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Psychotic Disorders and Co-occurring Substance Use Disorders
Published in Tricia L. Chandler, Fredrick Dombrowski, Tara G. Matthews, Co-occurring Mental Illness and Substance Use Disorders, 2022
Tricia L. Chandler, Fredrick Dombrowski
The causes of schizophrenia used to be considered a genetic issue, but gene studies have indicated that individual genes increase the risk of developing schizophrenia to less than two times that of the average population (Gilmore, 2010). Pre- and perinatal complications, along with environmental exposures, appear to be more relevant to developing the disorder, with maternal depression during the pregnancy increasing the risk in offspring up to 9% if a parent also had a psychotic disorder and environmental exposure, increasing the risk even more (Gilmore, 2010). Stressors or infections during pregnancy may contribute to neurological changes in the fetus, but these are not a sure outcome for the development of schizophrenia, and the genetic propensity does not ensure that schizophrenia will necessarily develop. Biological and neurological factors that have been considered in the development of schizophrenia, and the additional substance use disorders include the dysregulation of the brain chemical dopamine, although there are a number of neurotransmitters affected by the development of schizophrenia (Chambers et al., 2001). Psychotropic medications for the treatment of schizophrenia have significant adverse side effects that also affect brain chemistry. Considering the severity of the side effects of prescribed medications, many people may turn to illicit substances to cope with symptoms.
Evidence for Genetic Predispositions for Criminogenic Behavior
Published in Gail S. Anderson, Biological Influences on Criminal Behavior, 2019
We will explore many other protective factors as we delve deeper into specific biological factors associated with behavior, such as hormones, brain chemistry, brain trauma, birth defects, and inadequate diet, but many different and disparate environmental factors have been associated with reducing biological risks. For example, increased exposure to green space was found to be a protective factor against developing schizophrenia. The causes of schizophrenia have been shown to be multi-faceted, with both environmental and genetic factors increasing risk. In an analysis of proximity to green space over the life course, using satellite data from the landmass of Denmark, proximity to the least amount of green space was related to a 1.52-fold increase in risk of developing schizophrenia in comparison with people living closest to green space, even after adjusting for other known predisposers. This highlights the benefits of green space, which may relate to reduced pollution, decreased stress, improved immune functioning, and improved mental health—all known to relate to exposure to a more natural environment.67 This suggests that careful city planning and town planning could improve mental and physical health and well-being—as well as aesthetics—by increasing, or better planning, the amount and proximity of green space.
Life Care Planning for Depressive Disorders, Obsessive-Compulsive Disorder, and Schizophrenia
Published in Roger O. Weed, Debra E. Berens, Life Care Planning and Case Management Handbook, 2018
Schizophrenia is primarily a problem of brain functionality rather than brain structure. While the role of dopamine imbalance has been well documented, other neurotransmitters appear to be involved in schizophrenia as well, including serotonin, acetylcholine, norepinephrine, glutamate, and GABA. While the causes of schizophrenia are unknown, scientists believe it is a combination of genetic predisposition and environmental factors that most likely occur in utero during the development of the brain. Psychosocial stressors such as living in an urban area and dysfunctional family communication may also play a role (Tsuang, 2000).
Sublingual dexmedetomidine: repurposing an anesthetic as an anti-agitation agent
Published in Expert Review of Neurotherapeutics, 2023
Justin Faden, Meghan Musselman, Leslie Citrome
Acute agitation is broadly defined as abnormal and excessive motor and verbal activity, including feelings of restlessness, inner tension, hypervigilance, hyperarousal, and irritability [1,2]. It is not synonymous with aggression or violence, though if left untreated, it can evolve into it[3]. The etiology of agitation is multifactorial, including, but not limited to, substance intoxication or withdrawal, dementia, neurologic and metabolic conditions, traumatic brain injury, delirium, anxiety, and personality disorders[4]. Other common causes include schizophrenia and bipolar disorder. Individuals with schizophrenia may be predisposed to episodes of agitation and aggression due to low frustration tolerance, irritability, limited coping skills, persecutory delusions, or command hallucinations to harm others, whereas individuals with bipolar disorder may exhibit agitation or aggression due to emotional lability, alterations in energy levels, impulsivity, or irritability[5]. In presentations to the emergency department (ED) for agitation, bipolar disorder and schizophrenia have been estimated to be the underlying cause in 13% and 21% of occurrences, respectively[6]. More broadly, agitation is a common clinical presentation occurring in approximately 2.6% of ED presentations and 4.3% to 10% of psychiatric ED presentations [7–9].
Could low α-N-acetylgalactosaminidase plasma concentration cause schizophrenia?
Published in The World Journal of Biological Psychiatry, 2023
According to the neurodevelopmental hypothesis, although the causes of schizophrenia are related to abnormal prenatal changes, the onset of the disease occurs at advanced ages, such as the second decade of life. There might be several approaches related to this issue. It is thought that until postnatal brain development is complete (this process continues into late adolescence or even early adulthood), brain regions without the disease compensate for the impaired brain regions. Another approach is the interaction of disease-causing factors with normal neuronal development (Hariri et al. 1999; Lieberman 1999). In our study, the mean age of onset of the disease was 20.56 ± 1.91. And there was a positive correlation between disease onset age and α-NAGAL levels. Those with earlier disease onset had lower enzyme concentrations. The possible explanation for this result may be that low α-NAGAL levels exacerbate the underlying pathology, leading to the onset of the disease at an earlier age.
Do neurocognitive functions in cannabis induced psychosis groups differ from schizophrenia with cannabis use? A controlled cross-sectional study
Published in International Journal of Psychiatry in Clinical Practice, 2021
Raghav Shah, Abhishek Ghosh, Ajit Avasthi, Ritu Nehra, Chirag K. Ahuja, Niranjan Khandelwal
Cannabis increases the risk of psychosis by 2–3 times and it is one of the ‘component causes’ of schizophrenia (van Os et al. 2002; Zammit et al. 2002; Arendt et al. 2005). Nevertheless, a significant majority of patients who developed psychotic symptoms following exposure to cannabis had resolution of psychotic symptoms in 1–6 months (Arseneault et al. 2002). This group, as per the current nosology, is identified as cannabis induced psychosis (American Psychiatric Association 2013; World Health Organization 2019). Studies from the Swedish and Danish registries showed that the conversion rate of the diagnosis of cannabis induced psychosis to schizophrenia spectrum disorders was nearly 40–45%, when studied over a period of 3–7 years (Arendt et al. 2005; Kendler et al. 2019). Study from our clinic reported conversion in about 30% cases with the initial diagnosis of cannabis induced psychosis (Aggarwal et al. 2012). Therefore, a substantial proportion would retain the diagnosis of cannabis induced psychosis. This group needs research attention to examine potential reasons for non-conversion to schizophrenia. In our opinion the answer may lie on neurocognitive function.