Schizophrenia and Cannabis

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Do patients think cannabis causes schizophrenia? - A qualitative study on the causal beliefs of cannabis using patients with schizophrenia

Do patients think cannabis causes schizophrenia? - A qualitative study on the causal beliefs of cannabis using patients with schizophrenia

negated a causal link between schizophrenia and canna- bis. Thus, we suggest that clinicians consider these find- ings in their work with patients suffering from such co-occurring disorders. Frequently, cannabis use of patients with schizophrenia has only been seen as a mis- behavior leading to an untoward treatment outcome. Therefore, it often resulted and still results in withhold- ing treatment or excluding such patients from certain treatment settings like day-care facilities or fulltime hos- pitals (RS, personal communication). In view of the beliefs surrounding cannabis use described above the majority of this patient group may not understand such an intervention. Rather patients may construe this thera- peutic strategy as social rejection on the part of their therapists, which has been shown to significantly contri- bute to experiences of stigma and discrimination [29,30]. Stigma, then, has been found to act as an environmental risk factor for the onset and course of schizophrenia [31]. Further, treatment approaches which do not take account of patients ’ subjective illness models are not likely to enhance early help-seeking for psychosis and treatment collaboration [32]. Moreover, given the missing scientific evidence of deleterious effects of cannabis use on the course of schizophrenia [3], we think that such confron- tational approaches cause additional harm to this already heavily burdened patient group. In conclusion patients ’ causal attributions and individual recovery strategies should be routinely explored in the context of the doc- tor-patient-relationship.
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A clinical comparison of schizophrenia with and without pre-onset cannabis use disorder: a retrospective cohort study using categorical and dimensional approaches

A clinical comparison of schizophrenia with and without pre-onset cannabis use disorder: a retrospective cohort study using categorical and dimensional approaches

Socio-demographic characteristics, age at onset, num- ber of hospital admissions and personal history of sui- cide attempts were recorded on the basis of both medical notes and data extracted from the DIGS. Patients were also assessed for lifetime cannabis and other sub- stance use, and were asked to state precisely when use had begun, its duration and the mode of consumption. Patients were assigned to the “pre-onset CUD” group if they met lifetime DSM-IV-R criteria for cannabis use disorders (cannabis abuse or dependence) before or at the time of schizophrenia onset. Otherwise, they were assigned to the “no pre-onset” CUD group. Patients with other substance use disorders were excluded with an exception for tobacco smoking. Age at onset of schizo- phrenia was defined as the age at which the patient first met DSM-IV-R criteria for schizophrenia, according to medical case notes and interviews.
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Multimodal neuroimaging of frontal white matter microstructure in early phase schizophrenia: the impact of early adolescent cannabis use

Multimodal neuroimaging of frontal white matter microstructure in early phase schizophrenia: the impact of early adolescent cannabis use

The brain region of interest for this study is the left superior longitudinal fasciculus (SLF), a large bundle of white matter fibre tract located in the frontal lobe, trav- elling between the dorsal prefrontal and caudal-inferior parietal regions of the brain. Frontal regions undergo substantial myelination during the periods of adoles- cence and early adulthood [17,18], especially in the bilateral SLF [19]. Abnormal maturation of the SLF in adolescence may thus be crucial in the development of schizophrenia. Several DTI studies have found ab- normalities in the SLF in schizophrenia as well as in asymptomatic cannabis users, as reviewed below. We will investigate the SLF microstructure in early phase schizophrenia (less than five years since diagnosis) [20], focusing on the potential role of early adolescent
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Atypical course in severe catatonic schizophrenia in a cannabis dependent male adolescent: a case report

Atypical course in severe catatonic schizophrenia in a cannabis dependent male adolescent: a case report

