appunti del
dott. Claudio Italiano, internista
Gli studi appresso riportati
vogliono rispondere al quesito che un nostro gentile navigatore
ci pone, se cioè sia possibile e provato scientificamente, che
l'abuso del fumo di canna possa slatentizzare la schizofrenia.
Alcuni autori sembrano confermare questa ipotesi, che cioè
abusando droghe, in soggetti già predisposti geneticamente,
l'abuso della droga possa slatentizzare una psicosi latente. I
passi salienti degli abstracts sono stati riportati in rosso.
Cannabis abuse and risk for psychosis in a prodromal sample.
Kristensen K,
Cadenhead KS.
Department of Psychiatry, 0810, University of California San Diego,
9500 Gilman Drive, La Jolla, CA 92093-0810, USA.
.
The goal of the present study was to examine the rate of cannabis
use among participants in the Cognitive Assessment and Risk
Evaluation (CARE) Program, a longitudinal program for individuals
who are "at risk" for developing a psychotic disorder. Cannabis
abuse was assessed in 48 individuals identified as at risk for
psychosis based on subsyndromal psychotic symptoms and/or family
history. At 1 year follow-up, 6 of the 48 (12.5%) at risk subjects
had made the transition to psychosis. Of the 32 subjects who had no
use or minimal cannabis use, one subject (3.1%) converted to
psychosis. Of the 16 subjects who met criteria for cannabis
abuse/dependence, five (31.3%) converted to psychosis. The results
show a significant association between cannabis abuse and conversion
to psychosis in this sample. Nicotine use was also found to be
significantly associated with later conversion. The significant
associations between cannabis and nicotine abuse and conversion to
psychosis in individuals at risk for schizophrenia suggest that
early identification and intervention programs should screen for and
provide education about the deleterious effects of these substances.
Cannabis use and psychotic disorders: an update.
Hall W,
Degenhardt L,
Teesson M.
Office of Public Policy and Ethics, Institute for Molecular
Bioscience University of Queensland Australia. w.hall@imb.uq.edu.au
This paper evaluates three hypotheses about the relationship between
cannabis use and psychosis in the light of recent evidence from
prospective epidemiological studies. These are that: (1) cannabis
use causes a psychotic disorder that would not have occurred in the
absence of cannabis use; (2) that cannabis use may precipitate
schizophrenia or exacerbate its symptoms; and (3) that cannabis use
may exacerbate the symptoms of psychosis. There is limited support
for the first hypothesis. As a consequence of recent prospective
studies, there is now stronger support for the second hypothesis.
Four recent prospective studies in three countries have found
relationships between the frequency with which cannabis had been
used and the risk of receiving a diagnosis of schizophrenia or of
reporting psychotic symptoms. These relationships are stronger in
people with a history of psychotic symptoms and they have persisted
after adjustment for potentially confounding variables. The absence
of any change in the incidence of schizophrenia during the three
decades in which cannabis use in Australia has increased makes it
unlikely that cannabis use can produce psychoses that would not have
occurred in its absence. It seems more
likely that cannabis use can precipitate schizophrenia in
vulnerable individuals. There is also reasonable evidence for the
third hypothesis that cannabis use exacerbates psychosis.
Familial predisposition for psychiatric disorder: comparison of
subjects treated for cannabis-induced psychosis and
schizophrenia.
Arendt M,
Mortensen PB,
Rosenberg R,
Pedersen CB,
Waltoft BL.
Centre for Psychiatric Research, Aarhus University Hospital,
Skovagervej 2, Risskov, 8240 Risskov, Denmark.
mca@psykiatri.aaa.dk
.
CONTEXT: Cannabis-induced psychosis is considered a distinct
clinical entity in the existing psychiatric diagnostic systems.
However, the validity of the diagnosis is uncertain. OBJECTIVES: To
establish rate ratios of developing cannabis-induced psychosis
associated with predisposition to psychosis and other psychiatric
disorders in a first-degree relative and to compare them with the
corresponding rate ratios for developing schizophrenia spectrum
disorders. DESIGN: A population-based cohort was retrieved from the
Danish Psychiatric Central Register and linked with the Danish Civil
Registration System. History of treatment of psychiatric disorder in
family members was used as an indicator of predisposition to
psychiatric disorder. Rate ratios of cannabis-induced psychosis and
schizophrenia associated with predisposition to psychiatric
disorders were compared using competing risk analyses. SETTING:
Nationwide population-based sample of all individuals born in
Denmark between January 1,1955, and July 1, 1990 (N = 2,276,309).
Patients During the 21.9 million person-years of follow-up between
1994 and 2005, 609 individuals received treatment of a
cannabis-induced psychosis and 6476 received treatment of a
schizophrenia spectrum disorder. RESULTS: In general, the rate
ratios of developing cannabis-induced psychosis and schizophrenia
spectrum disorder associated with predisposition to schizophrenia
spectrum disorder, other psychoses, and other psychiatric disorders
in first-degree relatives were of similar magnitude. However,
children with a mother with schizophrenia were at a 5-fold increased
risk of developing schizophrenia and a 2.5-fold increased risk of
developing cannabis-induced psychosis. The risk of a schizophrenia
spectrum disorder following a cannabis-induced psychosis and the
timing of onset were unrelated to familial predisposition.
CONCLUSIONS: Predisposition to both
psychiatric disorders in general and psychotic disorders
specifically contributes equally to the risk of later treatment
because of schizophrenia and cannabis-induced psychoses.
Cannabis-induced psychosis could be an early sign of schizophrenia
rather than a distinct clinical entity.
.
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