Schizophrenia cannabis

Dean, B., Bradbury, R., and Copolov, D.L., Cannabis-sensitive dopaminergic markers in postmortem central nervous system changes in schizophrenia, Biol. Psychiatry, 53, 585, 2003. 

Andreasson S, Allebeck P, Engstrom A and Rydberg U (1987). Cannabis and schizophrenia A longitudinal study of Swedish conscripts. Lancet, 2, 1483-1486. 

Zammit S, Allebeck P, Andreasson S, Lundberg I and Lewis G (2002). Self reported cannabis use as a risk factor for schizophrenia in Swedish conscripts of 1969 Historical cohort study. British Medical Journal, 325, 1199-1201. 

Chronic use has been associated with an "amotivational syndrome" characterized by loss of interest in social activities, school, work, or other goal-directed activities. Cannabis use is cited as the cause of this phenomenon, but there is no evidence to support any causal relationship. There is evidence, however, that the symptoms of the "amotivational syndrome" are secondary to depression (Musty and Kraback 1995). In contrast to ethanol, there is no evidence to support that cannabis causes an increase in violent behavior (Murray 1986). However, cannabis use may be contraindicated in those with preexisting psychiatric disturbances such as bipolar disorder or schizophrenia. 

Psychosocial morbidity association. Cannabis dependence is a prevalent comorbid substance use disorder among patients early in the course of a schizophrenia-spectrum disorder. Among 29 eligible patients, 18 participated in the study. First-episode patients with comorbid cannabis dependence (n = 8) reported significantly greater childhood physical and sexual abuse compared with those without comorbid cannabis dependence (n = 10). The result indicated the preliminary evidence of an association between childhood maltreatment and cannabis dependence among this especially vulnerable population. Child-... 

Arendt M, Rosenberg R, Foldager L, Perto G Minuk-Jorgensen P (2005). Cannabis-induced psychosis and subsequent schizophrenia-spectrum disorders follow-up study of 535 incident cases. British Journal of Psychiatry, 187, 510-15... 

Several studies have investigated how cannabis use and/or the endocannabinoid system itself may be associated with schizophrenia. Although the endogenous cannabinoid system might be implicated in schizophrenia, relatively few studies have analyzed receptor expression or binding in postmortem brain. 

Using in situ radioligand binding, another study reported an increased CB1 density in DLPFC, an effect that was not dependent on previous cannabis use (Dean et al., 2001). In addition, an increased CB1 receptor density in the striatum has been reported, which may have been associated with recent cannabis intake (Dean et al., 2001). Postmortem studies of cannabinoid receptor expression, in particular for the CB1 receptor in PCC, ACC and DLPFC support the involvement of the cannabinoid system in the pathophysiology of schizophrenia. 

Dean B, Sundram S, Bradbury R, Scarr E, Copolov D. 2001. Studies on [3H] CP-55940 binding in the human central nervous system Regional specific changes in density of cannabinoid-1 receptors associated with schizophrenia and cannabis use. Neuroscience 103 9-15. 

Olanzapine has been compared with haloperidol in cannabis-induced psychosis (54), schizoaffective disorder (55), first-episode psychosis (56), and treatment-resistant schizophrenia (57) the two last studies were reanalyses of data from large clinical trials promoted by the manufacturers, Eli Lilly. In all cases olanzapine was better than haloperidol at reducing BPRS scores, but in patients with cannabis-induced psychotic disorders they were similar. Increased appetite was consistently reported more often in olanzapine-treated patients and extrapyramidal signs more often in those treated with haloperidol. 

In 10 patients, schizophrenia was acutely worsened after cannabis use, despite verified adequate depot treatment with neuroleptic drugs (637). 

Knudsen P, Vilmar T. Cannabis and neuroleptic agents in schizophrenia. Acta Psychiatr Scand 1984 69(2) 162-74. 

A 17-year-old man, with a history of paranoid schizophrenia and irregular abuse of cannabis and alcohol, took risperidone (202). Starting at 0.5 mg/day, the dose was titrated up to 4 mg/day over 3 weeks. In a few weeks, he stopped taking risperidone because of a recurrent inability to ejaculate, despite normal libido, erection, and sense of orgasm he also had difficulty in urinating. These effects disappeared after drug withdrawal. However, risperidone was restarted because of relapse of schizophrenia, and the ejaculatory disturbance recurred within a few days. 

The causal relation between cannabis abuse and schizophrenia is controversial. Cannabis abuse, and particularly heavy abuse, can exacerbate symptoms of schizophrenia and can be considered as a risk factor eliciting relapse in schizophrenia (110). Chronic cannabis use can precipitate schizophrenia in vulnerable individuals (111). 

Neurotrophins, such as nerve growth factor and brain-derived neurotrophic factor (BDNF), are implicated in neuronal development, growth, plasticity, and maintenance of function. Neurodevelopment is impaired in schizophrenia and vulnerable schizophrenic brains may be more sensitive to toxic influences. Thus, cannabis may be more neurotoxic to schizophrenic brains than to nonschizophrenic brains when used chronically. In 157 drug-naive first-episode schizophrenic patients there were significantly raised BDNF serum concentrations by up to 34% in patients with chronic cannabis abuse or multiple substance abuse before the onset of the disease (114). Thus, raised BDNF serum concentrations are not related to schizophrenia and /or substance abuse itself but may reflect cannabis-related idiosyncratic damage to the schizophrenic brain. Disease onset was 5.2 years earlier in the cannabis-consuming group. 

People with pre-existing coronary artery disease may have an increased incidence of attacks of angina (146). In individuals who are vulnerable to schizophrenia, cannabis can precipitate psychoses or aggravate schizophrenia. The control of epilepsy may be impaired. Users undergoing anesthesia may react unexpectedly and may have enhanced nervous system depression. Because of impairment of judgement and psychomotor performance, users should not drive or operate machinery for at least 24 hours after administration. 

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