Our experience with this case illustrates that adolescent schizophrenia can be challenging to classify in individuals with a history of smoking cannabis. The onset was acute with delusions and hallucinations, supporting a cannabis- related or possibly affective psychosis. Owing to the clin- ical picture, our patient was diagnosed with schizophrenia despite a history of heavy cannabis abuse. A catatonic sub- type was determined given the motor immobility, extreme negativism and mutism, and bizarre postures and facial expressions [15]. NMS was ruled out because changes in his level of consciousness, muscular rigidity (bizarre body postures), and autonomic instability (urine incontin- ence and salivation) began before therapeutic doses of antipsychotic medication were prescribed. The absence of leukocytosis, hyperthermia, and tachycardia along with a normal EEG supports other diagnostic alternatives [16]. After 3.5 years of social adjustment without psychiatric treatment, our patient’s first psychotic episode was more likely to be classified as cannabis-induced, despite the atyp- ically pronounced duration and severity of that first epi- sode [13, 14]. However, after relapsing into pronounced psychotic symptoms without any signs of substance abuse, he was re-diagnosed with catatonic schizophrenia.
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Schizophrenia like Cognitive, Trait and DNA Markers in Regular Cannabis Users

Schizophrenia like Cognitive, Trait and DNA Markers in Regular Cannabis Users

The current study aimed to address these issues and further explore the link between smoking cannabis and schizophrenic-like behaviours, by testing a group of cannabis users versus non- cannabis users, on LI and KB performance, to see if there are subtle differences between both groups. Based on the literature reviewed in Chapter 1, it is clear that cannabis use in some people may contribute to schizophrenia. Cannabis use is also frequently associated with acute and sub-acute psychotic-like experiences; in normal, non-pathologised individuals as well as in clinical populations. Such effects may be underpinned by alterations in dopamine produced by THC; acutely, sub-acutely and chronically. If cannabis use is producing such effects at a stable level, elevating schizotypy in many, leading to more serious disturbance in others, then we should also see noticeable differences amongst cannabis users, in other behaviours and cognitive processes affected by psychosis. As such, the filtering out of irrelevant information typically seen in normal healthy adults, but which has been shown to be disrupted in people diagnosed with schizophrenia, those administered with dopamine agonists and high schizotypy scorers may also be significantly affected by regular/frequent cannabis use. The hypothesis therefore is that cannabis users will show moderate impairments on the associative learning tasks for selective attention, namely LI and KB. In addition, both cannabis users and control participants will be classified as either having high or low psychotic-like traits from using their scores on the SPQ-B measure (Raine & Benishay, 1995), and this will be explored to look at differences between these groups on their LI and KB performance. Previous research has demonstrated that individual differences in psychotic-like personality traits results is linked to disrupted associative learning, namely for the LI and KB tests. Therefore it is predicted that those scoring higher for psychotic-like traits will also showed reduced LI and KB performance.
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Two cases of "cannabis acute psychosis" following the administration of oral cannabis

Two cases of "cannabis acute psychosis" following the administration of oral cannabis

retrospectively 200 patients hospitalized after the inges- tion of large dose of cannabis between 1963 and 1968. Other reports in different countries showed similar fea- tures after bhang ingestion [3,15]. It usually results from taking large amount of the drug, generally in food or drink. The symptoms have some similarity with paranoid schizophrenia, which could raise the hypothesis that " symptoms of schizophrenic illness might be caused by an abnormal over-activity of endogenous cannabinoid mechanism in the brain" (Iversen [10] citing Emrich [16]). However because of the poor quality of informa- tion on previous cannabis experience, cannabis dose intake, other drug consumption and previous psychiatric comorbidity, some commentators have criticized these case series [12,17,18]. Case-control studies have been conducted comparing people with cannabis psychosis with persons suffering from schizophrenia [19-21]. How-
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Cannabis and Mental Health: Put into context

