With increasing legalization and medicalization of cannabis use, there is need for greater public awareness of the short- and long-term effects of cannabis use on cognition. Recent research has comprised a renewed focus on increasing the safety profile of cannabis to reduce potential harms. In this chapter, we summarize recent evidence to support that acute exposure to cannabis impairs cognitive function in humans, particularly in the domains of learning, episodic memory, attention, and processing speed. The evidence for non-intoxicating residual effects of chronic cannabis use is less consistent and there is a need for further research to investigate risk factors that may slow or prevent recovery of cognitive impairment in some regular users. We then discuss factors that confer greater risk and resilience to cognitive impairment following cannabis use and field-wide methodological challenges that need to be tackled to delineate the cognitive domains that are most vulnerable to cannabis exposure. These future directions are necessary to inform targets for preventative interventions and public health policies to mitigate the harms that people can experience when using cannabis.

Cannabis sativa has been used for centuries for both its medicinal and psychomimetic effects. This chapter outlines the acute and subacute psychomimetic effects of cannabis in humans. Animal experiments with cannabis are not addressed here; the interested reader can find an account of such studies in Chapters 1 and 2 or refer to Adams and Martin (1996) or Chaperon and Thiebot (1999). Similarly, cannabis-associated psychotic disorders in humans are not dealt with here, as these are discussed in Chapters 5–7.

As we shall describe, the response of most people to cannabis is fairly stereotyped. Having said this, the experience of intoxication with any psychomimetic substance is influenced, inter alia, by dose; previous experience (and hence expectation of effect); the personal characteristics of the user (e.g. personality); and the context in which the drug is taken (O'Brien, 1996). Dose is particularly problematic with use of the plant C. sativa, as the proportional content of the major psychoactive compound (Δ9-tetrahydrocannabinol, or THC) varies widely between different strains of the plant, as well as being dependent upon the conditions under which the plant was cultivated. Furthermore, the part of the plant or the type of plant product consumed also affects the amount of THC ingested: for example, cannabis resin has a THC content of up to 10 times that of the traditional cigarette (Ashton, 2001).

The acute effects of cannabis on cognitive functioning have been reasonably well researched. The literature, though, is so vast that any attempt to summarize the findings will necessarily be an oversimplification. This review will selectively focus on those aspects of cognitive functioning that are of relevance to the research reported in Part 2 of this monograph. The substance of this research concerns the long-term cognitive effects of cannabis and accordingly the review of the literature on chronic effects in Chapter 5 is very thorough. While the premise that a knowledge of the acute effects of a drug may provide the basis for research into possible long-term consequences of use is reasonable, the acute and chronic effects of a drug need not necessarily be the same (Block et al., 1992; Block & Ghoneim, 1993) and can in fact be markedly different (Pomara et al., 1983). Also to be borne in mind is the fact that many factors impinge on the effects experienced by the user when acutely intoxicated. These include the dose, the mode of administration, the user's prior experiences with the drug, any concurrent drug use, the “set and setting”, i.e. the complex of user's expectations, attitudes towards drug effects and mood state, and the social environment in which the drug is used (Jaffe, 1990; O'Brien, 1996). Many of the effects of cannabis are also subject to the development of tolerance (Jones, 1983; O'Brien, 1996) and thus naive users may show a greater decrement in performance than experienced users.

A major concern about the recreational use of cannabis has been whether it may lead to functional or structural neurotoxicity or “brain damage” in ordinary language. Fehr & Kalant (1983a) defined neurotoxicity as “functional aberrations qualitatively distinct from the characteristic usual pattern of reversible acute and chronic effects, and that may be caused by identified or identifiable neuronal damage”. On this definition an enduring impairment of cognitive functioning could be interpreted as a manifestation of neurotoxicity if neuronal damage were also demonstrated. Cognitive deficits may be the end result of secondary changes associated with drug use, as opposed to a direct toxic effect on neurons. A thorough review of the cognitive literature in relation to long-term cannabis use is presented in Chapter 5. This chapter will concentrate on the direct investigations of neurological function and toxicity arising from exposure to cannabinoids.

The review begins with an examination of the evidence for functional neurotoxicity from animal behavioural studies. Neurochemical, electrophysiological and brain substrate investigations of functionality follow, and the chapter concludes with the findings of more invasive examinations of brain structure and morphology in animals, and of less invasive techniques for imaging the human brain.

Animal behavioural studies

Animal research provides the ultimate degree of control over extraneous variables; it is possible to eliminate factors known to influence research findings in humans, such as nutritional status, age, sex, previous drug history and concurrent drug use. The results, however, are often difficult to extrapolate to humans because of between species differences in brain and behaviour and in drug dose, patterns of use, routes of administration and methods of assessment.

Selective attention

Selective attention is one of a number of processes which collectively comprise the state of attending to the environment. William James described the essence of this process more than a century ago:

Thus, selective attention could simply be defined as those processes which allow some stimuli to be processed more rapidly and effectively than others, or “the predisposition of an organism to process selectively relevant, as compared to irrelevant, environmental information” (Harter & Aine, 1984). An entirely adequate model of selective attention has not yet been formulated. Selective attention may be viewed as a facilitatory mechanism that enhances the processing of relevant stimuli, or it may be viewed as a filtering mechanism protecting a limited capacity central processor from overload by irrelevant sources of information.

Early behavioural research and theorizing in the area was initiated by Broadbent (e.g. 1958). The aim of continuing research has been to elucidate the processes involved in the selection of relevant from irrelevant information, to determine where, how and when differential processing occurs, and to establish the fate of the irrelevant information or to what extent it is processed.

This concluding chapter integrates the findings of the original research reported here with the cumulative results of the research reviewed in Chapters 2 to 6. The synthesis of neuropsychological test data and eventrelated potential (ERP) indices of cognitive functioning with the results of other investigations of brain function and structure, enables the formulation of a preliminary model of neuropsychological function in long-term cannabis users. The evidence for long-term use of cannabis leading to subtle cognitive impairments is discussed together with the role of other possible confounds. The nature of the cognitive impairments is discussed in terms of proposed attentional / neuropsychological and neurophysiological / biochemical mechanisms. The implications of these findings for future research is discussed, as are implications for long-term cannabis users.

Summary and synthesis

Is the cognitive functioning of long-term regular cannabis users impaired in comparison to nonusers? What is the nature of this impairment?

Previous reviewers have generally concluded that there is insufficient evidence to conclude that cannabis produces any long-term cognitive deficits (e.g. Wert & Raulin, 1986a, b). This is probably a reasonable conclusion when gross deficits are considered: the weight of evidence suggests that the long-term use of cannabis does not result in any severe or grossly debilitating impairment of cognitive function. Recent reviewers agree, however, that there is now sufficient evidence that the long-term use of cannabis leads to a more subtle and selective impairment of cognitive functioning (Hall et al., 1994; Pope et al., 1995; Block, 1996).

The question of whether cognitive impairments associated with long-term use of cannabis are reversible on cessation of use has not been entirely resolved. The previous experiment assessed event-related potential (ERP) measures of selective attention in a group of ex-cannabis users, examining the effects of past duration of use and the length of abstinence. The group result suggested partial recovery of function, but there was also evidence for individual differences in the extent of reversibility of impairment. A subset of the sample (those who had used for the greatest number of years) did not differ from the current long-term cannabis users of Experiment 2 in their ERP signature reflecting unnecessary processing of complex irrelevant information. The impairment was progressive with the number of years of use in both current users and ex-users, and ex-users showed no indication of gradual improvement with increasing abstinence. It was hypothesized that if partial recovery did occur, it must occur fairly rapidly upon cessation of use.

The previous study did not assess subjects before and after the cessation of cannabis use and therefore it is not known to what extent individual subjects showed the deficit in selective attention prior to giving up, or indeed what other factors might contribute to the manifestation or resolution of such an impairment. The present study therefore was designed to investigate in detail changes in cognitive functioning following cessation of cannabis use in an individual subject.