One Aspect of Family Environment That Has Been Found to Be Important in Schizophrenia Is

Schizophrenia

Rick D. Kellerman MD , in Conn's Current Therapy 2021 , 2021

Treatment

At present there is no cure for schizophrenia. Although there is meaning clinical heterogeneity inside the disorder, schizophrenia is usually a chronic status that requires long-term handling. Comprehensive treatment involves outpatient medication management and psychotherapy, psychosocial interventions, involvement of the family/support system, inpatient intendance for astute crisis intervention/affliction exacerbation, and collaboration with primary care physicians. Currently, there is a vigorous research effort for diagnostic, prognostic and theranostic biomarkers in schizophrenia, toward a more "personalized medicine" approach for patients.

Antipsychotic medications play an important role in the pharmacologic management of schizophrenia. So-called first-generation antipsychotics (FGAs) have been in clinical apply since the introduction of chlorpromazine (Thorazine) in the 1950s. These agents block the dopamine D2 receptor, and common side effects include extrapyramidal side effects (EPS) (e.g., Parkinsonism, dystonia). The newer or "second-generation antipsychotics" (SGAs), in addition to D2 receptor blockade, are also serotonin five-HT2 receptor antagonists. While the run a risk of EPS is lower for SGAs than FGAs, SGAs are associated with a heightened risk of weight gain and the metabolic syndrome.Table i provides a more detailed description of antipsychotic medications. The Texas Medication Algorithm Project (TMAP) currently recommends a trial of a single (not-clozapine) SGA for newly diagnosed patients with schizophrenia, or patients never before treated with an SGA. Nevertheless, neither the TMAP nor the American Psychiatric Clan (APA) guidelines for the treatment of schizophrenia preferentially endorse a detail antipsychotic. Clozapine (Clozaril) is primarily used for "treatment-refractory" schizophrenia, commonly defined every bit a lack of/fractional response to an adequate trial of monotherapy with two or 3 different antipsychotics.

Adjunctive medications may too play an important role in the pharmacologic handling of some patients with schizophrenia. These include antidepressants for depression and anxiety, mood stabilizers for depression or mood summit, benzodiazepines for feet or agitation, beta-blockers for akathisia, and anticholinergics for EPS.

Medication nonadherence is a major treatment issue in patients with schizophrenia at all phases of the illness. Reasons for nonadherence are complex and multifaceted only may include medication side effects, dumb insight into illness, psychopathology in all three symptom domains, lack of efficacy, and comorbid substance employ. Over 70% of patients in the Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Schizophrenia Trial discontinued medication inside the first eighteen months of treatment. Medication nonadherence leads to dramatically increased risk of illness relapse, hospitalization, and suicidal behavior and should be routinely assessed in clinical visits. The use of rapid-dissolving oral or long-acting injectable medications may improve adherence in some patients.

Schizophrenia

D.R. Combs , ... M.R. Basso , in Encyclopedia of Human Behavior (2d Edition), 2012

Genetics

Schizophrenia is a complex disorder with a number of interrelated causes, with many stemming back to prenatal development. There are hundreds of theories about the causes and potential mechanisms of schizophrenia, each with varied levels of enquiry support. There has been considerable interest in genetic factors involved in schizophrenia due to findings that a person's gamble for developing schizophrenia is higher if a get-go-degree relative (parents, siblings, and children) has the condition. Children born from two parents with schizophrenia accept an estimated 46% greater risk for developing the disorder themselves (ane% lifetime adventure in the general population). Twin studies accept proven useful in understanding genetic factors in schizophrenia. Studies examining rates of schizophrenia amidst monozygotic (MZ; 100% genetic similarity) and dizyotic (DZ; l% genetic similarity) twins show pairwise concordance rates of 28% and 6%, respectively. In MZ twins, the ane who is discordant (i.e., does not accept the disorder) for schizophrenia has a 17% chance of having children who develop the disorder even though they themselves are salubrious. Twins who are reared autonomously still have an elevated risk for developing schizophrenia above that accounted for shared environmental factors. Adoption studies conducted in Scandinavia evidence a rate of schizophrenia of about 16% if i of the biological parents has schizophrenia. Environmental factors such as communication deviance (i.due east., incomprehensible speech) and stressful family events in combination with a genetic predisposition led to the highest risk for developing schizophrenia in adoption studies. Despite the clear role of genetics and family history in schizophrenia, the genetic relationship is modest at all-time and schizophrenia is considered a polygenetic construct. In fact, information technology is possible that at that place may be different types of schizophrenia each with their ain profile of genetic abnormalities. Current research has focused on several chromosomes such as 6, 8, thirteen, and 22, but research to place a specific genetic locus has proved largely disappointing. Chromosome 22 is of particular interest equally it contains the COMT (catechol- o-methyltransferace) gene that metabolizes dopamine. Persons with a detail type of COMT genetic profile (valine/valine allele type) are at an increased take chances for developing schizophrenia.

