Any medicine containing THC may produce similar acute cognitive effects to recreational cannabis if taken in sufficient dosage. These effects include: euphoria, sensory enhancement, increased social conviviality, and a sense of relaxation and contentment; perceptual effects including distorted time and space estimation and alteration in sensory modalities; impairment in both sustained and divided attention; impairment in reaction time, motor control and dexterity; impairment in various aspects of memory and higher cognitive function including associative and abstractive processes, planning and organisational strategies (reviewed by Solowij 1998: pp 29-40). The possible implications for those receiving cannabis-based medicines who wish to continue driving have been reviewed by Hadorn (2004). Interestingly, analysis of responsibility for traffic collisions has repeatedly indicated that drivers with only cannabis in their systems (and especially no alcohol) were, if anything, less culpable than drug-free drivers. In prospective studies using driving simulators or road tests, cannabis does impair subjects' ability to maintain road position and constant following distances. However, cannabis users generally seem aware of being impaired and compensate by driving more cautiously. Alcohol consistently produced greater impairment than cannabis in comparable social doses, tended to induce more aggressive driving and, in contrast to cannabis smokers, alcohol subjects lacked insight into their impairment and thus made no attempt to compensate. These studies suggest that, as should be the case with many other prescribed drugs, patients receiving cannabis-based medicines should simply be warned to avoid driving and other potentially hazardous tasks at any time they feel impaired.
Do any of these acute deficits persist after cannabis has been discontinued and fully metabolised? A large and expanding scientific literature has still not fully resolved this question. Recognising the methodological shortcomings that have dogged much of this research, Gonzalez et al. (2002) proposed seven "minimal criteria" which should be applied to any study purporting to explore non-acute cognitive effects of cannabis: only 13 out of 40 eligible studies met these basic criteria. The authors point out that negative results have been disseminated in the media without any acknowledgement of these serious shortcomings.
A major problem lies in distinguishing long-lasting but reversible residual effects (due to slow metabolism of cannabis components or withdrawal phenomena) from irreversible effects. Pope et al. (2002) tested 77 current heavy users and 87 controls. The former showed significant memory deficits at 0, 1 and 7 days of abstinence, but by day 28 were virtually indistinguishable from control subjects. There was no association between duration of cannabis use and cognitive performance after 28 days of abstinence. This conflicts with the finding of Solowij et al. (2002) that deficits on several neuropsychological measures were correlated with lifetime duration of cannabis exposure. In seeking to explain this, Pope et al. (2002) point out that even well-controlled studies depend on the assumption that, after adjustment for more obvious confounding factors, cannabis users and non-users are comparable on all factors other than exposure to cannabis. Additionally, heavy use of an illegal drug may produce non-pharmacological deficits such as family alienation or school drop-out that impact outcome measures. Grant et al. (2003) carried out a meta-analysis of studies examining non-acute cognitive effects, and found no substantial, systematic or detrimental effect of recreational cannabis on neuropsychological performance. They concluded:
The small magnitude of effect sizes from observations of chronic users of cannabis suggests that cannabis compounds, if found to have therapeutic value, should have a good margin of safety from a neurocognitive standpoint under the more limited conditions of exposure that would likely obtain in a medical setting.
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