Cannabis and Mental Health: Put into context

Although most people treated for schizophrenia during the follow-up period did not use cannabis during adolescence, those who did use cannabis heavily (i.e. more than 50 times before the age of 18) were six times more likely to be hospitalised for schizophrenia by the age of 33 than those who had not used cannabis. Moreover, those who had used cannabis more than ten times (but less than 50 times) were three times more likely to be hospitalised for schizophrenia. However, these represent crude values that do not take confounding factors into account (see Appendix 1 for an explanation of these concepts). Once psychiatric factors, social and family background, and alcohol, tobacco and inhalant use were controlled for, the relative risk associated with being hospitalised for schizophrenia among those who had used cannabis at least ten times was reduced to just over two times and was no longer statistically significant. The adjusted relative risk for those who had used cannabis more than 50 times was not reported (for explanations of relative risks and odds ratios, including the concept of adjustment, see Appendix 1).
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Harm reduction-the cannabis paradox

Harm reduction-the cannabis paradox

The use of cannabis – and any mind-altering drug – by young developing minds rightfully remains an area of focus and concern. For example, is there a relationship between cannabis use and schizophrenia? Schizophrenia is characterized by distortions of reality, disturbances of language and thought processes, and social withdrawal. Certainly, aspects of cannabis intoxication parallel these symptoms. It is feared that cannabis can precipitate this state [129], especially in susceptible individuals [130]. It has been suggested that schizophrenics (or potential schizophrenics) fall into two categories with respect to cannabis use [131]. One group may find symptomatic relief in the use of cannabis, while the other may actually take the risk of inducing the onset of the disease. The com- plexities of this issue are illuminated by the unpredictable behavior of interacting complex systems such as the nerv- ous and immune systems, as will be considered below. In an important recent study, De Marchi et al [132], exam- ined the endocannabinoid levels in healthy volunteers and compared them to that of schizophrenic patients, both before and after successful antipsychotic treatment. Patients suffering with acute disease had significantly higher anandamide levels in their blood than did the nor- mal individuals or patients in clinical remission. Might these elevated cannabinoid levels be contributing to the disease symptoms, and what might be causing them? Can- nabinoids act homeostatically across biological subsys- tems. A possible immune involvement in schizophrenia has long been suspected, and immunological parameters have been implicated in the disease. For example, there is an inverse correlation between schizophrenia and rheu- matoid arthritis; an individual generally does not get both illnesses [133]. Interestingly, schizophrenia has been cor- related with HLA type, Toxoplasma gonodii infection, and exposure to cats [133]. Toxoplasma gonodii infects brain neurons, and is best controlled with a strong pro-inflam- matory immune response. Endocannabinoids modulate the pro-inflammatory TH1 response by up-regulating the anti-inflammatory Th2 response. Hence, it is likely that some individuals idiosyncratically respond to Toxoplasma gonodii infections by producing excess endocannabinoids and suffering the associated abnormal mental state. Antipsychotic drugs have actually improved the outcome of infection with this parasite[134].
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Cannabis, psychosis and schizophrenia : unravelling a complex interaction

Cannabis, psychosis and schizophrenia : unravelling a complex interaction

The authors used this military conscript registry to analyse data from two questionnaires that were given to a cohort of 45 570 Swedish men at the point of their conscription between 1969 and 1970. Seven per cent of this cohort refused to answer questions relating to drug use and were excluded from the study. Clearly, this 7% could have altered the results signi fi cantly if they refused to participate due to fear of disclosing cannabis use. However, 4290 (9.4%) of the conscripts con fi rmed that they had used cannabis on at least one occasion prior to their conscription into the army. Andréasson was keen to explore level of exposure to cannabis and any consequent diagnosis of schizophrenia. He and his co-authors distinguished between infrequent and frequent use. Frequent use was de fi ned as using cannabis on 50 or more occasions, a cut-off inherited from research into smoking cigarettes at the time. Although level of exposure had been explored previously it had not been investigated in a cohort of this size. By exploring two levels of exposure to cannabis among the conscripts, Andréasson was able to show that there was a dose – response relationship between cannabis use and schizophrenia. This was an important fi nding, and helped to direct future research which con fi rmed this association [11].
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An appraisal of the use of cannabis on construction sites