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Schizophrenia

Fred F. Ferri Md, FACP , in Ferri's Clinical Advisor 2022 , 2022

Chronic Rx

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Relapse prevention is a major goal of treatment. Nonadherence is common and leads to loftier relapse rates. Long-acting injectable preparations given biweekly, monthly, or every three mo are currently underutilized and may better adherence and reduce hospitalizations.

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There is considerable individual variability with regard to antipsychotic response and vulnerability to specific adverse furnishings.

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Clozapine is the most effective antipsychotic currently available and requires monitoring to forestall life-threatening adverse effects (agranulocytosis, myocarditis, seizure, orthostatic hypotension). Routine labs including absolute neutrophil count (ANC) during therapy is required to monitor for agranulocytosis. Additional notable side effects include constipation, metabolic syndrome, and sialorrhea. Olanzapine stands out as particularly constructive but too has substantial adverse metabolic effects.

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Neurocognitive comeback associated with antipsychotic treatment amidst patients with schizophrenia is modest and does not differ between first-generation and 2nd-generation antipsychotics.

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The treatment of negative symptoms is challenging. A recent meta-analysis demonstrated modest effects of all antipsychotics (with particular benefits for clozapine, amisulpride, and olanzapine). Given the similarity of negative symptoms to depression (and the frequent co-occurrence of depression in schizophrenia), antidepressants accept been used. A Cochrane review on the topic demonstrated only modest benefits. Preliminary analyses suggest that some newer antipsychotics (cariprazine, lumateperone) may have some benefit, although more rigorous studies are needed.

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Mood stabilizers may be considered for a clinical presentation with high agitation or aggression, or for patients with schizoaffective disorder. Lithium has known antisuicidal properties and may be trialed in patients with comorbid major depressive disorder or dysthymia, or for those with a depressive subtype of schizoaffective disorder. Clinically, valproate is about often considered if a patient has a vehement or agitated history or presentation; still, this utilise has not been backed past rigorous study. Utilise of valproate has not been shown to pb to improved long-term symptom control; show in support of its use has been of low quality to engagement.

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Rational polypharmacy of antipsychotics may be benign to reduce symptoms and rehospitalization. For instance, the combination of aripiprazole and clozapine is ordinarily used and may help to mitigate the metabolic side-effect burden of clozapine.

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Anticholinergic agents, though oftentimes used acutely to prevent or mitigate acute motor side furnishings of antipsychotics, should not be used long term due to their cognitive side effects and disability to prevent motor side furnishings in the long term.

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Tardive dyskinesia (TD) (i.e., choreoathetoid movements of the muscles of tongue and face and occasionally of other muscle groups) is common amid patients on chronic antipsychotics—this consequence is more pronounced with first-generation than second-generation antipsychotics (incidence of 6.3% per twelvemonth with first-generation vs. two.vi% per yr with second-generation antipsychotics). Stepwise handling of TD involves reduction of antipsychotic dose if possible, consideration of transition to clozapine or quetiapine, trial augmentation with vitamin E and vitamin B_six, and apply of a vesicular monoamine transporter 2 (VMAT2) inhibitor (valbenazine, tetrabenazine, deutetrabenazine).

