299
Cannabis and Psychopathology : Update 2004
Sandeep Grover1
, Debasish Basu*2
1
Senior Resident
*2
Additional Professor, Drug De-addiction & Treatment Centre, Department of Psychiatry, Postgraduate Institute of Medical Education & Research,
Chandigarh 160012. E-mail : db_sm@satyam.net.in
*Correspondence
REVIEWARTICLE Indian Journal of Psychiatry, 2004, 46(4)299-309
Cannabis is the world's most commonly used illicit drug,
with approximately 200 to 300 million regular users. It
occupies fourth place in worldwide popularity among
psychoactive drugs, after caffeine, nicotine and alcohol
(Macfadden et al., 2000). The prevalence of lifetime use
of cannabis by young adults has increased in many
developed countries over the past several decades (Hall et
al., 1999). The ready availability of the drug, the increasing
social disapproval of cigarette smoking, stern drinking laws,
and perceptions that cannabis is safe or less harmful than
cigarettes or alcohol may explain these changes (Rey and
Tennant, 2002).
Cannabis is also associated with significant psychiatric co-
morbidity. In a review published in this Journal 10 years
ago (Basu et al., 1994), the authors had reviewed the status
of various psychopathologies associated with cannabis. A
lot of new research has been published since then, partly
settling some of the old controversies while raising new
ones. The topic is relevant because psychopathology and
comorbid psychiatric disorders are still very common among
heavy cannabis users in treatment settings, both in India
(Sarkar et al., 2003) and abroad (Arendt and Munk-
Jorgensen, 2004). It was felt that an update was necessary
to take a stock of the situation and to direct new research
in this area. In the current update we specifically focus on
research in this area over the last 10-15 years. Only very
ABSTRACT
The study of cannabis use and psychopathology remains an interesting area from both academic and pragmatic perspectives. This
article provides an update on the progress made in this area over the past decade or so. Psychopathology and psychiatric syndromes
associated with cannabis use that have received research attention in recent years include cannabis withdrawal, cannabis and psychotic
disorders (especially schizophrenia), depression, anxiety, and cognitive impairment. Status of a specific cannabis withdrawal syndrome
and a specific `cannabis psychosis' remains controversial. Current evidence indicates that there is a clinically significant association
between cannabis use disorders and psychotic syndromes, depression, anxiety and possibly mild cognitive impairment. However, the
nature of this association is often not clear. Several hypothesis related to the cannabis-schizophrenia association are examined.
Cannabis use might be casually related to the later development of schizophrenia in an indirect way in a few heavy users, but more
commonly, its use may precipitate disorders in persons who are vulnerable to developing psychosis and worsen the course of the
disorder.
Key Words : Cannabis, psychopathology, withdrawal, psychosis, schizophrenia, depression, mania, anxiety.
relevant articles or those of historical interest published
before that period are cited.
The search strategies for this update included both search
of electronic databases as well as manual search of relevant
publications or cross references. Electronic search included
both PUBMED searches and searches using other search
engines. Cross-searches of key references (both electronic
and hand-search) often yielded other relevant material. The
search terms used (in various combinations) were: cannabis,
marijuana, cannabinoids; use, abuse, dependence,
withdrawal; psychopathology, psychiatric syndromes;
psychosis, schizophrenia, depression, mania, anxiety;
cognition, neuropsychology, cognitive impairment;
flashback, amotivational syndrome. While it cannot be
guaranteed that all relevant articles could be located,
considering the huge number of publications, an attempt
has been made to provide a balanced update within the
constraints of search strategies employed and the demands
on journal space. Although there is a plethora of laboratory
and biochemical studies using cannabinoids, both exogenous
(cannabis-derived) and endogenous (e.g., anandamide), we
have focused mostly on the clinical studies keeping in view
the scope of the subject covered.
Cannabis and Psychopathology
Both DSM-IV-TR (American Psychiatric Association,
2000) and ICD-10 (World Health Organization, 1992) have
Introduction
300
given various categories of disorders associated with the
use of cannabis, with ICD-10 having a wider approach.
The most important thing which is apparent from the
classification is that cannabis is implicated as the causative
agent for all the categories, but on the contrary, research
has shown that it may not only act as a causative agent, but
may also worsen the pre-existing mental illness or may
unmask the mental illness in predisposed subjects. Johns
(2001) has accordingly divided the untoward mental effects
of cannabis in three broad categories i.e. psychological
responses (panic, depression, psychosis) related to excess
consumption of the drug, effect of cannabis on pre-existing
mental illness, and dependency or withdrawal effects. In
this article we will use the standard nosological categories
to describe the various effects of cannabis and wherever
required will refer to the Johns system of classification.
CANNABIS USE DISORDERS
Cannabis intoxication
It is one of the least controversial issues in the research
related to cannabis and have been divided into severe
cannabisintoxicationandpathologicalcannabisintoxication.
Details of the clinical picture have been described in the
previous review (Basu et al., 1994). Recent research has
shown that the duration of intoxication would be longer in
persons with previous history of schizophrenia or personality
disorder (Johns, 2001).
Cannabis withdrawal syndrome
Early clinic-based reports of cannabis abstinence syndrome
were non-conclusive. Recently a number of clinical and
community-basedstudieshaveexaminedthisissue,targeting
various elements of withdrawal syndrome such as onset,
duration, and offset of symptoms; symptom pattern or
presentation; and alternative explanations.
The studies reporting the onset and abatement of symptoms
are very few, and the little available data are inconsistent.
Earlier studies (Jones et al., 1976) reported symptoms
starting at 4 hours and returning to baseline at 4 days, but
the recent studies have reported a peak at 4-7 days (Haney
et al., 1999; Kouri et al., 1999). A recent study on 18
outpatient cannabis users found that onset typically occurred
between days 1-3 and peak effects between days 2-6, and
most effects lasted 4-14 days (Budney et al., 2003). The
remainder of the main withdrawal studies (e.g., Wiesback
et al., 1996) makes no mention of time scale. Further, onset
of withdrawal symptoms at 4 hours and lasting for a week
is not supported by the pharmacokinetic properties of
cannabinoids such as long half-life and multiple bioactive
metabolites (Grotenhermen, 2004).
Offset of symptoms, the cessation of symptoms on
reintroduction of cannabis, has received limited attention
with contradictory findings. In contrast to earlier anecdotal
reports (Jones et al., 1976), a DSM-IV field trial (Cottler et
al., 1995) found that reintroduction of cannabis could relieve
such symptoms only in 11% of individuals, although these
lower rates could be due to the use of dependent and
nondependent users. However, in a recent well-designed
laboratory study, it was found that oral tetrahydrocannabinol
and not divalproex reduced the symptoms of putative
cannabis withdrawal (Haney et al., 2004).
Regarding the withdrawal symptoms, early outpatient and
laboratory studies reported sleep reduction or various other
sleep problems, restlessness, irritability, sweating and chills,
decreased appetite or change in appetite (Jones et al., 1976).
Some of the recent studies have also confirmed the
existence of similar symptoms (Wiesbeck et al., 1996;
Budneyetal.,1999;Haneyetal.,1999).Additionally,studies
that have looked for withdrawal symptoms with oral
preparations have found stomach pain as one of the
symptoms, which is not seen with smoked preparations
(Haney et al., 1999). Autonomic symptoms have not been
reported reliably. However, the specificity of these
symptoms is again questionable. Studies which have
examined the symptomatology in individuals who become
dependent on non-substance behaviours, such as gambling,
also reveal a cluster of symptoms centered around anxiety
and irritability upon ceasing these behaviours (Gilbert et
al., 1998) and absence of autonomic symptoms, similar to
that of cannabis and due to the same withdrawal states in
cannabis are questionable in not being distinct from general
anxiety reaction.
