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Cannabis Cognition and Psychosis

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Cannabis Cognition and Psychosis Powered By Docstoc
					Conversion of ultra-high Risk state (prodromal) to psychosis: How does
                         cannabis play a role?


                                         Amresh Srivastava
                                          Megan Johnston



1. Abstract
          Cannabis abuse causes a number of acute and chronic health problems. Links between
cannabis abuse, psychosis and cognitive dysfunction are not yet clearly investigated. This pilot
project proposes: a) to study the pattern of cannabis usage in relation to development of psychosis
and its risk factors. b) To investigate the neuro-cognitive status of people abusing cannabis. And
its relationship to development of psychosis, if any.

2. Background
2.1. Prevalence, Health Effects and Misconceptions Regarding Cannabis Use
         Cannabis is one of the most commonly used illicit drugs. Its active compound
‘cannabidols’ has 64 active isomers, each having different effects on human health and behaviour.
Effects of cannabis have traditionally been seen as less harmful than alcohol abuse, drugs and
other illicit substances. Consequently, less attention has been focused on developing and
evaluating interventions related to cannabis use [1, 2]. There is a strong link between cannabis
and the exacerbation of psychosis as well as other mental health conditions such as anxiety and
depression. However, further research is needed to determine the underlying neurochemical
processes of cannabis exposure as a possible causative and/or exacerbating factor in the
development and progression of psychosis in young adults.
          HBSC data over the past 12 years suggest that experimentation with marijuana has continued to
rise for Grade 10 boys (50 percent) but has leveled off for girls (40 percent) (Figure 6.18). Earlier regional
studies in Canada indicate that approximately 40 percent of adolescents have tried marijuana by the age of
15 (The McCreary Centre Society, 1999). Some authors suggest that the popularity of marijuana as a social
drug among adults is contributing to the availability and acceptance of its use as a safe recreational activity
by adolescents (Tonkin, 2002). However, data on the impact of long-term marijuana use on adolescent
health are not yet available. Data derived from clinical reports has demonstrated an association between
marijuana use and declining performance in school, decreased motivation, and increased absenteeism
(Tonkin, 2002). Figures 6.19 and 6.20 show increasing use of marijuana by grade. One-third of boys and
one-quarter of girls in Grade 10 had used marijuana three or more times in the past year. (Public health
agency of Canada (http://www.phac-aspc.gc.ca/dca-dea/publications/hbsc-2004/chapter_6_e.html)


Grade 10 students who ever tried marijuana, by year of survey (%)
         A recent study conducted over 27 years (between 1976 and 2002) reported that
approximately 50% of 12th grade students had been exposed to cannabis in the United States [3].
These statistics are likely reflective of the Canadian population and have serious health
implications for our youth. Substance abuse disorders have high co morbidity with various
psychiatric disorders and are associated with substantial functional impairments [3]. For instance,
there is growing evidence that early and regular use of cannabis is associated with subsequent
increases in depression, suicidal behavior, psychotic illness, and may also accelerate the onset of
schizophrenia. It is important to note that the vast majority of recent studies reject the view that
marijuana is used to self-medicate psychotic or depressive symptoms and that; in fact, cannabis
appears to be causative and/or exacerbating of mental illness. To date, research on cannabis
exposure and its associated psychiatric disorders remains limited as does research regarding
treatments and rehabilitation for cannabis users and co morbid mental illnesses [4, 5, 6].

2.2. The Effects of Cannabis on Neurocognition and Neurophysiology
         There is little information on the neurocognitive and neurophysiological effects of
cannabis. Preliminary neuro-imaging studies (in mainly nonpsychotic populations) show that
cannabis does not affect gross brain anatomy. But cannabis does acutely increase cerebral blood
flow and long-term exposure causes an overall reduction of cerebral blood flow. In terms of
cognition, acute cannabis administration induces memory impairments, which can persist for
weeks and months following abstinence, though there is little evidence of residual effects
following years of abstinence. Animal studies using an active cannabidol (delta9-
tetrahydrocannabinol) demonstrate enhanced dopaminergic neurotransmission in brain regions
known to be implicated in psychosis. In humans, delta9-tetrahydrocannabinol induces psychotic
like states and memory impairments in healthy volunteers [7]. Overall, the current body of
research literature does not provide evidence of significant, long-term effects due to cannabis use.
However, several acute effects are noted and some are suggestive of negative mental health
consequences. For these reasons, the proposed study aims to look at acute mental health patients
with and without cannabis use.
         In addition, the acute and long-term effects of cannabis are unknown in individuals that
may be genetically or biochemically predisposed to mental illness. The proposed study will also
examine linkages between serum biochemical markers and mental health status (with and without
cannabis exposure). This is an important line of investigation as studies in humans show that
genetic vulnerability may add to increased risk of developing psychosis and cognitive
impairments following cannabis consumption. For instance, continued cannabis use by persons
with schizophrenia causes a small increase in psychotic symptom severity but not vice versa [8].
Cognitive dysfunction associated with long-term or heavy cannabis use is similar in many
respects to the cognitive endophenotypes that have been proposed as vulnerability markers of
schizophrenia [9]. Closer examination of the cognitive deficits associated with specific
parameters of cannabis use and interactions with neurodevelopmental stages and neural substrates
will better inform our understanding of the nature of the association between cannabis use and
psychosis. Further research in this field will enhance our understanding of underlying
pathophysiology and improving treatments for substance abuse and mental illness [9].