An appraisal of the use of cannabis on construction sites

Several challenges, including what constitutes private use, arise from the court ruling in South Africa. Technically, if individuals in possession of cannabis step outside their home, retain the substance in their pocket, and it is for personal use, they have not broken the law. Possession in itself would no longer carry the previous legal censure. Further, allowing people to purchase marijuana would amount to the court sanctioning dealing in the substance. Should the users want to grow their own cannabis, they would have to purchase the seeds or small plants from another party who would be deemed to be a dealer in marijuana. This is still an illegal practice. The purchaser would be an accomplice to dealing in cannabis. The South African government would need to make a decision about what quantities are allowed per person strictly for personal use.
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CANNABIS A REVIEW AND ITS THERAPEUTIC POTENTIALS

CANNABIS A REVIEW AND ITS THERAPEUTIC POTENTIALS

436 | P a g e The effects of cannabis on thought processes are characterized initially by a feeling of increased speed of thought, flights of ideas which may seem unusually profound and crowding of perceptions [8]. With higher doses of cannabis, thoughts may get out of control, become fragmented and lead to mental confusion. It causes a specific deficit in short term memory, an effect which is demonstrable even after small doses in experienced cannabis users. The deficit appears to be in acquisition of memory and may result from an attentional deficit combined with an inability to filter out irrelevant information and intrusion of extraneous thoughts [9]. Impaired motor performance have been shown in many studies in humans, including tracking ability, pursuit rotor performance, hand-eye coordination, physical strength and many others [10]. The observable effects immediately after consumption are reddening of eyes, reduction in body temperature, dry mouth and throat, hunger, slightly elevated heart rate and blood pressure when lying down and a drop in heart rate and blood pressure when standing [11][12][13]. Heart rate may increase to 20%-50% over baseline and this tachycardia occurs within a few minutes and can last up to 3 hours [5]. If dose is of low potency, effects can be subtle and brief although if repeated smoking is done, the effects can last for hours [14].
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Developing limits for driving under cannabis

Developing limits for driving under cannabis

There are several potential indicators of cannabis use and its potential impact on driving skills. Because of its good correlation with measured impairment during the later phase of a cannabis high, i.e. more than 2 hours after cannabis consumption, the concentration of THC in blood is still the most meaningful indicator of impairment during that period [7]. Note that during the first hour of a cannabis ‘high’ no unimodal relationship between impairment and THC concentration exists. However, during this phase, THC concentrations in blood clearly exceed the range considered by the authors for a legal limit. Thus, drivers under the acute impact of cannabis and presenting with THC concentrations in the serum of 20 ng/ml or more would invariably be found in violation. Commercially available less invasive alternatives to measuring THC concentration in blood, such as testing
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The cannabis withdrawal syndrome: current insights

The cannabis withdrawal syndrome: current insights

Abstract: The cannabis withdrawal syndrome (CWS) is a criterion of cannabis use disorders (CUDs) (Diagnostic and Statistical Manual of Mental Disorders – Fifth Edition) and cannabis dependence (International Classification of Diseases [ICD]-10). Several lines of evidence from ani- mal and human studies indicate that cessation from long-term and regular cannabis use precipitates a specific withdrawal syndrome with mainly mood and behavioral symptoms of light to moderate intensity, which can usually be treated in an outpatient setting. Regular cannabis intake is related to a desensitization and downregulation of human brain cannabinoid 1 (CB1) receptors. This starts to reverse within the first 2 days of abstinence and the receptors return to normal functioning within 4 weeks of abstinence, which could constitute a neurobiological time frame for the duration of CWS, not taking into account cellular and synaptic long-term neuroplasticity elicited by long-term cannabis use before cessation, for example, being possibly responsible for cannabis craving. The CWS severity is dependent on the amount of cannabis used pre-cessation, gender, and heritable and several environmental factors. Therefore, naturalistic severity of CWS highly varies. Women reported a stronger CWS than men including physical symptoms, such as nausea and stomach pain. Comorbidity with mental or somatic disorders, severe CUD, and low social functioning may require an inpatient treatment (preferably qualified detox) and post-acute rehabilitation. There are promis- ing results with gabapentin and delta-9-tetrahydrocannabinol analogs in the treatment of CWS. Mirtazapine can be beneficial to treat CWS insomnia. According to small studies, venlafaxine can worsen the CWS, whereas other antidepressants, atomoxetine, lithium, buspirone, and divalproex had no relevant effect. Certainly, further research is required with respect to the impact of the CWS treatment setting on long-term CUD prognosis and with respect to psychopharmacological or behavioral approaches, such as aerobic exercise therapy or psychoeducation, in the treatment of CWS. The up-to-date ICD-11 Beta Draft is recommended to be expanded by physical CWS symptoms, the specification of CWS intensity and duration as well as gender effects.
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Executive functions and cannabis use in adolescents