The prevalence of these withdrawal symptoms again has
wide variation ranging from 14% to 85% in the recent
studies (Wiesbeck et al., 1996; Budney et al., 1999; Cottler
et al., 1995), depending on the type of measurement used
(self report/structured standardized tools), sample size, type
of sample (cannabis users/ cannabis dependent subjects),
amount of cannabis used and mode of cannabis use. Studies
that have used standardized clinical instruments to measure
severity reveal mild symptoms pattern (Kouri et al., 1999).
Most of the withdrawal studies have made some form of
psychiatric evaluation prior to selection of the samples and
have found various psychiatric disorders ranging from 41%
Sandeep Grover & Debasish Basu
301
to 79% (Budney et al., 1999; Stephens et al., 1993). The
only controlled study using standardized instrument to omit
participants with psychiatric disorders found no withdrawal
symptoms (Greenberg et al., 1976).
Further, many studies have limitations in the form of lack
of operational definition for withdrawal symptoms, lack of
control group, use of cannabis of poorer strength, use of
oral forms rather than smoked form, and lack of blindedness
because most studies have used self administration.
From the above, it can be concluded that because of lack
of severity of symptoms, the inconsistent onset and offset
of such symptoms and the possibility of alternative
explanations such as comorbidity, there is no unequivocal
support for cannabis withdrawal syndrome under current
definitions. In future, more rigorous research is required
with a preset criteria for withdrawal syndrome and then
measured with use of control participants, measuring the
plasma levels of the drugs and correlating the same with
the withdrawal symptoms. Recently published good-quality
research under controlled conditions can shed more light
on this currently `hot' topic (e.g., Haney et al., 2004).
CANNABIS AND PSYCHOSIS
Cannabis Psychosis
One of the most heated debates in cannabis research
concerns the existence of a distinct nosological entity that
could be rightfully identified as cannabis psychosis. Earlier
evidence of existence of this entity came from case reports
(for details see Basu et al., 1994). The authors of these
case reports attributed the psychosis to cannabis use for
combination of the following reasons: the onset of the
symptomsfollowedcloselyuponingestionoflargequantities
of cannabis; the affected individuals often exhibited
"organic" symptoms, such as confusion, disorientation and
amnesia; some had no reported personal or family history
of psychosis prior to using cannabis; their symptoms rapidly
remitted after a period of enforced abstinence from cannabis
use, usually within several days to several weeks; recovery
was usually complete with the person having no residual
psychotic symptoms of the type often seen in persons with
schizophrenia; and if the disorder recurred, it was after the
individual started using cannabis.
A number of controlled studies have been conducted over
the past 25 years. Some case-control studies have either
compared persons with "cannabis psychosis" with persons
who have schizophrenia (Imade & Ebie, 1991; Thornicroft
et al., 1992; McGuire et al., 1995; Basu et al., 1999) or
compared psychosis occurring in persons who do and do
not have biochemical evidence of cannabis use prior to
presenting for treatment (Chaudry et al., 1991; Mathers et
al., 1991; Tien & Anthony, 1990; Thomas, 1996). Their
results have been mixed. Studies in favour of a distinct
entity have shown the cannabis psychosis to be short-lasting,
presentingwithapredominantlypolymorphicclinicalpicture,
presence of more odd and bizarre behaviour, violence, panic,
but reactive and congruent affect, less evidence of
schizophrenic formal thought disorder, and swift complete
recovery compared to schizophrenia (Basu et al., 1999).
The negative studies report that there are no differences in
sociodemographic picture and symptoms that are unique to
cannabispsychosis,andnonethatenabledthemtodistinguish
a `cannabis psychosis' from schizophrenia (Thornicroft et
al., 1992).
The entity has been criticized by various authors
(Thornicroft, 1990; Gruber & Pope 1994; Poole & Brabbins
1996; Schuckit, 1994) for the poor quality of information on
cannabis use and its relationship to the onset of psychosis,
and the person's premorbid adjustment and their family
history of psychosis. They also emphasize the wide variety
of clinical pictures of "cannabis psychoses" reported by
different observers of the case reports and case series.
Overall, it can be concluded that the existence of a "cannabis
psychosis" is still a matter for debate. In its favour are
case series of "cannabis psychoses", and a small number
of controlled studies that compare the characteristics of
"cannabis psychoses" with those of psychoses in individuals
who were not using cannabis at the time of hospital
admission/ treatment/ evaluation. Critics of the hypothesis
emphasizethefallibilityofclinicaljudgmentsaboutaetiology,
the poorly specified criteria used in diagnosing these
psychoses, the dearth of controlled studies, and the striking
variations in the clinical features of "cannabis psychoses"
(Poole & Braddins, 1996). It is plausible that high doses of
cannabis may produce psychotic symptoms but the evidence
for a specific clinical syndrome that is identifiable as a
cannabis psychosis is much less compelling.
Cannabis and schizophrenia
Clinical research has shown that high proportions of persons
with schizophrenia report regular cannabis use and meet
criteria for cannabis use disorders (Fowler et al., 1998;
Mueser et al., 1990; Ziedonis and Trudeau, 1997).
Epidemiological studies have also found an association
between cannabis use and psychosis in the general
population (Anthony & Helzer, 1991; Cuffel et al., 1993;
Degenhardt & Hall, 2001; Tien & Anthony, 1990). There
CannabisandPsychopathology:Update2004
302
has been considerable debate about the reasons for this
association (Batel, 2000; Blanchard et al., 2000; Gruber &
Pope, 1994; Hall, 1998; Hall & Degenhardt, 2000; McKay
&Tennant, 2000; Mueser et al., 1998; Rosenthal, 1998).
Depending upon the nature of the relationship between
cannabis use and psychosis, four hypotheses have been
proposed to explain the association. These are: cannabis
use causes psychosis, cannabis use precipitates psychosis
among vulnerable individuals, cannabis use worsens the
prognosis of persons with schizophrenia and regular
cannabis use is more likely among persons with psychosis.
According to the first hypothesis there is a causal link
between cannabis use and schizophrenia in the sense that
cannabis use causes cases of the disorder that would not
have otherwise occurred. This hypothesis has arisen from
reports of `cannabis psychoses'. This hypothesis predicts
that the age of onset of schizophrenia would decline in recent
birth cohorts because of the age of cannabis initiation has
declined, rising prevalence of cannabis use among persons
with schizophrenia, an increase in incidence of
schizophrenia because of increase in cannabis use among
young adults and ultimately an increase in prevalence of
schizophrenia. Studies have shown that subjects with first-
episode schizophrenia who use cannabis are younger than
those who do not (Linszen et al., 1994; Mathers et al., 1991;
Rolfe et al., 1993), which supports this hypothesis. But there
have been contradictory findings regarding the change in
the incidence of schizophrenia. Numerous studies conducted
in many countries have reported declines in the incidence
of schizophrenia over the past 30 years (Geddes et al., 1993;
Kendell et al., 1993; Munk-Jorgensen, 1995; Suvisaari et
al., 1999). However, this has not been universal, with some
reporting stable or increased rates (Bamrah et al., 1992;
Harrison et al., 1991). Given uncertainty about whether
there has been a decrease in incidence, the most
conservative conclusion is that the incidence rates of
schizophrenia have remained stable and possibly decreased
over the past several decades.
