psychopathology

A Historical Perspective of Schizophrenia

| Jen L'Insalata
schizophrenia1by Jen L’Insalata

Schizophrenia cannot be explained in its entirety by one particular theoretical model and the underlying neurobiological foundation for the disease is still relatively unknown.  Rather it is the descriptions and observations of the primary psychotic symptoms that have allowed several theories surrounding schizophrenia to evolve (Mishara, & Schwartz, 2013). Historically, schizophrenia was considered to be constructive in which anomalous experiences provide the construct of one self. Early clinical observations emphasized subjective self-experiences and altered self-awareness. The concept of self-experience is still referenced in modern work with schizophrenia. (Parnas, & Henriksen, 2014).

The earliest depictions of schizophrenia were recorded in France during the 12th century but were not linked to any particular disorder. Writing described individuals who deviated from what was considered to be normal self-perception; anomalous self-experiences. In many cases writing illustrate a disunity of consciousness in which a person’s thinking, perception, movement, and vision were disjointed and incongruent with presented stimuli (Parnas, & Henriksen, 2014).

The modern understanding of schizophrenia rose form the work of Emil Krapelin, an influential German psychiatrist working in the late 19th and early 20th century. Krapelin research surrounding the combination of symptoms and psychiatric illness from a biological origin highlighted two forms of psychosis; manic depression and dementia praecox (Ebert, & Bär, 2010). The disturbance known as Krapelin’s dementia praecox consisted of the phenomenon currently recognized as schizophrenia. During his research, Krapelin described the deterioration of what he believed to be perception and attention in combination with muscular tension (Mishara, & Schwartz, 2013).

Throughout the late 1800’s and early 1900’s core symptoms were studied by individuals from a psychodynamic perspective such as Carl Jung, Josef Berze, and Hans Walter Gruhle. Many of these theorists called attention to various cognitive and affective characteristics of the disorder. Jung in particular was fascinated by patients displaying confused speech which he described as a state of sleep-drunken-ness and confusion. Their theories critiqued by many other early psychotheorists and the phenomenon later was renamed schizophrenia in 1908 by Eugen Bleuler (Mishara, & Schwartz, 2013).

Bleuler theorized individuals with schizophrenia experienced a general loose association with a fissure personality which was highly influenced by Jung’s work. Bleuler believed that such loose associations allowed aspects of the unconscious to invade the consciousness and lead to an ego disorder. The unconscious invasion would erode the functioning of the ego to the level in which it exists in dreams. Gruhle added to Bleuler’s work and theorized that the primary symptoms of schizophrenia operated independently and observed a dysfunction between the cognitive and the affective components of the disorder (Mishara, & Schwartz, 2013).

Josef Berze criticized Jung’s work and theories believing that the symptoms were due to a reduction in mental activity rather than attention. He theorized that mental activity is more closely related to consciousness than affect and highlighted the concept of a disruption in self as the essences of schizophrenia. Berze also noted diminished mental activity in goal setting, linguistic coherence, and the ability to access the autobiographical self. Much of his work was inspired by emerging neurobiological research. He theorized that schizophrenia symptoms originated at a subcortical area, specifically the thalamus which gave rise primitive drives and motivations (Mishara, & Schwartz, 2013).

Jaspers integrated and critiqued his predecessors work in his book General Psychopathology published in 1913. (Mishara, & Schwartz, 2013). Highly influenced by the philosopher Descartes, he solidified the concept of self-experience pertaining to schizophrenia. Jaspers recognized that an individual may have and recognize experiences that are invalid and referred to positive symptoms as first person symptoms (Parnas, & Henriksen, 2014).

During the 1940s Freud’s psychoanalytic work continued to influence much of the theories surrounding schizophrenia and emphasized an etiological root stemming from early relationships. Psychoanalytic writers produces detailed descriptions of the schizophrenic experience including disruptions in interpersonal relationships and the self-experience due to the psychosis (Hamm, & Lysaker, 2016).