Executive functions and cannabis use in adolescents

some cognitive functions, affecting performance on divided attention, verbal memory, and working memory (Broyd et al., 2016; Hindocha et al., 2017; Lundqvist et al., 2005; Solowij et al., 2002; Bull et al., 2002; Ilan et al., 2004). In particular, working memory suffers the effects of substance abuse, especially because its impairment also affects other cognitive functions. According to some studies, this impairment causes below-average academic performance (Grant et al., 2003), declarative memory deficit (Grant et al., 2012) and persistent decline in global cognitive functioning (Meier et al., 2012). Studies showing that impairment persists in adulthood are particularly worrying, (Alloway et al., 2010; Ullman et al., 2014) and with greater severity among chronic cannabis users (Cousijn et al., 2014; Solowij et al., 2008). Pope &Yurgelun (1996), document one of the fewer studies comparing adolescents with a chronic and a occasional cannabis consumption behaviour. In more recent studies, Pope et al., (2001) undergo to cannabis administration and after a 19 hours time frame of abstinence, detected an impairment affecting memory capabilities, particularly attention and executive functions. Successively Pope et al., (2002) widened the sample using more specific and sensitive tests founding a greater specific impairment of visual-spatial memory in chronic consumers than in occasional ones. Chronic cannabis usage in adolescence may cause permanent changes to neuronal circuits in specific brain areas and such changes may increase the likelihood of developing psychiatric disorders in adulthood (Gardner & Steinberg, 2005; Rubino et al., 2011). Evidence also suggests that individuals who start consuming cannabis at an early age may be more vulnerable to long-term neuropsychological deficits than individuals who started using it later (Porath-Waller, 2009). In this study investigated how cannabis abuse (chronic and occasional consumption, as well as absence) can influence global cognitive functioning, also through executive functions. The methodology used was the administration of WISC-IV (Orsini, Pezzuti and Picone, 2012) in two groups of adolescents with occasional and chronic cannabis usage. In particular, working memory indexes (WMI), processing speed (PSI) and intellectual quotient (IQ) were investigated by comparing scores with a control group that did not consume substances, to understand the impairment magnitude that the abuse may cause to cognitive functions. We also performed a neuropsychological study through the administration of the BVN Battery 12-18 to investigate whether planning skills and memory capacities (visuo-spatial) were affected by the consumption of cannabinoid substances.
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Deterrence and Deviance:  The Example of Cannabis Prohibition

Deterrence and Deviance: The Example of Cannabis Prohibition

In summary, this research has shown that more severe penalties and higher perceived certainty of punishment do not have the effect of reducing the likelihood of subsequent cannabis use a[r]

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Introduction:cultivation, medication, activism and cannabis policy

Introduction:cultivation, medication, activism and cannabis policy

Some of the organisations behind the parliamentary protest, like the United Patients Alliance who are now spearheading the medical reform movement in the UK, are open in their support for commercial players. Others are reluctant, and fear that legislative change, if it does come, will only facilitate corporate profit, without establishing the right to grow your own. For instance, the UKCSC (2016), who advocate for medical and non-medical use, have established a ‘Right2Grow’ campaign, which emphasises the right to grow, share and collectively consume cannabis.

