Cannabis psychosis (Acute and Long term) Flashcards
What are examples of temporary psychotic symptoms that one may develop?
Hallucinations
Delusions
With temporary psychotic symptoms, around how long do hallucinations and delusions last?
Resolve themselves within hours or a few days without any help
Often psychotic problems are long lasting and can develop into what?
Severe mental illness. These cases can be complex and depend of the individuals symptoms, including their use of cannabis which could be a possible trigger for psychosis
How is C-psychosis caused?
Increased dopaminergic drive
Prolonged and excessive stimulation of the CB1 receptor
How does increased dopaminergic drive get elicited?
Cannabinoids
How does increased dopaminergic drive cause an increase in positive psychotic symptoms?
The increased drive get elicited bg cannabinoids which underlie the addictive/ misuse property of the drug and therefore increases positive psychotic symptoms induced by THC
(Lynch et al 2012)
The excessive stimulation of what receptor causes a disruption to the endocannabinoid system function?
Murray et al 2007)
The CB1 receptor
Several novel lines of evidence exist to suggest a role of cannabis kids and their receptors in the pathophysiology of schizophrenia (Lynch et al 2012)
Several novel lines of evidence exist to suggest a role of cannabis kids and their receptors in the pathophysiology of schizophrenia (Lynch et al 2012)
Has been proposed that this CB1 receptor overstimulation may be a contributing factor in triggering THC- induced psychosis
(Morrison and Murray 2009)
Has been proposed that this CB1 receptor overstimulation may be a contributing factor in triggering THC- induced psychosis
(Morrison and Murray 2009)
Developmental psychopathology through early onset use show dysfunction in what?
Low extracellular GABA from disruption of the CB system resulting in poor tone in the PFC
(EGERTON ET AL 2006)
Early exposure CB agonist causes a higher expression of dopamine and dysfunction in other neural transmitters such as GABA, serotonin, glutamate and acetylcholine leading to the endocannabinoid hypothesis of schizophrenia (working memory problems, cognitive deficits and startle reflex).
Theorised early onset use in adolescents could have long term consequences (Muller-Vahl, 2008, Burns, 2013)
Early exposure CB agonist causes a higher expression of dopamine and dysfunction in other neural transmitters such as GABA, serotonin, glutamate and acetylcholine leading to the endocannabinoid hypothesis of schizophrenia (working memory problems, cognitive deficits and startle reflex).
Theorised early onset use in adolescents could have long term consequences (Muller-Vahl, 2008, Burns, 2013)
What is the proposed model for vulnerability for cannabis psychosis (Burns, 2013) ?
Proposed model for vulnerability for cannabis psychosis (Burns 2013)
Factors that are key to the various pathways include:
Early initiation/ lifetime use of cannabis versus recent cannabis use
Underlying genetic vulnerability to psychosis/schizophrenia
Ongoing cannabis use after psychosis onset versus stopping cannabis use
Proposed model for vulnerability for cannabis psychosis (Burns 2013)
Factors that are key to the various pathways include:
Early initiation/ lifetime use of cannabis versus recent cannabis use
Underlying genetic vulnerability to psychosis/schizophrenia
Ongoing cannabis use after psychosis onset versus stopping cannabis use