According to the second hypothesis, regular cannabis use
precipitatesschizophreniaamongvulnerableindividuals,that
is, among persons who would have developed the disorder
regardless of whether they used cannabis or not (Hall, 1998).
According to this hypothesis, an increase in regular
cannabis use in the general population would not affect the
incidence of schizophrenia but it would reduce the age of
onset of psychotic illness among those who used cannabis.
That is, the incidence rates of persons using cannabis would
be `brought forward'. If this led to more chronic psychotic
disorders (e.g. because earlier onset cases are more likely
to relapse), the prevalence of chronic cases of psychosis
would increase. This would increase the prevalence of
regular cannabis use among persons with schizophrenia.
The most convincing evidence that cannabis use may
precipitate schizophrenia came from a 15-year prospective
study of cannabis use and schizophrenia in 50,465 Swedish
conscripts (Andreasson et al., 1988). This study investigated
the relationship between self-reported cannabis use at age
18 and the risk of receiving a diagnosis of schizophrenia in
the subsequent 15 years, and the authors after controlling
for the confounding variables concluded that cannabis use
precipitates schizophrenia in vulnerable individuals. They
also found a dose-response relationship between a diagnosis
of schizophrenia and the number of times that cannabis
had been used by age 18. In a recent follow-up of the same
cohort it has been concluded that heavy cannabis users by
the age of 18 years were 6.7 times more likely than non-
users to be diagnosed with schizophrenia 27 years later
(Zammit et al., 2002); and the risk remained significant after
controlling for other potential confounding factors such as
disturbed behaviour, low IQ score, growing up in a city,
cigarette smoking and poor social integration. Similar
increases in risk of development of schizophrenia after
cannabis use have also been reported by other
epidemiological follow-up studies ranging from 3 years to
more than 20 years (Fergusson et al., 2003; van Os et al.,
2002) and have also found evidence for the presence of
dose-response relationship (van Os et al., 2002). Other
supporting evidence for this hypothesis is that persons with
first-episode schizophrenia who use cannabis are younger
than those who do not (Linszen et al., 1994; Mathers et al.,
1991; Rolfe et al., 1993); cannabis use usually precedes
the development of psychotic symptoms (Allebeck et al.,
1993; Hambrecht and Haefner, 2000; Linszen et al., 1994);
among first-episode cases of psychosis, those who used
cannabis were more likely to have a family history of
psychosis (McGuire et al., 1995; Boutros & Bowers,1996);
their better premorbid adjustment, their fewer negative
symptoms, and their better treatment response. This
hypothesis is also consistent with the stress-diathesis model
of schizophrenia (Boutros & Bowers, 1996; Gottesman,
1991) in which the likelihood of developing schizophrenia is
the product of stress acting upon a genetic diathesis to
develop schizophrenia.
According to the third hypothesis, cannabis use would
worsen the prognosis of schizophrenic persons by increasing
relapse to schizophrenia. This hypothesis does not predict
an increased incidence of schizophrenia among regular
cannabis users. Instead, it predicts that persons with
schizophrenia who are regular cannabis users will be more
likely to have a relapse after their initial episode. This could
increase the number of persons in the population with
Sandeep Grover & Debasish Basu
303
chronic schizophrenia. It would not affect the age of onset
of psychosis. The prevalence of cannabis use among
persons with schizophrenia would increase because there
would be more cannabis users among chronic cases. It is
supported by evidence that persons with schizophrenia who
use cannabis are more likely to suffer a relapse (Jablensky
et al., 1992; Linszen et al., 1994; Negrete et al., 1986) and
stable incidence of schizophrenia as discussed above. It is
also biologically plausible. Psychotic disorders involve
disturbances in the dopamine neurotransmitter systems,
since drugs that increase dopamine release produce
psychotic symptoms when given in large doses, and
neuroleptic drugs that reduce psychotic symptoms also
reduce dopamine levels (Stahl, 1996). Cannabinoids, such
as THC increase dopamine release (Hamara et al., 1995).
The major cause of uncertainty about this relationship is
assessing the contribution of confounding factors. It may
be, for example, that the difference in psychotic symptoms
between schizophrenia patients who do and do not use
cannabisisduetodifferencesinpremorbidpersonality,family
history and other characteristics (Kavanagh, 1995). The
other difficulty is about separating the contributions that
cannabis and alcohol make to exacerbations of
schizophrenicsymptoms.Itisrareforaschizophrenicpatient
to only use cannabis (Mueser et al., 1992). The concurrent
use of alcohol is common, and the heavier their cannabis
use, the more likely they are to use psychostimulants and
hallucinogens. The only study [Linszen et al. (1994)]
statistically adjusted for the effects of concurrent alcohol
and drug use and found that the relationship persisted.
According to the fourth hypothesis, persons with
schizophrenia are more likely to become regular cannabis
users, if they use the drug. There is no causal relationship
between cannabis use and psychosis, so increasing rates
of cannabis use will have no effect upon the incidence or
prevalence of schizophrenia and there would not be a
change in age of onset. There would be an increased
prevalence of cannabis use among persons with psychosis.
Findings in favour of the hypothesis is the evidence that
some schizophrenic patients report using cannabis because
its euphoric effects relieve negative symptoms and
depression (Dixon et al., 1990). Dixon et al. (1990) surveyed
83 patients with schizophrenia who reported that cannabis
reduced anxiety and depression, and increased a sense of
calm but at the cost of increased suspiciousness.
Although recent, double-blinded, randomized,
counterbalanced laboratory studies have clearly
demonstrated the psychotomimetic properties of intravenous
tetrahydrocannabinol (D'souza et al., 2004), these cannot
answer the question: what happens to people long-time
after they have been using cannabis? Prospective cohort
studies can possibly answer this question. Two recent
publications (Arseneault et al., 2004; Smit et al., 2004) have
reviewed the few original high-quality longitudinal cohort
studies available in this area from four countries: Sweden
(Andreasson et al., 1988; Zammit et al., 2002); Israel
(Weiser et al., 2002); Netherlands (van Os et al., 2002);
and New Zealand (Arseneault et al., 2002; Fergusson et
al., 2003). The follow-up period varied from 3 - 15 years
across studies. Outcome was defined differently, varying
from a count of number of psychotic symptoms to full-
fledged ICD or DSM-defined schizophrenia or
schizophreniform disorder. All these studies had eliminated
effect of prior history of psychosis, and most (other than
Weiser et al., 2002) had eliminated the effect of other
substances. Except one (Arseneault et al., 2002), all studies
had controlled for the possible confounding effects of several
sociodemographic and clinical variables such as gender, age,
ethnicity, marital status, education, employment, IQ, social
network, urbanicity, etc. Based on these, both the reviewers
concluded that cannabis use in adolescence leads to at least
a twofold increase in the relative risk of schizophrenia or
related psychoses in adulthood (adjusted pooled Odds ratio
= 2.34; 95% CI = 1.69 - 2.95). Although confounding effects
cannot be totally eliminated, the overall evidence suggests
cannabis was more harmful in vulnerable subjects, i.e., those
`atrisk'fordevelopingpsychoticillnessesbyvirtueoffamily
history or adverse past history. Cannabis did not appear to
represent a sufficient or a necessary cause for the
development of psychosis but forms parts of a causal
constellation. Although the risk of developing psychotic
disorders was numerically small, this minority was
significant from both the clinical point of view and at the
population level. Arseneault et al. (2004) even estimated
that about 8% of schizophrenia could be prevented by
elimination of cannabis use in the population.