2.3. Cannabis and Psychosis
         Many studies now show a robust and consistent association between cannabis
consumption and the development of psychosis. Furthermore, our understanding of cannabis
biology allows the proposal of a plausible hypothetical model, based notably on possible
interactions between cannabis and dopaminergic neurotransmission [10]. Cannabis use can induce
and exacerbate psychotic symptoms and accelerate the disease process. In one such study of first-
episode schizophrenia, it was observed that patients with long-term cannabis consumption were
significantly younger at disease-onset, mostly male, and suffered more often from paranoid
schizophrenia (with a better prognosis) than those without cannabis consumption. The
significance of higher serum neurotrophin levels in cannabis consuming schizophrenics as
compared to those without cannabis consumption remains equivocal so far. The cognitive
functions of this patient group are at least not worse than in those with schizophrenia alone.
Hence, the proposed study has been planned to understand the complex interaction of cannabis
and psychiatric disorders via cognition and other behavioural components.

3. Hypothesis
       Cannabis use is a potential risk factor for development of Psychosis Cognitive
dysfunctions occurs in early and prodromal psychosis, which remains fairly stable, a
dconsistent thoughout the course. It is hypothesized that cannabis abusers who have
cognitive deficits are the candidates who go on to develop psychosis.
       . In further studies, it is intended to explore whether cognitive challenge pre-exist
Cannabis abuse or occur later.
Future Directions
         The data and findings derived from this pilot study will be presented and disseminated
via mental health research conferences (e.g. Canadian Psychiatric Association, American
Psychiatric Association and World Psychiatric Association conferences) and in clinical journals
such as Addiction and British Journal of Psychiatry. This project contributes to overall program
of research that seeks to address two major themes: 1) to study the interrelationship of addictive
behaviours (including substance abuse), cognitive status and underlying psychiatric disorders, 2)
to examine the changes in brain functions/mechanisms of cannabis users and the relationship to
mental illness. This is an important area of research as information available regarding the health
effects of cannabis abuse is not currently sufficient to manage and treat cannabis abusers. We
expect that this project will reveal the interrelationship of addictive behaviour, cognitive status
and underlying psychiatric disorders in cannabis abusers. This work will also establish an
expertise at the University of Western Ontario for targeted approaches to mental health research
and services in rural areas. Furthermore, as students will be collecting and analyzing the data,
they will be gaining valuable experience which will serve them well as their careers progress as
scientists and clinicians. In addition, this grant money will serve as an invaluable stepping stone
to establish collaborations within London’s medical research community and to collect
preliminary data which will, in turn, assist in competing for external grants at provincial, national
and international levels.

9. References
    1. Shrivastava A, Rao S, 1997, Ind J Clinical Practice, 2 Supplement, 66-70.
    2. Raphael B et al, 2005, J Psychiatr Pract, 11, 161-167.
    3. Roberts RE et al, 2007, Drug Alcohol Depend, 88 Suppl 1, S4-S13.
    4. Rey JM et al, 2004, J Am Acad Child Adolesc Psychiatry, 43, 1194-1205.
    5. Wittchen HU et al, 2007, Drug Alcohol Depend, 88 Suppl 1, S60-S70.
    6. Gregg L et al, 2007, Clin Psychol Rev, January 18, Epub ahead of print, PMID:
        17240501.
    7. Linszen D, van Amelsvoort T, 2007, Curr Opin Psychiatry, 20, 116-120.
    8. Degenhardt L et al, 2007, Psychol Med, 9, 1-8.
    9. Solowij N, Michie PT, 2007, J Psychiatry Neurosci, 32, 30-52.
    10. Jockers-Scherubl MC, 2006, Prax Kinderpsychol Kinderpsychiatr, 55, 533-543.

				
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