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An estimated 60% to fourscore% of individuals with schizophrenia utilize tobacco, which is the major contributor to the nearly 30-yr bloodshed gap betwixt those with schizophrenia and the general population. Varenicline has been shown to be specially efficacious in achieving smoking cessation in this population.

Schizophrenia

M.A. Schreiber , ... D.Due west. Tsuang , in Brenner's Encyclopedia of Genetics (Second Edition), 2013

Abstract

Schizophrenia is a common, lifelong, and frequently disabling psychiatric disease that affects the about critical college level functions of humans. Scientific understanding of the underlying molecular etiologies of schizophrenia continues to be limited despite intensive inquiry. Genetic studies offer the hope of gaining new insight into the mechanisms that increment a person'due south susceptibility to develop schizophrenia, in particular past identifying potential new targets for treatment, but the genetic ground of schizophrenia has proven exceptionally difficult to unravel. Given the rapid evolution of molecular genetic research technologies, quantum progress is imminent in the near time to come.

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Management of Depression and Psychoses in Pregnancy and in the Puerperium

Robert Resnik MD , in Creasy and Resnik's Maternal-Fetal Medicine: Principles and Exercise , 2019

Schizophrenia and Schizoaffective Disorder

The same caveats for studies of bipolar disorder in pregnancy are relevant for studies in pregnant and postpartum women who endure from schizophrenia. Bachelor literature suggests that women with schizophrenia accept worse nativity outcomes than women without the disorder, but some of this may be attributable to poor health habits, including the use of licit and illicit substances. ^63-66 In a linked Danish database, ⁶⁵ women with schizophrenia had a 46% higher RR for preterm birth (95% CI, 1.nineteen to 1.79), a 57% higher likelihood of delivering a low-birth-weight baby (95% CI, 1.36 to 1.82), and a 35% college risk for an SGA fetus (95% CI, 1.17 to 1.53) compared with the overall population of women, findings consistent with other reports. ^63,67 In a study that compared pregnancy outcomes in women with schizophrenia who were or were non treated with antipsychotic agents ⁶⁶ to an unaffected comparing group, women with schizophrenia, regardless of treatment, had college rates of low-birth-weight and SGA deliveries than the comparing group. Boosted complications reported for women with schizophrenia include placental abruption ⁶³ and fetal malformations. ⁶⁷

Some, ^64,68 simply not all, ⁶⁷ studies evidence an increased adventure for stillbirth and neonatal death for women with psychotic disorders, including women with schizophrenia and bipolar disorder. ⁶⁸ The literature besides notes differences in the rates of post-neonatal deaths for infants built-in to women with schizophrenia (0.73%) compared with mortality rates for the general population (0.26%) (RR = 2.76; 95% CI, 1.67 to 4.56). ⁶⁷ Almost of the deaths were attributable to sudden infant death syndrome, which occurred at a rate of 0.46% for children born to women with schizophrenia and 0.1% for the general population (RR = five.23; 95% CI, two.82 to nine.69).

Schizophrenia

Lisa T. Eyler Zorrilla , Dilip Five. Jeste , in Encyclopedia of the Human Brain, 2002

3. Theories of Etiology

Iii.A. Genetics

Schizophrenia has a potent familial component. Siblings and parents of patients accept an viii–ten% chance of developing the disorder and offspring take a 12–fifteen% risk, compared to a 1% run a risk in the general population. Evidence from twin and adoption studies suggests that a portion of the familiality of the disorder is genetic. Specifically, monozygotic (MZ) twins have a 40–sixty% concordance rate, whereas dizygotic (DZ) twins have a 12–15% concordance. In addition, the offspring of schizophrenic mothers who are adopted abroad have a higher risk of schizophrenia than those from nonschizophrenic mothers.