From the above review it can be concluded that cannabis
use might be causally related to development of
schizophrenia in an indirect way, but its use may precipitate
disorders in persons who are vulnerable to developing
psychosis and worsen the course of the disorder among
those who have already developed it.
CANNABIS AND AFFECT
Depression
The association between cannabis and depression has
received much less attention than potential links between
cannabis use and psychosis, probably because of depressed
CannabisandPsychopathology:Update2004
304
cannabis users seeking much less treatment and
underreporting of cannabis use by depressed patients
because of its illegal status.
Findings from the convenient community sample have
provided conflicting evidence on the association between
cannabis use and depression. Studies have shown that life
time use of cannabis increases the risk of depression in
females (Rowe et al., 1995), leads to greater suicidal
ideations(Fieldetal.,2001),increasesthelevelofdepression
with increasing involvement with cannabis use (Troisi et
al., 1998; Milich et al., 2000). On the contrary, no difference
was found between light and heavy users in the number of
depressive symptoms reported (Musty and Kaback, 1995),
depression and suicidal ideations (Galaif et al., 1998).
However, the above findings cannot be generalized because
of small sample size (Kouri et al., 1995), use of specific
populations like college students (Kouri et al., 1995), young
adult males (Green & Ritter, 2000), army draftees (Troisi,
1998), and lack of comparative groups (Troisi, 1998; Kouri
et al., 1995).
Studies from general population are more forthcoming about
the association between depression and cannabis use. The
Epidemiologic Catchment Area (ECA) and the National
Comorbidity Survey (NCS) reported association between
drug use disorders (which included cannabis and other
substance use disorders) and depression. Chen et al. (2002)
reanalyzed the NCS data with a specific focus on cannabis
use and major depressive disorder and found that greater
number of occasions of cannabis use were associated with
a higher risk of having experienced a major depressive
episode and that life time DSM III R cannabis dependence
was associated with a 3.4 times increased risk of major
depression. In another epidemiological study Grant et al.
(1995) found that people meeting criteria for DSM IV
cannabis abuse or dependence within the past year had 6.4
times the odds of meeting criteria for DSM IV major
depression than those who did not meet criteria for drug
abuse/ dependence. Degenhardt et al. (2001) examined the
relationship between different levels of cannabis use (no
use, use, abuse or dependence) and depression in the
Australian National Survey of Mental Health and found
that those who were more heavily involved with cannabis
use were more likely to meet criteria for DSM-IV mood
disorders. Similar findings have been reported from
adolescent population using cannabis (Rey et al., 2002).
Fergusson et al. (2003) found that adolescents who had
used cannabis 10 or more times by the age of 15-16 years
were more likely to also meet criteria for a mood disorder
at that age. A study of Patton et al. (2002) using a
representative cohort of young adults (aged 20-21 years)
in Victoria found that 68% of females who reported daily
cannabis use in the past year were depressed - an odds
ratio of 8.6 compared to non-users. Brook et al. (1998) in a
10-year follow up study of students aged 12-14 years found
that, reporting lifetime cannabis use had higher depression
scores, and 42% met criteria for DSM-IV major depression
at some point in their lives.
To summarize, there is increasing recent evidence that
regular cannabis use and depression occurs together more
often than we might expect by chance. While not all studies
have found a significant association, the weight of evidence
indicate that there is an increased chance of depression
among people who report heavy or problematic cannabis
use. The strength of the association is, however, only
modest,especiallyaftercontrollingforpotentialconfounding
variables; hence, it is still too early to rule out the hypothesis
that the association is due to common social, family and
contextual factors that increase risks of both heavy cannabis
use and depression (Degenhardt et al., 2003).
Accordingly, it is important to try to understand the basis of
this association between cannabis and depression. Three
hypothesis or possible theories of association are cannabis
use may be a contributory cause of depression; depression
may be a contributory cause of cannabis use and there is
no direct relationship between the two, with the observed
association explained by shared risk factors that increase
the risk of both disorders. Various cross-sectional and
longitudinal studies have examined the association and have
provided mixed evidence on the nature of the association
between cannabis use and depression. Cross-sectional
studies (Degenhardt et al., 2001; Rowe et al., 1995; Green
et al., 2000; Rey et al., 2002) have suggested that the
relationship can be explained by other factors such as the
use of other drugs. Longitudinal studies (Bovasso, 2001;
Merikangas & Angst, 1995; McGee et al., 2000) have
consistently indicated that the `self-medication' hypothesis
does not fit the pattern of cannabis use over time among
cohorts of adolescents and young adults. There is more
mixed evidence that heavy cannabis use increases the risk
of depression during follow-up, and this relationship is partly
but not completely explained by confounding variables. A
recent study by Sullivan et al. (2000) suggested that the
association between depression and cannabis dependence
may be explained partially by a high degree of overlap in
genetic factors predisposing to cannabis use and depressive
disorders, landing support to the hypothesis of shared risk
factors.
Sandeep Grover & Debasish Basu
305
Mania
Strakowski et al. (1996) reported that among the various
drugs of abuse, cannabis was more commonly associated
with mania, but the cannabis use did not affect the age of
onset of bipolar disorders. In a later study they showed
that duration of cannabis abuse was positively correlated
with duration of mania in new-onset bipolar disorder cases
(Strakowski et al., 2000). A recent study from India (Sarkar
et al., 2003) found that of the 244 patients with cannabis-
related diagnosis attending their centre, 12% received a
diagnosis of bipolar disorder - mania with psychosis, the
third common psychiatric condition after cannabis-induced
psychosis (21%) and schizophrenia (14%). Even the
commonest presentation of cannabis-induced psychosis in
their series was that of predominantly manic type. It is
possible that acute psychotic agitation with mania brings
the condition to early treatment attention. Interestingly,
cannabis has been anecdotally suggested to have mood-
stabilizing property in bipolar disorder (Grinspoon and
Bakalar, 1998), though no such studies are available.
Panic and anxiety
Anxiety is probably the commonest adverse reactions with
cannabis use, but most cases do not seek medical attention
and resolve spontaneously. Panic attacks constitute the most
frequent acute anxiety syndrome associated with cannabis
use (Thomas, 1993; Hall and Solowij, 1998), and 20-30%
of consumers present with acute and brief anxiety reactions
after smoking cannabis (Thomas, 1996). Other studies have
suggested that cannabis use may be associated with long-
lasting anxious symptomatology. In a study of persons who
regularly used cannabis for at least 10 years, Reilly et al.
(1998) found that 21% of these subjects had high levels of
state anxiety, and several case reports have described
cannabis-induced agoraphobia (Moran, 1986) and panic
disorder (Deas et al., 2000; Langs et al., 1997). A
speculative hypothesis regarding the association of cannabis
use and agoraphobia concerns the emergence of
anticipatory anxiety secondary to previous cannabis induced
panic-like symptoms. Few epidemiological investigations
have examined the comorbidity of anxiety disorders and
cannabis use in the general population. Using data from
the Australian National Survey of Mental Health and Well-
Being, Degenhardt et al. (2001) have reported an association
between cannabis use over the past year and increased
prevalence of anxiety disorders. Among individuals with
cannabis dependence, 17% had at least one anxiety disorder
compared to 5% of non-users. However, this association
disappeared after adjustment for demographic
characteristics, personality disorder and use of others drugs.
