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CHAPTER 15 ■ Schizophrenia Spectrum and Other Psychotic Disorders
ANTIPSYCHOTIC MEDICATIONS—cont’d Second Generation (Atypical) Antipsychotics Clozapine, olanzapine, quetiapine, aripiprazole, risperidone, iloperidone, ziprasidone, paliperidone, asenapine, lurasidone, and cariprazine (ameliorate positive symptoms with some improvement in negative symptoms— particularly cariprazine)
Strong 5-HT Low to moderate D 2 Varying degrees of affinity for: ACh α -adrenergic H 1 Partial agonist at D 2 , D 3 , and HT 1A (associated with more improvement in negative symptoms than other atypical antipsychotics)
Weight gain, sedation Low potential for ejaculatory difficulty Sexual dysfunction, GI disturbance, headache Low potential for EPS Anticholinergic effects Tachycardia, tremors, insomnia, postural hypotension
some cases of schizophrenia following infection from a neurotoxic virus (particularly prenatal exposure to Toxoplasma gondii ) (Matheson et al., 2014). Symp- toms of NMDA glutamate receptor autoimmune encephalopathy mimic the psychotic symptoms in schizophrenia, which supports the impact of immune system involvement in mental symptoms. The role of cytokines in inflammation and the specific effects of these chemicals in the brain are still being explored
Typical (first generation) antipsychotic medica- tions largely target the dopamine receptors in the brain. Newer, atypical (second generation) antipsy- chotics have a weaker affinity for dopamine receptors and a stronger affinity for serotonergic receptors. The glutamate model of schizophrenia suggests pos- sibilities for new biomarkers signaling early illness and for new approaches to prevention and early treatment. Physiological Factors A number of potential physiological factors have been identified in the medical literature. However, their specific mechanisms and implications in the eti- ology of schizophrenia are unclear. Current theories suggest that it “is likely that these genetic risks, envi- ronmental risks and vulnerability factors are cumula- tive and interactive with each other and with critical periods of neurodevelopmental vulnerability” (Davis et al., 2016, p. 185). Viral Infection Boland and Verduin (2022) report that epidemiolog- ical data indicate a high incidence of schizophrenia after prenatal exposure to influenza. They stated: Other data supporting a viral hypothesis are an increased number of physical anomalies at birth, an increased rate of pregnancy and birth complications, seasonality of birth consistent with viral infection, geographical clusters of adult cases, and seasonality of hospitalizations. (p. 360) The effect of autoimmune antibodies in the brain is being studied within the field of psychoneuroim- munology, and evidence suggests that such antibod- ies may be influential in the development of at least
through ongoing research. Anatomical Abnormalities
With the use of neuroimaging technologies, struc- tural brain abnormalities have been observed in indi- viduals with schizophrenia. Ventricular enlargement is the most consistent finding; however, some reduc- tions in gray matter are also reported. As previously discussed, reduction in the volume of the hippocam- pus has also been identified in neuroimaging studies and may signal transition to a first psychotic episode (Harrisberger et al., 2016). Studies that focus on risks for a first psychotic episode are important, as early treatment is associated with better outcomes. Ulti- mately it is hoped that these studies will also point to preventive strategies. Magnetic resonance imaging (MRI) has revealed reduced symmetry in several lobes of the brain and reductions in size of structures within the limbic system of individuals with schizophrenia. Consider- able evidence from postmortem studies has shown abnormalities in the prefrontal cortex, and people who have had prefrontal lobotomies are reported to manifest many symptoms common to schizophrenia (Boland & Verduin, 2022), including flat affect and cognitive deterioration.
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