Despite strong back up for the role of genes in the disorder, the search for a particular gene related to schizophrenia has been disappointingly unfruitful. Linkage analyses have revealed several candidate markers that have not been confirmed in subsequent studies. The nigh studied have been the long arm of chromosome 22, chromosome 6p, and genes for various dopamine receptors.At that place are several methodological issues that complicate the search for a "schizophrenia factor." First, there is swell heterogeneity of symptom presentation among those diagnosed with schizophrenia. It is quite possible that dissimilar symptom profiles are related to abnormalities in different sets of genes. Thus, by combining all subtypes into one category, potentially relevant genes may be missed. Relatedly, the boundaries of schizophrenia are not well-divers. Results of linkage analyses are likely to be strongly influenced by how broadly the schizophrenia spectrum is defined. Thirdly, schizophrenia is not likely to be caused by just i factor. Multiple genes, interacting with one some other, are the advisable targets for genetic research in this disorder. Finally, although genes clearly play some role in the etiology of schizophrenia, results from twin and adoption studies too betoken to the importance of environmental factors. For instance, the cyclopedia charge per unit for MZ twins is but half of that expected in a purely genetic disorder, and adoption studies have found that characteristics of the adoptive parents contributed substantially to the risk of developing schizophrenia. Thus, even if genes related to schizophrenia are discovered, they are unlikely to explicate fully the etiology of the disorder.

Three.B. Environment

Early theories regarding environmental risk factors for schizophrenia focused solely on the role of parenting styles (especially, "schizophrenogenic" mothering). These theories were eventually supplanted, still, by hypotheses centering on biological precursors. Nearly current inquiry has focused on influences in the perinatal menses of development. There are three master reasons for this emphasis. Start, as reviewed earlier, the nature of the brain abnormalities in schizophrenia suggests neurodevelopmental aberrations instead of neurodegenerative processes. Second, patients with schizophrenia have an increased prevalence of minor physical anomalies and neurological soft signs, pointing to a gestational origin. Tertiary, birth-accomplice and high-risk studies that followed subjects into the risk period for development of symptoms have consistently demonstrated that patients with schizophrenia bear witness deficits long before the onset of the disorder. By using techniques such as the retrospective review of home movies and records as well equally prospective studies, it has been shown that individuals who later develop schizophrenia demonstrate at an early historic period motor and psychomotor abnormalities, cerebral ventricular enlargement, neurological soft signs, cognitive deficits including lower IQ and attentional dysfunction, and social and emotional disturbances at school.

Exploration of perinatal environmental influences on the development of schizophrenia has centered on two chief candidates: obstetric complications and viruses. History of obstetric complications (OCs) is more than common in patients with schizophrenia than in good for you individuals. Specifically, prematurity, low birth weight, and complications involving trauma or oxygen impecuniousness are frequently establish. Considering the medial temporal lobe is known to exist specially sensitive to hypoxia, the prevalence of OCs among patients provides a potential origin of the neurodevelopmental deficits seen in this region. A viral origin of schizophrenia has besides been proposed. Support for this hypothesis comes from epidemiological studies showing an increased rate of schizophrenia amidst the offspring of women who were in the 2d trimester of pregnancy during an influenza epidemic. In addition, it has been argued that the increased risk of schizophrenia found amidst those born in the wintertime, in urban areas, and during times of famine supports a viral etiology. Finally, adult patients with schizophrenia show a wide diversity of immunologic abnormalities, although the specificity of these deficits is not determined. Despite these pieces of circumstantial evidence, no virus has been identified that explains about cases of schizophrenia.