Although these studies suggest that an association may exist
between cannabis use and high levels of trait or state anxiety,
they are not informative concerning the direction of this
association (Compton et al., 2000; McGee et al., 2000;
Mueser et al., 1998). Thus, it is currently unclear if anxiety
is best conceptualized as a consequence of cannabis use in
vulnerable subjects, or conversely, if anxiety disorders may
favour cannabis use. An additional possibility is that both
cannabis use and anxiety disorders may be independently
induced by a shared risk factor, such as specific pre-existing
personality traits. Tournier et al. (2003) examined the
association of cannabis and anxiety and found that a
diagnosis of agoraphobia was significantly associated with
increased likelihood of cannabis use, independent of state
anxiety and other confounding factors. No evidence was
found for an anxiolytic or anxiogenic effect of cannabis in
daily life. This finding does not support the hypothesis that
subjects with high levels of anxiety use cannabis as a means
of self-medication. The association between agoraphobia
and cannabis use in daily life may be explained by
anticipatory anxiety secondary to previous cannabis-induced
panic-like symptoms. Importantly, cannabis-precipitated
panic disorder (both with or without agoraphobia) has been
shown to be as responsive to treatment with paroxetine as
panic disorder not associated with cannabis in a recent study
(Dannon et al., 2004).
CANNABIS AND OTHER PSYCHOPATHOLOGY
Amotivational syndrome
This presumed psychological syndrome is believed to be a
direct result of regular, heavy cannabis use and leaves those
so affected reduced in motivation and capacity for the usual
activities required for achievement and success in today's
world. Although many anti-cannabis campaigners accept,
a priori, the existence of the `amotivational syndrome', there
is considerable doubt as to whether it is an actual nosological
entity and whether all cannabis users are so affected. Some
authors do not consider it to be a single nosological entity
but rather a change in cognitive style emerging as a result
of cannabis's ability to facilitate a unique attentional state
favoured by those who have a higher than average level of
a personality factor referred to as `trait absorption'.
Exaggeration of the absorptive style of cognition through
cannabis use, when taken in the context of either a pre-
existing or a reactive depression, may be what has been
mistakenlycategorizedas`amotivationalsyndrome'(Nelson
et al., 1993)
CannabisandPsychopathology:Update2004
306
Echo or Flashback phenomenon
First reported by Keeler et al. (1968), these consist of re-
experiencing the various perceptual and cognitive effects
of the drug at a later date while not under its influence any
more. Although better known with hallucinogens, several
reports of cannabis flashback have also been published (for
details see Basu et al., 1994).
The newer understanding of the pharmacokinetics of
cannabinoids puts in doubt the existence of truly drug-less
flashback reactions. It seems quite possible that such
experiences may be the result of a continuous or intermittent
release of psychoactive component from adipose tissues
where they are stored during periods of active usage
(Thomas, 1993). According to the available data they occur
rarely and require a thorough differential diagnostic
evaluation in each individual case, especially to rule out
concomitant hallucinogen consumption (Fischer &
Taschner, 1991). A recent interesting case report from
Switzerland described a young man who offended a friend
without any objective reason. The report of the forensic
psychiatrist demonstrated that the offense was committed
under the influence of a cannabis flashback, proven
subsequently by laboratory detection of cannabinoids in
plasma during another flashback, thus highlighting the
medicolegalimplicationsofthephenomenon(Niveau,2002).
Cognitive impairments
The cognitive effects of long-term cannabis use and their
implications are insufficiently understood (Malhotra &
Basu, 1997). In contrast to the heated polarization that
characterized this debate, most well-designed studies concur
that modest cognitive deficits occur with heavy and
prolonged use of cannabis and persist at least several weeks
after stopping heavy cannabis use. The most consistent
findings are impairment of performance on tests of focused
attention,short-termmemory,perceptuomotorfunctions,and
`executive functions' such as set-shifting (Block and
Ghoneim, 1993; Fletcher et al., 1996; Solowij et al., 1995;
Pope & Yurgelun-Todd, 1996; Ehrenreich et al., 1999).
Solowij et al. (1995) further assessed the persistence of
the cognitive deficits after stopping cannabis and found
partial recovery of function but the past duration of cannabis
use continued to have an adverse effect on the ability to
effectively reject complex irrelevant information. There was
no indication of improvement with increasing length of
abstinence. It must, however, also be noted that the
impairment in these areas are mostly modest in magnitude,
often just reaching statistical significance. Their clinical
significance remains uncertain (Kouri et al., 1995; Pope &
Yurgelun-Todd, 1996).
Conclusion
What has changed in the last 10 years regarding cannabis
and psychopathology? It may depend upon how one looks
at the field. Stoics may not see a sea change in our
knowledge in this area. However, considering the very
substantive difficulties and challenges involved in clinical
research with cannabis (Basu et al., 1994), it is remarkable
that such a substantial volume of reasonably well-designed
research has taken place in the last decade. An important
area of stride has been the extending the locus of studies
from purely clinic-based and laboratory-based to the large,
community-based epidemiological studies conducted in the
1990s. This has helped us to confirm, refute or modify the
hypotheses formed from the clinic-based studies in many
cases. Another important area opened up during the last
decade is the establishment of an association between
cannabis use and non-psychotic psychopathology,
predominantly depression and anxiety. The nature of this
association, however, remains speculative. The need for
further research in this important area has been
demonstrated in a convincing manner. Mild residual
cognitive impairment resulting from chronic cannabis use
has also been demonstrated, although its clinical significance
remains to be demonstrated. The evidence and informed
opinion regarding cannabis withdrawal and the putative
`cannabis psychosis' seems to weigh against the latter at
least. Regarding the established association between
cannabis and schizophrenia, the research during the last
decade has shown that cannabis use might be causally
related to the later development of schizophrenia in an
indirect way in a few heavy users, but its use may
precipitate disorders in persons who are vulnerable to
developing psychosis and worsen the course of the disorder
among those who have already developed it. All these have
clear-cut academic as well as purely pragmatic implications.
The future decade should, hopefully, be able to throw new
light on this important area. Considering the fact that India
remains a traditional cannabis use country, the importance
of research from our country cannot be overestimated.
References
Allebeck, P., Adamsson, C., Engstrom, A., Rydberg, U. (1993) Cannabis
and schizophrenia: a longitudinal study of cases treated in Stockholm
County. Acta Psychiatrica Scandinavica, 88, 21-24./
American Psychiatric Association. (2000) Diagnostic and Statistical Manual
of Mental Disorders, Text Revised (DSM-IV TR). American Psychiatric
Association, Washington, DC.
Sandeep Grover & Debasish Basu
307
Andreasson, S., Allebeck, P., Engstrom, A., Rydberg, U. (1988) Cannabis
and schizophrenia: A longitudinal study of Swedish conscripts. Lancet, 2,
1483-1486.
Anthony, J.C., Helzer, J. (1991) Syndromes of drug abuse and dependence.
In: Robins, L.N., Regier, D.A. (Eds.), Psychiatric Disorders in America.
The Free Press, New York, pp. 116-154.
Arendt, M., Munk-Jorgensen, P. (2004) Heavy cannabis users seeking
treatment- prevalence of psychiatric disorders. Social Psychiatry and
Psychiatric Epidemiology, 39, 97-105.
Arseneault, L., Cannon, M., Poulton, R., Murray, R., Caspi, A., Moffitt,
T.E. (2002) Cannabis use in adolescence and risk for adult psychosis:
longitudinal prospective study. British Medical Journal, 325, 1212-1213.