Writers such a Freud and Searles illustrate individuals that were detached from the world and redirected psychic energies inward during psychosis. Such writings provide the concept of an altered self-experience from which the schizophrenic individual is unable to integrate life experiences. Psychodynamic approaches took a pessimistic view of schizophrenia treatment which failed to produce empirically supported and measurable treatment modalities. Eventually, such treatment modalities fell out of favor and were replaced by psychosocial and cognitive behavioral perspectives (Hamm, & Lysaker, 2016).

With the publication of the ICD 8 and 9, Schizophrenia was recognized as a disturbance of personality and involved disorder concepts of individual uniqueness and self-direction. During that time the term personality referred to a subjective self rather than the personality descriptions used in contemporary psychology. Research surrounding a subjective self could be measured using systematic approached however lacked reliability in its methods. This notion soon fell out of favor and was replaced with an operational model following the publication of the DSM-III in 1980 (Parnas, & Henriksen, 2014).

The DSM-III emphasized behavioristic components of schizophrenia which stress observable features over the subjectivity and inference of previous theories. Biological concepts such as genetics in the etiology of schizophrenia were highlighted and lead to the emergence of a spectrum of observable features and predictors. Among the most noted were deficits in emotion, eccentricity, and thought disorder which caused interpersonal difficulties in social and occupational function. The inclusion of the diathesis stress model illustrated how core vulnerability combined with environmental stressors and produce cognitive changes observed in schizophrenia (Parnas, & Henriksen, 2014).

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References

Asenjo Lobos, C., Komossa, K., Rummel-Kluge, C., Hunger, H., Schmid, F., Schwarz, S., & Leucht, S. (2010). Clozapine versus other atypical antipsychotics for schizophrenia. The Cochrane Database of Systematic Reviews, (11), CD006633. Advance online publication. http://doi.org.library.capella.edu/10.1002/14651858.CD006633.pub2

Ebert, A., & Bär, K.-J. (2010). Emil Kraepelin: A pioneer of scientific understanding of psychiatry and psychopharmacology. Indian Journal of Psychiatry, 52(2), 191–192. http://doi.org/10.4103/0019-5545.64591

Hamm, J. A., & Lysaker, P. H. (2016). Psychoanalytic phenomenology of schizophrenia: Synthetic metacognition as a construct for guiding investigation. Psychoanalytic Psychology, 33(1), 147-160. doi:10.1037/a0038949

Mishara, A. L., & Schwartz, M. A. (2013). Jaspers’ critique of essentialist theories of schizophrenia and the phenomenological response. Psychopathology, 46(5), 309-19. doi:http://dx.doi.org.library.capella.edu/10.1159/000353355

Parnas, J., & Henriksen, M. G. (2014). Disordered Self in the Schizophrenia Spectrum: A Clinical and Research Perspective. Harvard Review of Psychiatry, 22(5), 251–265. http://doi.org.library.capella.edu/10.1097/HRP.0000000000000040

Spencer, E. K., & Campbell, M. (1994). Children with schizophrenia: Diagnosis, phenomenology, and pharmacotherapy. Schizophrenia Bulletin, 20(4), 713-725.

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Stress!!!!

| Jen L'Insalata
mental-illnesses-disorders-drawn-real-monsters-toby-allen-thumb640
Artwork by Toby Allen
By Jen L’Insalata

Stress has been cited for many adverse physical and mental health conditions and is linked to the proliferation of non-communicable disease epidemics in recent years. During the 1800’s most deaths were related to poor sanitary and hygienic conditions. Most deaths were attributed to outbreaks of cholera, Influenza, typhoid, and tuberculosis spread through unsanitary drinking water (Shern, Blanch, & Steverman, 2016).

In the 21st century, public health is still at risk. The US ranked 36th out of 194 for life expectancy in 2012 with the vast majority of deaths related to obesity, coronary heart disease, lung disease, and substance abuse. Most contemporary chronic illness has its roots in stress and it is estimated that nearly half of Americans will develop resulting mental health and addiction issues at some point during their lifetime (Shern, Blanch, & Steverman, 2016).

It is widely understood that a combination of genetic predisposition coupled with environmental influence shape over all human development. Many alterations in genetic material correlate with environmental stressors. In other words, genetic mutation and expression is strongly influenced by the environments which people are exposed to.

