy
Degree level
The association between stimulant drug use and the presence of a psychotic disorder raises questions about causation. Substance-induced psychosis may differ etiologically from schizophrenia despite similar phenotypic presentation. It is possible that stimulant drug users who develop symptoms of psychosis have a pre-existing vulnerability to schizophrenia. A recent theory building on the neurodevelopmental hypothesis of schizophrenia proposes that a second insult in conjunction with a pre-existing vulnerability may be necessary to trigger the onset of psychosis. Stimulant dependence may be one of these exogenous triggers for psychosis. This study investigated the possibility that stimulant dependence can trigger psychosis biologically by using proton magnetic resonance spectroscopy, and cognitively by using a battery of cognitive assessments. It was hypothesized the stimulant drug users who develop psychotic symptoms have a pre-existing vulnerability to psychosis that manifests when the substance use triggers abnormal neuropathological development. Evidence of this pathology should be found biologically in proton magnetic resonance spectroscopy measures of N-acetylaspartate, glutamate and choline, and cognitively in measures of processing speed and executive functioning. Abstinent stimulant-dependent users were recruited from the community and compared to a healthy control group and a group of non-substance-induced first episode psychosis patients. Results of this study provide support for the association between methamphetamine use and psychosis. The stimulant-dependent group had worse performance on measures of executive function and processing speed compared to healthy controls, but only processing speed was related to the presence of psychotic symptoms, providing support for processing speed as a potential endophenotype for psychosis. The stimulant-dependent group also had abnormal neurochemical profiles as measured by N-acetylaspartate and glutamate. Finally, in comparison between stimulant-dependent users with symptoms of psychosis and a de novo schizophrenia, the factors predicting severity of psychotic symptoms differed substantially between groups. These results suggest that the cognitive and biological correlates of a substance-induced psychosis differ from a non-substance-induced psychosis, suggesting that a vulnerability to substance-induced psychosis may differ from the neurodevelopomental pathology associated with schizophrenia.
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