Arseneault, L., Cannon, M., Witton, J., Murray, R.M. (2004) Causal
association between cannabis and psychosis: examination of the evidence.
British Journal of Psychiatry, 184, 110- 117.
Bamrah, J., Freeman, H., Goldberg, D. (1992). Epidemiology of
schizophrenia in Sanford, 1974-/84: changes in an urban community over
10 years. British Journal of Psychiatry, 159, 802-/810.
Basu, D., Malhotra, A., Bhagat, A., Varma, V.K. (1999) Cannabis psychosis
and acute schizophrenia: a case-control study from India. European
Addiction Research, 5, 71-73.
Basu, D., Malhotra, A., Varma, V.K. (1994) Cannabis related psychiatric
syndromes: A selective review. Indian Journal of Psychiatry, 36, 121-128.
Batel, P. (2000). Addiction and schizophrenia. European Psychiatry, 15,
115-/122.
Blanchard, J., Brown, S., Horan, W., Sherwood, A. (2000) Substance use
disorders in schizophrenia: review, integration, and a proposed model.
Clinical Psychological Review, 20, 207-/234.
Block, R.I. & Ghoneim, M.M. (1993) Effects of chronic marijuana use on
human cognition. Psychopharmacology, 110, 219-228.
Boutros, N.N. & Bowers, M.B. (1996) Chronic substance-induced psychotic
disorders: state of the literature. Journal of Neuropsychiatry and Clinical
Neurosciences, 8,262-269.
Bovasso, G. (2001) Cannabis abuse as risk factor for depressive symptoms.
American Journal of Psychiatry, 158, 2033-2037.
Brook, J.S., Cohen, P., Brook, D.W (1998) Longitudinal study of Co-
ocurring Psychiatric disorders and substance use. Journal of the American
Academy of Child and Adolescent Psychiatry, 37, 322-330
Budney AJ, Moore BA, Vandrey RG, Hughes JR. (2003) The time course
and significance of cannabis withdrawal. Journal of Abnormal Psychology,
112, 393-402.
Budney, A.J., Novy, P.L. & Hughes, J.R. (1999) Marijuana withdrawal
among adults seeking treatment for marijuana dependence, Addiction, 94,
1311-1321.
Chaudry, H.R., Moss, H.B., Bashir, A., Suliman, T. (1991) Cannabis psychosis
following bhang ingestion. British Journal of Addiction, 86, 1075-1081.
Chen, C. Y., Wagner, F & Anthony, J. (2002) Marijuana use and the risk of
major depression episode: epidemiological evidence from the United States
National Comorbidity Survey. Social Psychiatry and Psychiatric
Epidemiology, 37, 199-206.
Compton, W.M., Cottler, L.B., Phelps, D.L., Ben Abdallah, A., Spitznagel,
E.L. (2000) Psychiatric disorders among drug dependent subjects: are they
primary or secondary? American Journal on Addictions, 9, 126-134.
Cottler, L.B., Schuckit, M.A., Hlzer, J.E., Crowley, T., Woody, G., Nathan,
P., Hughes, J. (1995) The DSM-IV field trial for substance use disorders:
major results. Drug and Alcohol Dependence, 38, 59-69.
Cuffel, B.J., Heithoff, K.A., Lawson, W. (1993) Correlates of patterns of
substance abuse among patients with schizophrenia. Hospital Community
Psychiatry, 44 , 247-/251.
Dannon, P.N., Lowengrub, K., Amiaz, R., Grunhaus, L., Kotler, M. (2004)
Comorbid cannabis use and panic disorder: short term and long term follow-
up study. Human Psychopharmacology, 19, 97-101.
Deas, D., Gerding, L., Hazy, J. (2000) Marijuana and panic disorder. Journal
of the American Academy of Child and Adolescent Psychiatry, 39, 1467.
Degenhardt, L., Hall, W., Lynskey, M. (2003) Exploring the association
between cannabis use and depression. Addiction, 98, 1493-1504.
Degenhardt, L., & Hall, W., (2001) The association between psychosis and
problematical drug use among Australian adults: Findings from the National
Survey of Mental Health and Well-Being. Psychological Medicine, 31,
659-/668.
Degenhardt, L., Hall, W., Lynskey, M. (2001) The relationship between
cannabis use, depression and anxiety among Australian adults: findings
from the National Survey of Mental Health and Well-Being. Social Psychiatry
and Psychiatric Epidemiology, 36, 219-227.
Dixon, L., Haas, G., Wedien, P.J., Sweeney, J., Frances, A.J. (1990) Acute
effects of drug abuse in schizophrenic patients: clinical observations and
patients' self-report. Schizophrenia Bulletin, 16,69-79.
D'Souza, D.C., Perry, E., MacDougall, L., Ammerman, Y., Cooper, T.,
Wu, Y.T., Braley, G., Gueorguieva, R., Krystal, J.H. (2004) The
psychotomimetic effects of intravenous delta-9-tetrahydrocannabinol in
healthy individuals: implications for psychosis. Neuropsychopharmacology,
June 2, 2004 [Advance online publication]. Doi: 10.1038/sj.npp.1300496.
Ehrenreich, H., Rinn, T., Kunert, H.J., Moeller, M.R., Poser, W., Schilling,
L., Gigerenzer, G., Hoehe, M.R. (1999) Specific attentional dysfunction in
adults following early start of cannabis use. Psychopharmacology, 142,
295-301.
Fergusson, D.M., Horwood, L.J., Swain-Campbell, N.R. (2003) Cannabis
dependence and psychotic symptoms in young people. Psychological
Medicine, 33,15-21.
Field, T., Diego, M., Sanders, C. (2001) Adolescent suicidal ideation.
Adolescence, 36, 241-248.
Fischer, J., Taschner, K. L. (1991) Flashback following use of cannabis - a
review. Fortschrift Neurologie Psychiatrische, 59, 37-46 [article in German].
Fletcher, J.M., Page, B., Francis, D.J., Copeland, K., Naus, M.J., Davis,
C.M., Morris, R., Krauskopf, D., Satz, P. (1996) Cognitive correlates of
long-term cannabis use in Costa Rica men. Archives of General Psychiatry,
53, 1051-1057.
Fowler, I., Carr, V., Carter, N., Lewin, T. (1998) Patterns of current and
lifetime substance use in schizophrenia. Schizophrenia Bulletin, 24, 443-/
455.
Galaif, E., Chou, C.P. Sussman, S., Dent, C. (1998) Depression, suicidal
ideation, and substance use among continuation high school students. Journal
of Youth and Adolescence, 27, 275-299.
Geddes J, Black, R., Whalley, L., Eagles, J. (1993) Persistence of the
decline in the diagnosis of schizophrenia among first admissions to Scottish
hospitals from 1969 to 1988. British Journal of Psychiatry, 163, 620-626.
Georgotas, A. & Zeidenberg, P. (1979) Observations on the effects of four
weeks of heavy marijuana smoking on group interaction and behaviour.
Comprehensive Psychiatry, 20,427-432.
Gilbert, D.G., Gilbert, B.O., Schultz, V.I. (1998) Withdrawal symptoms:
individual differences and similarities across addictive behaviours. Personality
and individual Differences, 24, 351-356.
Gottesman, I.I. (1991) Schizophrenia Genesis: The origins of madness.
W.H. Freeman and Co, New York.
Grant, B.F. (1995) Comorbidity between DSM-IV drug use disorders and
major depression: results of a national survey of adults. Journal of Substance
Abuse, 7,481-497.