III.C. Interactive

Due to the complexity of schizophrenia, it is unlikely that genes or ecology factors alone cause the disorder. Rather, some interaction of these factors probably leads to the heterogeneity of symptom profiles, grade, and outcome. The diathesis–stress theory posits that environmental factors combine with an underlying genetic vulnerability to produce schizophrenia. In support of this theory, inquiry suggests that the offspring of mothers with schizophrenia who also endure delivery complications are the most likely to develop schizophrenia later in life. In addition, early on separation from caregivers increases the take chances of schizophrenia merely amidst those individuals with a family history of the disorder. Finally, studies have suggested that individuals at genetic risk for the disorder who receive poor parenting are more likely to develop schizophrenia. Thus, ecology risks at many stages of evolution appear to collaborate with genetic factors to promote the genesis of schizophrenia.

3.D. Developmental

A complete understanding of the etiopathology of schizophrenia must include an explanation of the age at onset of characteristic symptoms. As reviewed earlier, most known risk factors have their effects perinatally. In addition, subtle abnormalities of performance are evident in childhood and adolescence in those individuals who are eventually diagnosed with schizophrenia. The pathognomonic signs and symptoms of schizophrenia, however, practice non usually arise until late adolescence or early adulthood and typically erupt rather forcefully in the form of a "first break." In addition, in some individuals onset is earlier (childhood onset), and in others, especially women, onset is later in life (late onset). 1 form of theories that attempts to explicate these facts hypothesizes that perinatal events (either genetic, environmental, or an interaction) create a brain vulnerability that only becomes apparent after normal developmental changes occur near the historic period at onset. In search of support for these hypotheses, the role of developmental hormones in the onset of schizophrenia has been investigated. In childhood-onset schizophrenia, the onset of puberty is related to the onset of the disorder, though merely in girls. In add-on, the preponderance of women among late-onset patients with schizophrenia has led to the suggestion that female reproductive hormones, such as estrogen, may be protective factors against onset of the disorder. It is posited that the decrease in estrogen levels during menopause promotes the onset of schizophrenia. Related theories advise that the nature of the congenital abnormality is a disruption of normal developmental changes, such equally a delayed expression of aberrant genes or failure of normal synaptic pruning that should occur around the second decade of life. Finally, other theories emphasize an accumulation of agin events that eventually reach a threshold, leading to onset of the disorder. At this time, no definitive evidence has been found that favors any of these theories over others.

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Schizophrenia

B.A. Ellenbroek , in Encyclopedia of Behavioral Neuroscience, 2010

Genetic Models

Schizophrenia has a strong genetic component, and although the genes that are involved in the etiology accept non been unequivocally identified, some genetic changes have been establish in several clinical studies. Table 2 lists the nearly important genes that have been associated with schizophrenia. Without going into too much item, it is important to notation that for virtually genes, more than i single nucleotide polymorphism (SNP) has been linked to schizophrenia. A good example is the regulator of G-protein signaling iv (RGS-4) gene of which iv SNPs accept been linked to schizophrenia (commonly denoted by i, 4, 7, and xviii). However, in one study, the haplotype One thousand–G–1000–Chiliad was institute to exist more common in schizophrenic patients, whereas in another study the haplatype A–T–A–A was seen more often in patients. Some other problem is that in nigh cases, the functional consequence of this mutation is non known, and could correspond both proceeds-of-part likewise as loss-of-function mutations. In several cases, increases or decreases in expression of the protein or mRNA of the candidate cistron have been establish, but it is not clear whether this is actually due to the SNP.

Table 2. Candidate genes for schizophrenia and genetic simulation models

Gene	Location (human)	Functional issue of SNP	Beast model	DA resp.	PPI	P50	Retentivity	Soc Isol	Anhedonia
COMT	22q11	Val158 SNP has reduced enzyme action	COMT−/−	−	−	Ø	Ø	Ø	Ø
			COMT+/−	Ø	Ø	Ø	Ø	Ø	Ø
DAOO	12q24	Increased activity and expression?	None
DISC-one	1q42	Not clear at present	DISC-L100P	Ø	+	Ø	+	−	−
			DISC-Q31L	Ø	+	Ø	+	+	+
			DISC-KO	+	+	Ø	Ø	+	Ø
DTNBP1	6q22	Reduced mRNA and protein expression?	Sdy mutant	−	−	Ø	Ø	+	Ø
G72	13q32-34	Not clear at nowadays	None
mGluR3	7q21-22	Reduced poly peptide expression?	mGluR3−/−	Ø	Ø	Ø	Ø	Ø	Ø
NRG1	8p12-21	Increased mRNA expression?	III-NRG1+/−	Ø	+	Ø	+	Ø	Ø
			TM-NRG1+/−	Ø	+	Ø	−	Ø	Ø
			CRD-NRG1+/−	Ø	+	Ø	+	Ø	Ø
RGS4	1q21-22	Reduced protein expression?	RSG−/−	−	−	Ø	−	Ø	Ø

