Psychological Medicine

Original Articles

Opposite relationships between cannabis use and neurocognitive functioning in bipolar disorder and schizophrenia

P. A. Ringena1a2, A. Vaskinna2, K. Sundeta3, J. A. Engha1a4, H. Jónsdóttira1a4, C. Simonsena3a4, S. Friisa1a4, S. Opjordsmoena1a4, I. Mellea1a4 and O. A. Andreassena1a4 c1

a1 Institute of Psychiatry, University of Oslo, N-0318 Oslo, Norway

a2 Oslo University Hospital – Aker, Clinic for Mental Health, N-0514 Oslo, Norway

a3 Institute of Psychology, University of Oslo, N-0317 Oslo, Norway

a4 Oslo University Hospital – Ulleval, Division of Psychiatry, N-0407 Oslo, Norway


Background Cannabis use is associated with altered neurocognitive functioning in severe mental disorders, but data are still inconclusive and there are no studies of bipolar disorder. The aim of this study was to investigate the association between cannabis use and neurocognition in bipolar disorder compared with schizophrenia in a naturalistic setting.

Method A total of 133 patients with bipolar disorder and 140 patients with schizophrenia underwent neuropsychological assessments and clinical characterization including measures of substance use. Relationships between cannabis users and neurocognitive function were explored in the two diagnostic groups. Possible interactions between diagnosis and cannabis use were investigated, and findings were controlled for possible confounders.

Results In bipolar disorder subjects, cannabis use was associated with better neurocognitive function, but the opposite was the case for the schizophrenia subjects. There was a statistically significant interaction effect of diagnosis and cannabis use on focused attention (p=0.019), executive functioning (verbal fluency – set shifting) (p=0.009), logical memory-learning (p=0.007) and on logical memory-recall (p=0.004). These differences in neurocognitive function could not be explained by putative confounders.

Conclusions The findings suggest that cannabis use may be related to improved neurocognition in bipolar disorder and compromised neurocognition in schizophrenia. The results need to be replicated in independent samples, and may suggest different underlying disease mechanisms in the two disorders.

(Received April 28 2009)

(Revised August 18 2009)

(Accepted September 15 2009)

(Online publication November 06 2009)


c1 Address for correspondence: O. A. Andreassen, Psychosis Research Section – TOP, Building 49, Department of Psychiatry, Oslo University Hospital – Ulleval, Kirkeveien 166, N-0407 Oslo, Norway. (Email: