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Psychological Disorders
Published in Mohamed Ahmed Abd El-Hay, Understanding Psychology for Medicine and Nursing, 2019
The essential cause of schizophrenia appears to be genetic and constitutional but a large number of biopsychosocial factors may predispose a person to manifest the illness at a particular time in a person’s life. Schizophrenia is widely believed to have a neurobiological basis. The most notable theory is the dopamine hypothesis, which postulates that positive symptoms of schizophrenia are due to hyperactivity of the dopamine D2 receptor neurotransmission in the subcortical and limbic brain regions, whereas negative and cognitive symptoms of the disorder can be ascribed to the hypofunctionality of the dopamine D1 receptor neurotransmission in the prefrontal cortex (Toda & Abi-Dargham, 2007). In support of this, studies have shown an increased density of the dopamine D2 receptor in post-mortem brain tissue of schizophrenia sufferers. This theory is also partly supported by the efficacy of antipsychotic drugs (which block dopamine receptors) and the ability of drugs (such as cocaine or amphetamines) that stimulate dopaminergic activity to induce psychosis. Many recent studies have revealed a lot of structural and functional brain abnormalities evidenced through brain imaging of schizophrenic patients. Psychosocial and environmental factors may hinder or help to make the predisposition to schizophrenia, these include various psychosocial stressors and unfavorable early experiences, abnormal parental attitudes, physical illness, head injury, and intoxications. No one finding or theory to date is fully adequate in explaining the etiology and pathogenesis of this complex disease.
Psychotic disorders
Published in Bhaskar Punukollu, Michael Phelan, Anish Unadkat, MRCPsych Part 1 In a Box, 2019
Bhaskar Punukollu, Michael Phelan, Anish Unadkat
Dopamine: Hypothesis states there is excess dopaminergic activity in the mesolimbic–mesocortical pathways. All effective antipsychotics block D2 receptors. Other evidence: amphetamines (dopamine agonists) can cause an acute psychosis; only the cis isomer of flupenthixol which is a dopamine antagonist has antipsychotic properties; postmortem studies reveal increased D2 receptors in the basal ganglia and limbic system. PET studies have also suggested increased D2 receptors in striatum.
Multiple Commitments
Published in Hanna Pickard, Serge H. Ahmed, The Routledge Handbook of Philosophy and Science of Addiction, 2019
This chapter charts currents of continuity and discontinuity, unity and disunity, obduracy and plasticity important in the conceptual history of addiction neuroscience. Despite attempts to unify object and approach, the social and affective complexity of addiction exceeds them. Social and cultural histories of diverse moments of translation in clinical and research-oriented sciences perhaps tell us as much about the societies in which these concepts emerge as they do about the ontological objects under study. Despite the so-called NIDA paradigm—and concomitant notions of brain reward circuitry, allostasis, and the dopamine hypothesis—shifts in acceptance of the view that addiction is a brain disease are underway (Lewis 2015; Szalavitz 2016). Explanatory frameworks for addiction have long been inadequate to account for the entwined psychological and emotional effects that comprise the addictions; differences between acute and prolonged exposure; individual variation in response to drugs; and social learning about these effects at the individual and societal levels. Recent efforts to elucidate the neurochemobiological processes and mechanisms thought to underlie the changes that move non-addicted brains into addictive states have been multiple and are not easily subsumed into the brain disease model.
Potassium channel modulators and schizophrenia: an overview of investigational drugs
Published in Expert Opinion on Investigational Drugs, 2023
Meghan Musselman, Eric Huynh, Rachana Kelshikar, Eric Lee, Mohammed Malik, Justin Faden
The dopamine hypothesis, however, is not a complete explanation for the etiology of schizophrenia symptoms. Currently available antipsychotic medications, which act through dopamine blockade, do not typically have a significant impact on the negative and cognitive symptoms of schizophrenia [22]. Additionally, there is evidence suggesting the involvement of additional neurotransmitters and pathways. The glutamate hypothesis, also referred to as the NMDA hypoactivity theory, suggests that decreased functioning of NMDA receptors that sit on GABA interneurons in the prefrontal cortex cause increased glutamate signaling [22]. This increase in glutamate leads to hyperactivity of the ventral tegmental area and thus stimulates the mesolimbic pathway. In this theory, the same positive symptoms are elicited. However, the cause is further upstream, thus addressing the source of dopaminergic dysfunction rather than the downstream sequelae. Evidence supporting this theory is that dissociative drugs such as PCP and ketamine are NMDA receptor antagonists, block glutamate receptors, and can mimic the positive, negative, and cognitive symptoms of schizophrenia [23,24]. While the glutamate theory appears promising, therapeutic interventions based on this have not yet demonstrated consistent clinical efficacy though a recent meta-analysis yielded positive findings with significant differences between individual glutamatergic agents [25,26].
More than a Half-Century with Haloperidol: Glories, Disparities, and Use Today
Published in Issues in Mental Health Nursing, 2023
These days, it might be difficult to imagine the initial glory of haloperidol, but it was a sensation in the realms of psychiatry and mental health (Seeman, 2021; Tyler et al., 2017). It is now thought the medication aided in understanding how dopaminergic changes result in the desired effects of antipsychotics, paving the way for many medications to come; haloperidol also probably furthered the biochemistry understanding of psychosis and schizophrenia spectrum disorders, helping kickstart the dopamine hypothesis of schizophrenia (Tyler et al., 2017; Seeman, 2021). Additionally, in the first decades of use, the antipsychotic effects of haloperidol may have offered relief to so many individuals that it was a major player in accelerating deinstitutionalization, which ultimately occurred across the United States (Tyler et al., 2017).
Is there a therapeutic potential in combining bupropion and naltrexone in schizophrenia?
Published in Expert Review of Neurotherapeutics, 2022
Samer A. El Hayek, Malek A. Shatila, Jana A. Adnan, Luna E. Geagea, Firas Kobeissy, Farid R. Talih
Schizophrenia has been treated so far based on the ‘Dopamine Hypothesis’ which states, in short, that excess of dopamine (DA) in mesolimbic pathways is responsible for the positive symptoms seen in schizophrenia, and deficiency of DA in the mesocortical pathways is at the basis of negative symptoms [5]. According to this theory, schizophrenia occurs secondary to alterations in DA D2 and D3 receptor activity in the cortical and striatal regions, with D2 receptors being the main culprit [6]. This is supported by findings of studies showing that the efficacy of antipsychotics is proportional to their D2 receptor occupancy; when there is no occupancy of D2 receptors, these drugs have no therapeutic effect. In parallel, findings from imaging studies show doubled radiotracer displacement from D2 receptors and increased baseline D2 receptor occupancy by DA in patients with schizophrenia compared to healthy controls [7,8], accounting for positive symptoms. Alternatively, D1 receptors exist in the cortical areas of the brain and are underactive in schizophrenia. Findings from imaging studies in individuals with schizophrenia suggest chronic low levels of DA and a resultant upregulation of D1 receptor density [6]. These findings have traditionally been associated with the cognitive and negative symptoms of schizophrenia [6,9].