+: the sign or symptom observed in the patients tin can also be observed in the brute model; −: the sign and symptom observed in the patients was non observed in the animal model; Ø: the sign or symptoms has not been investigated in the brute model. Abbreviations: DA resp.: hyper-reactive response to dopamine agonists; PPI: deficit in prepulse inhibition; P50: deficit in P50 auditory gating; memory: deficit in memory tests; Soc Isol: social isolation.

Since neither the specific nature of the SNPs nor the functional consequences of those associated with schizophrenia is generally known, information technology has proven difficult to develop animal models based on genetic mutations known to be associated with schizophrenia. Most studies take therefore been carried out with either homozygous or heterozygous knockout mice. In particular, the homozygous knock-out animals may not fairly represent schizophrenia equally none of the genes so far identified in schizophrenia lead to a complete loss of part. This has led to some intriguing though hard-to-interpret finding. The schizophrenia-associated neuregulin haplotype, for example, is associated with increased levels of neuregulin. Withal, the heterozygous neuregulin knock-out mouse shows some schizophrenia-like features (such as increased locomotor activity and decreased prepulse inhibition).

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Schizophrenia

D.I. Shapiro , ... E.F. Walker , in Encyclopedia of Adolescence, 2011

Introduction

Schizophrenia is a complex, heterogeneous mental disease that is typically first diagnosed in late adolescence or early on adulthood. While approximately 1% of the world's population is diagnosed with schizophrenia, it is an affliction that is poorly understood. It can be severe and debilitating, merely a big proportion of individuals with schizophrenia learn to manage their illness and lead normal lives with the help of medications, mental health interventions, and supportive families and friends. In the post-obit sections, the nature of schizophrenia, what is known about its causes and outcomes, and its early on class in adolescence/young machismo are discussed.

Descriptions of atmospheric condition like to schizophrenia date as far back as the ancient Greeks and Egyptians. However, the first psychiatric classification arrangement to recognize what is now called schizophrenia was adult past Emil Kraepelin, a German psychiatrist, at the end of the nineteenth century. According to this system, nigh severe mental illnesses were classified into one of the two categories: manic depression, which encompassed severe mood disorders, similar the current diagnoses of Bipolar Disorder and Major Depressive Disorder, and dementia praecox, which was a broad category that included what is now referred to as schizophrenia, as well as some other non-mood-related mental disturbances. While this organization was an comeback on those that came before information technology in terms of the validity and uniformity of the syndromes it identified, it still lacked specificity. It is for this reason that Eugen Bleuler, a Swiss psychiatrist, coined the term schizophrenia effectually the plow of the twentieth century. The term is derived from the Greek language and literally ways 'split mind,' though this term can be misleading. Many people believe that schizophrenia is characterized by multiple or 'split' personalities, but this is non the example. Others believe that information technology entails aroused, violent, or psychopathic traits. These are misunderstandings that likely contribute to the stigma associated with the illness.

Schizophrenia is in a class of illnesses called the psychotic disorders. The term 'psychotic' is some other term that is ofttimes misunderstood. Briefly, psychosis is conceptualized as a meaning departure from reality and often includes false perceptions or beliefs, impairments in normal affect, thought, oral communication, and initiative, as well as anxiety, depression, and sleep disturbances. Approximately 1% of the population meets criteria for a psychotic disorder (i.e., has clinically meaning positive symptoms, which are described below), only does not meet criteria for schizophrenia.