Green, B.E. & Ritter, C. (2000) Marijuana use and depression. Journal of
Health Social Behaviour, 41, 40-49.
CannabisandPsychopathology:Update2004
308
Greenberg, I., Mendelson, J.H., Kuehnle, J.C., Mello, N., Babor, T.F. (1976)
Psychiatric and behavioural observations of causal and heavy marijuana
users in a controlled research setting. Annals of the New York Academy of
Sciences, 282, 72-84.
Grinspoon, L., Bakalar, J.B. (1998) The use of cannabis as a mood stabilizer
in bipolar disorder: anecdotal evidence and the need for clinical research.
Journal of Psychoactive Drugs, 1998, 30, 171-177.
Grotenhermen, F. (2004) Pharmacology of cannabinoids.
Neuroendocrinology Letters, 25(1-2), 14-23.
Gruber, A.J., & Pope, H.G. (1994) Cannabis psychotic disorder. Does it
exist? American Journal of the Addiction, 3, 72-83.
Hall, W. (1998) Cannabis use and psychosis. Drug Alcohol Review, 17,
433-/444.
Hall, W. & Degenhardt, L. (2000) Cannabis use and psychosis: a review of
clinical and epidemiological evidence. Australian and New Zealand Journal
of Psychiatry, 34, 26-/34.
Hall, W. & Solowij, N. (1998) Adverse effects of cannabis. Lancet, 352,
1611-1616.
Hall, W., Degenhardt, L., Lynskey, M. (2001) The Health and Psychological
Consequences of Cannabis Use. Canberra: Australian Publishing Service.
Hall, W., Johnston, L., Donnelly, N. (1999) The epidemiology of cannabis
use and its consequences. The health effects of cannabis (Ed H. Kalan, W.
Hall & R. Smart) Addiction Research Foundation, Toronto, pp. 69-125.
Hambrecht, M., & Haefner, H. (2000) Cannabis, vulnerability, and the
onset of schizophrenia: an epidemiological perspective. Australian and
New Zealand Journal of Psychiatry, 34, 468-/475.
Hamera, E., Schneider, J.K., Deviney, S. (1995) Alcohol, cannabis, nicotine
and caffeine use and symptom distress in schizophrenia. Journal of Nervous
and Mental Disease, 183, 559-565.
Haney, M., Hart, CL., Vosberg S,K., Nasser J., Bennett A., Zubaran C.,
Foltin R.W., (2004) Marijuana withdrawal in human; Effects of oral THC
or divalproex, Neuropsychopharmacology, 29 : 158-70
Haney, M., Ward, Corner, S.D., Foltin, R.W., Rischman, M.W. (1999)
Abstinence symptoms following smoked marijuana in humans.
Psychopharmacology, 141, 395-404.
Harrison, G., Cooper, J., Gancarczyk, R. (1991) Changes in the
administrative incidence of schizophrenia. British Journal of Psychiatry,
159, 811-/816.
Imade, A.G.T. & Ebie, J.C. (1991). A retrospective study of symptom
patterns of cannabis-induced psychosis. Acta Psychiatrica Scandinavica, 8,
134-136.
Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Karten, A., Cooper,
J.E., Day, R., Bertelsen, A. (1992) Schizophrenia: manifestations, incidence
and course in different cultures. A World Health Organization Ten-Country
Study. Psychological Medicine Monograph, Suppl 20, 1-97.
Johns, A. (2001) Psychiatric effects of cannabis. British Journal of
psychiatry, 178, 116-122.
Jones, R.T., Benowitz, N., Bachman, J. (1976) Clinical studies of cannabis
tolerance and dependence. Annals of the New York Academy of Sciences,
282, 221-239.
Kavanagh, D.J. (1995) An intervention for substance abuse in schizophrenia.
Behaviour Change, 12, 20-30.
Keeler, M. H., Reifler, C. B., Liptzin, M.B. (1968) Spontaneous recurrence
of marihuana effects. American Journal of Psychiatry, 125, 384-386.
Kendell, R., Malcolm, D., Adams, W. (1993) The problem of detecting
changes in the incidence of schizophrenia. British Journal of Psychiatry,
162,212-/218.
Kouri, E., Pope, H., Yurgelun-Todd, D., Gruber, S. (1995) Attributes of
heavy vs. occasional marijuana smokers in a college population. Biological
Psychiatry, 38, 475-481.
Kouri, E.M., Pope, H.G., Lukas, S.E. (1999) Changes in aggressive behaviour
during withdrawal from long-term marijuana use. Psychopharmacology,
143, 302-308.
Langs, G., Fabish, H., Fabish, K., Zapotoczky, H.G., (1997) Can cannabis
trigger recurrent panic attacks in susceptible patients? European Psychiatry,
12, 415-419.
Linszen, D.H., Dingemans, P.M., Lenior, M.E. (1994) Cannabis abuse and
the course of recent-onset schizophrenic disorders. Archives of General
Psychiatry, 51, 273-/279.
Macfadden, W., Woody, G.E. (2000) Cannabis related disorders. In.
Comprehensive textbook of Psychiatry by Kaplan & Sadock (7th
edition).
990- 998.
Malhotra, A., Basu, D. (1997) Cannabis use and performance. In, Cannabis:
Health Damage? (Eds. Mohan, D. & Pal, H.). New Delhi, All India Institute
of Medical Sciences; 98-109.
Mathers, D.C, Ghodse, H., Caan, A.W., Scott, S.A. (1991) Cannabis use in
a large sample of acute psychiatric admissions. British Journal of Addiction,
86, 779-784.
McGee, R., Williams, S., Poulton, R., Moffitt, T. (2000) A longitudinal
study of cannabis use and mental health from adolescence to early adulthood.
Addiction, 95,491-503.
McGuire, P., Jones, R., Harvey, I., Williams, M., McGuffin, P., Murray, R.
(1995) Morbid risk of schizophrenia for relatives of patients with cannabis
associated psychosis. Schizophrenia Research, 15, 277-281.
McKay, D.R., Tennant, C.C. (2000) Is the grass greener? The link between
cannabis and psychosis. The Medical Journal of Australia, 172, 284-/286.
Merikangas, K. & Angst, J. (1995) The challenge of depressive disorders
in adolescence. In: Rutter, M., ed. Psychosocial Disturbances in Young
People, Cambridge: Cambridge University Press.
Milich, R., Eynam, D., Zimmerman, R., Logan, T., Mattin, C., Leukefield,
C., Portis, C., Miller, I., Clayton, R. (2000) Difference in young adult
psychopathology among drug abstainers, experimenters, and frequent users.
Journal of Substance Abuse, 11, 69-88.
Moran, C. (1986) Depersonalization and agoraphobia associated with
marijuana use. British Journal of Medical Psychology, 59,187-196.
Mueser, K., Yarmnold, P., Levinson, D., Singh, H., Bellack, A., Kee, K.,
Morrison, R., Yadalam, K. (1990) Prevalence of substance abuse in
schizophrenia: demographic and clinical correlates. Schizophrenia Bulletin
16, 31-/56.
Mueser, K.T., Beflack, A.S., Blanchard, J.J. (1992) Comorbidity and
substance abuse: Implications for treatment. Journal of Consulting and
Clinical Psychology, 60, 845-856.
Mueser, K.T., Drake, R.E., Wallach, M.A. (1998) Dual diagnosis: a review
of etiological theories. Addictive Behaviour, 23, 717-/734.