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Absorptive stripping voltammetry for cannabis detection

Absorptive stripping voltammetry for cannabis detection

-tetrahydrocannabinol (THC), the active constituent of cannabis, is known to reduce psychomotor function and cognition thus greatly impairing driving ability [1, 2]. As would be expected, reports indicate that the de- gree of impairment is related to the amount of THC present in the body; as low as 0.95 μM of THC in blood has been found to cause equivalent driving impairment to an alcohol blood concentration of 11.5 mM, the legal limit in most European countries [1]. At the same time, studies have also shown that cannabis is not only one of the most commonly used illegal drugs [3, 4] but that it is also associated with many drug driving motor ve- hicle accidents [5]. There is hence a great need for both accurate and low-concentration detection as well as the development of methodologies suitable for road- side detection.
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Cannabis as a substitute for alcohol and other drugs

Cannabis as a substitute for alcohol and other drugs

The survey sample for this study consisted of 350 medical cannabis patients between the ages of 18 and 81 from the San Francisco Bay Area, California. Participants are mem- bers of Berkeley Patients Group (BPG), a medical canna- bis dispensing collective in Berkeley, CA. The sample was 68.4% male (N = 238), 66.2% White (N = 231) and 14.6% Multi-racial (N = 51). The mean age was 39.43. A survey was created by the researcher, with portions adapted from a patient survey administered by Dr. Frank Lucido at his medical practice in Berkeley, CA. The survey had five sections: demographic information, medical information, cannabis use pattern, alcohol and drug use and service utilization. Participants were asked the quan- tity and frequency of alcohol, tobacco and drug (prescrip- tion and illicit) use as well as current and past alcohol and/or drug treatment. Participants were also asked about whether they use cannabis as a substitute for alcohol, illicit drugs or prescription drugs and why to investigate medical cannabis as a treatment for alcohol and/or drug dependence.
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Public opinion and medical cannabis policies: examining the role of underlying beliefs and national medical cannabis policies

Public opinion and medical cannabis policies: examining the role of underlying beliefs and national medical cannabis policies

In addition to this emerging, albeit weak, evidence base, social movements have fought for legal access to medical cannabis. Public pressure to change medical cannabis policies has succeeded in many jurisdictions, yet medical cannabis continues to be controversial be- cause of the potential detrimental public health effects [9, 30–33] and the evolving, yet still weak, evidence base just mentioned. In the midst of these debates and policy changes, and at a time when much is unknown about the future of medical cannabis policies and their poten- tial effects, it is essential to gain a more nuanced under- standing of the nature, extent and rationale for public opinion related to medical cannabis policies. Indeed, a better understanding of public opinion can provide a framework for an improved understanding of current and future policy developments.
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Cannabis-based medicines and the perioperative physician

Cannabis-based medicines and the perioperative physician

Health Organisation (WHO) have been inconsistent in their approach. The WHO’s Expert Committee on Drug Dependences’ recent review (Ghebreyesus 2019) recom- mended to the United Nations Office on Drugs and Crime (UNODC) that the rescheduling within the Inter- national Drug Control Conventions occurs for cannabis and cannabis resin, dronabinol, tetrahydrocannabinol and extracts and tinctures of cannabis. They also re- peated their recommendation to remove cannabidiol (CBD) preparations (with not more than 0.2% delta-9- THC) from the International Drug Control Conventions. The UNODC subsequently delayed its vote on these rec- ommendations, but despite this, many countries are pro- ceeding to legalise or reschedule cannabis and/or CBMs, broadening public availability, with the UK the most re- cent country to reschedule CBMs. Table 1 details the current status of cannabis and CBMs in selected coun- tries for medical use. The recreational use of cannabis is currently legalised in Uruguay, Canada and certain states within the USA (United Nations Office on Drugs and Crime 2019).
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