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Schizophrenia

J.L. Padmanabhan , M.S. Keshavan , in Encyclopedia of Mental Health (2d Edition), 2016

Introduction

Schizophrenia is a mental disorder marked past severe disturbances in idea, emotion, perception, and behavior. The most characteristic symptoms of schizophrenia include hallucinations, delusions, and disorganized language and behavior. Historical references to a psychosis-like affliction appointment dorsum to ancient Egypt, with the Egyptian Volume of Hearts in the Ebers papyrus (around 1500 BCE) describing a psychosis-like syndrome ( Okasha, 1999; Kyziridis, 2005). Ancient texts from other cultures as well refer to psychotic symptoms, indicating that psychosis has been a part of human history throughout the world. Yet, it was not until the late ninteenth century that schizophrenia was first conceptualized equally a singled-out illness separate from other mental disorders. The German psychiatrist, Emil Kraepelin, used the phrase 'dementia praecox' (or premature dementia) for the affliction now known as schizophrenia, and believed it could exist distinguished from mood disorders past its cognitive symptoms and deteriorating course. In 1908, the disorder was reconceptualized and named 'schizophrenia' by the Swiss psychiatrist Eugen Bleuler, who noted that not all individuals with the disorder deteriorated over fourth dimension (Figures 1 and 2). The discussion 'schizophrenia' is derived from the Greek root 'schizo', meaning 'split', and 'phrenia', meaning 'mind', and refers not to a divide in personality or identity, merely to fragmented thinking.

Figure i. Emil Kraepelin, a German psychiatrist, differentiated 'dementia praecox' (an early name for schizophrenia) from mood disorders.

Figure 2. Eugen Bleuler was a Swiss psychiatrist who coined the term 'schizophrenia'.

Schizophrenia tin be highly disabling and has life-altering consequences for patients and their families. Due to its typical emergence during early machismo, schizophrenia tin can rob people of their autonomy and productivity during their prime working years, and can interfere with their chapters to form meaningful relationships. According to the World Health System, schizophrenia ranks every bit ane of the top ten global causes of disability for both men and women (World Health Organization, 2008). Understanding the origins and handling of schizophrenia is therefore important not simply for afflicted individuals and their families, only for lodge at large.

This article will review the symptoms, course of illness, diagnosis, and handling of schizophrenia. It volition also cover epidemiology, etiology, and neurobiology, with an aim of broadly summarizing the electric current scientific understanding of this devastating disorder.

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Schizophrenia

Fred Picayune , in xPharm: The Comprehensive Pharmacology Reference, 2007

Etiology

Schizophrenia is likely due to a genetic vulnerability, coupled with environmental and psychosocial stresses, the so-called diathesis-stress model. The Neurodevelopmental theory of schizophrenia posits that the pathology results from insults during critical times of gestation, resulting in the impairment of connections or correlations between brain regions that must human activity in harmony for normal brain function. This asynchrony becomes compounded over time due to subsequent dysregulation of dopamine and glutamate transmitter systems, leading to the clinical moving-picture show plant in early adulthood Weinberger et al (2001), Meyer-Lindenberg et al (2001). Family, twin, and adoption studies support the role of genetic influences in schizophrenia. Immediate biological relatives schizophrenics have about ten times greater risk than that those in the general population, which suggests a substantial genetic component to the disorder. The current consensus is that multiple genes, which take not even so been positively identified, are responsible for this disorder Henderson and Goff (2000), Weinberger et al (2001). Maternal stresses, such equally prenatal poverty, poor nutrition, and affective illness, may predispose an baby to schizophrenia. Other stresses implicated in this condition include exposure to influenza and Rh-gene incompatibility Henderson and Goff (2000). Low birth weight, brusk gestation, and delivery complications, are associated with the development of schizophrenia. Viral infections of the key nervous system may as well be associated with greater risk for this condition Henderson and Goff (2000).

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