Munk-Jorgensen, P. (1995) Decreasing rates of incident schizophrenia
cases in psychiatric services: a review of the literature. European Psychiatry,
10,129 -/141.
Musty, R.E., Kaback, L. (1995) Relationship between motivation and
depression in chronic marijuana users. Life Sciences, 56, 2151-2158.
Negrete, J.C., Knapp, W.P., Douglos, D.E., Bruce-smith, W. (1986) Cannabis
affects the severity of schizophrenic symptoms: results of a clinical survey.
Psychological Medicine, 16, 515-520.
Nelson, P. L. (1993). A Critical Review of the Research Literature
Concerning Some Biological and Psychological Effects of Cannabis, In
Advisory Committee on Illicit Drugs (Eds.), Cannabis and the Law in
Queensland: A Discussion Paper, Criminal Justice Commission, Brisbane,
Australia, 113-152.
Niveau G. (2002) Cannabis-related flash-back, a medico-legal case.
Encephale, 28, 77-79.
Sandeep Grover & Debasish Basu
309
Patton, G., Coffey, J., Degenhardt, L., Lynskey, M., Hall, W. (2002)
Cannabis use and mental health in young people: cohort study. British
Medical Journal, 325, 1195-1198.
Poole, R., & Brabbins, C. (1996) Drug induced psychosis. British Journal of
Psychiatry, 168, 135-138.
Pope, H.G. Jr, Yurgelun-Todd, D. (1996) The residual cognitive effects of
heavy marijuana use in college students. Journal of American Medical
Association, 275, 521-527.
Reilly, D., Didcott, P., Swift, W., Hall, W. (1998) Long-term cannabis use:
characteristics of users in an Australian rural area. Addiction, 93, 837-846.
Rey, J.M., &Tennant, C.C. (2002) Cannabis and mental health. British
Medical Journal, 325, 1183-1184.
Rey, J., Sawyer, M., Raphael, B., Patton, G., Lynsky, M. (2002) Mental
Health of teenagers who use cannabis: results of an Australian survey.
British Journal of Psychiatry, 180, 216-221.
Rolfe, M., Tang, M., Sabally, S., Todd, J., Sam, E., Hatib N'Jie, A. (1993)
Psychosis and cannabis abuse in the Gambia: a case-control study. British
Journal of psychiatry 1993, 163, 798-/801.
Rosenthal, R. (1998) Is schizophrenia addiction prone? Current Opinion
in Psychiatry, 11, 45-/48.
Rottanburg, D., Robins, A.H., Ben-Arie, O., Teggin, A., Elk, R. (1982)
Cannabis-associated psychosis with hypomanic features. Lancet, 2, 1364-
1366.
Rowe, M., Fleming, M., Barry, K., Manwell, I., & Kropp. S. (1995)
Correlates of depression in primary care. Journal of Family Practice, 41,
551-558.
Sarkar, J., Murthy, P., Singh, S.P. (2003) Psychiatric morbidity of cannabis
abuse. Indian Journal of Psychiatry, 45, 182-188.
Schuckit, M.A. (1994) Can marijuana cause a long-lasting psychosis? Drug
Abuse and Alcoholism Newsletter, 23, 1-4.
Solowij, N., Michie, P.T., Fox, A.M. (1995) Differential impairments of
selective attention due to frequency and duration of cannabis use. Biological
Psychiatry, 37,731-739.
Smit, F., Bolier, F., Cuijjpers, P. (2004) Cannabis use and the risk of later
Schizophrenia : a review Addiction, 99, 425-30.
Solowij, N. (1995) Do cognitive impairments recover following cessation
of cannabis use? Life Sciences, 56, 2119-2126.
Stahl, S.M. (1996) Essential Psychopharmacology. Cambridge University
Press, Cambridge.
Stephens, R.S., Roffman, R.A., Simpson, E.E. (1993) Adult marijuana
users seeking treatment. Journal of Consulting and Clinical Psychology,
61, 100-114.
Strakowki, S.M., McElroy, S.L., Keck, P.E. Jr., West, S.A. (1996) The
effects of antecedent substance abuse on the development of first episode
mania. Journal of Psychiatric Research, 30, 59-68.
Strakowski, S.M., DelBello, M.P., Fleck, D.E., Arndt, S. (2000) The impact
of substance abuse on the course of bipolar disorder. Biological Psychiatry.
2000, 48, 477-485.
Sullivan, P.F., Neale, M.C., Kendler, K.S. (2000) Genetic epidemiology of
major depression: review and meta-analysis. American Journal of Psychiatry,
157, 1552-1562.
Suvisaari, J., Haukka, J., Tanskanen, A., Lonnqvist, J. (1999) Decline in
the incidence of schizophrenia in Finnish birth cohorts born from 1954 to
1965. Archives of General Psychiatry 56, 733-/740.
Thomas, H. (1993) Psychiatric symptoms in cannabis users. British Journal
of Psychiatry, 163, 141-149.
Thomas, H. (1996) A community survey of adverse effects of cannabis
use. Drug and Alcohol Dependence, 42, 201-207.
Thornicroft, G., Meadows, G., Politi, P. (1992) Is cannabis psychosis a
distinct category? European Psychiatry, 7,277-282.
Thornicroft, G. (1990) Cannabis and psychosis: is there epidemiological
evidence for an association? British Journal of Psychiatry, 157, 25 -/33.
Tien, A.Y., Anthony, J.C. (1990) Epidemiological analysis of alcohol and
drug use as risk factors for psychotic experiences. Journal of Nervous and
Mental Disease, 178, 473-480.
Tournier, M., Sorbara, F., Gindre, C., Swendsen, J.D., Verdoux, H. (2003)
Cannabis use and anxiety in daily life: a naturalistic investigation in a non-
clinical population. Psychiatry Research , 118, 1-8.
Troisi, A., Pasini, A., Saracco, M. & Spalletta, G. (1998) Psychiatric
symptoms in male cannabis users not using other illicit drugs. Addiction,
93, 487-492.
Van Os, J., Bak, M.,Hanssen, M., Bijl, R.V., De Graff, R., Verdoux, H.
(2002) Cannabis use and psychosis: a longitudinal population-based study.
American Journal of Epidemiology, 156, 319-327.
Weiser, M., Knobler, H.Y., Noy, S., Kaplan, Z. (2002) Clinical characteristics
of adolescents later hospitalized for schizophrenia. American Journal for
Medical Genetics, 114, 949-955.
Wiesbeck, G.A., Schuckit, M.A., Kalmi J.A. Tipp, J.E., Bucholz, K.K.,
Smith T. (1996) An evaluation of the history of a marijuana withdrawal
syndrome in a large population. Addiction, 91, 1469-1478.
World Health Organization (1992) ICD-10 Classification of Mental and
Behavioural Disorders: Clinical Description and Diagnostic Guidelines.
Geneva: World Health Organization.
Wray, I. & Dickerson, M.G. (1981) Cessation of high frequency gambling
and withdrawal symptoms. British Journal of Addiction, 76, 401-405.
Zammit, S., Allebeck, P., Andreasson, S., Lundberg, I., Lewis, G. (2002)
Self-reported cannabis use as a risk factor for schizophrenia further analysis
of the 1969 Swedish conscript cohort, British Medical Journal, 325, 1199-
1201.
Ziedonis, D., Trudeau, K. (1997) Motivation to quit using substances among
individuals with schizophrenia: implications for a motivation-based
treatment model. Schizophrenia Bulletin, 23, 229-238.
CannabisandPsychopathology:Update2004