While manageable stress is considered important for healthy human development, toxic stress is not. Frequent, intense, and prolonged exposure to adversity including but not limited to physical and emotional abuse or violence, neglect, and economic hardship account for the source of much toxic stress. Acute or chronic exposure to traumatic events including death and sexual abuse also fall into the toxic stress category as does the persistence of less sever stressors including family instability and income insecurity (Shern, Blanch, & Steverman, 2016).

Stress alters development   over the course of a lifetime. Prenatal exposure to stress impacts developing structures of the fetus leading to adverse effects on memory and cognition. Early childhood stress often results in diminished behavioral, emotional, and impulse control. Individuals exposed to toxic stress during late adolescence and early adulthood develop a heightened fear response and are hyper responsive to stress stimuli (Shern, Blanch, & Steverman, 2016). Additionally, stress amplifies the aging process on both the brain and the body as a whole.

Stress causes structural remodeling of the brain and weakens neuro-connections within in the brain. Exposure to stress activates stress hormones and raises cortisol levels. Persistent elevation of cortisol levels increases the adverse effects on the connective structures within the amygdala; a structure commonly linked to cognitive and emotional regulation (Shern, Blanch, & Steverman, 2016 & Pagliaccio, Luby, & … Barch, 2015).

Genetic mutations occur throughout the short alleles of the serotonin transport promoter and produced heightened monoamine oxidise A activity. Heightened activity along the Hypothalamic-Pituitary-Adrenal Axis greatly effects the monoamine/serotonin structures and leads to additional cortisol release. It is the relationship between cortisol and amygdala connectivity that is believed to be a foundational component of internalizing pathology (Pagliaccio, Luby, & … Barch, 2015).

Internalizing pathology such and depression and anxiety contribute additional stress to an individual’s life. Symptoms of both disorders have dehabilitating effects on one’s ability to function in a socioeconomic capacity and produce feeling of dependency on unhealthy relationships and substances. Thus the cycle of stress, cell malfunction, and disorder is perpetuated.

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Resources

Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey, M. S., Belden, A. C., & … Barch, D. M. (2015). Amygdala functional connectivity, HPA axis genetic variation, and life stress in children and relations to anxiety and emotion regulation. Journal Of Abnormal Psychology, 124(4), 817-833. doi:10.1037/abn0000094

Shern, D. L., Blanch, A. K., & Steverman, S. M. (2016). Toxic stress, behavioral health, and the next major era in public health. American Journal Of Orthopsychiatry, 86(2), 109-123. doi:10.1037/ort0000120

 

A General Diagnostic Understanding: Schizophrenia and Related Psychotic Disorders

| Jen L'Insalata
schizophreniaJen L’Insalata

Schizophrenia is a psychotic disorder characterized by the disruption of an individual’s sense of self and perception. Psychotic symptoms manifest in the form of auditory, visual, and sensational hallucinations, disordered or delusional thoughts, and disruptions in language and communication. An individual with schizophrenia is not always incoherent. Most individuals experience periods of active symptoms and symptom remission, while many experience at least one period of relapse (NIMH, 2009).

Schizophrenia is sometimes confused with having a split of multiple personality which are characteristic of another disorder. Diagnosing in an emergency room setting can be difficult as symptoms manifest differently in varying individuals. Involuntary hospitalization can only occur legally if a professional witnesses psychotic behavior which can take the form of the vocalization of delusional thoughts (NIMH, 2009).

295.90 (F20.9) Schizophrenia is characterized by delusions, hallucinations, disorganized speech that is easily derailed or incoherent, grossly disorganized or catatonic behavior, and negative symptoms including flat affect and diminished emotional expression. The symptoms must be severe enough to impact normal day to day function such as interpersonal relationships and self-care (APA, 2013). In an emergency room scenario it may be difficult to assess the impact of the symptoms on education and employment. It may be easier to visually assess the appearance of the individual to gather the extent of the symptoms on daily functionality. Schizophrenia can be distinguished from other psychotic disorders based on severity and length of duration of the symptoms. In schizophrenia the symptoms persist continuously for six months and meet the full diagnostic criteria for at least one month. If the duration and severity of the symptoms is less than the diagnostic criteria, a diagnosis of schizophrenipform disorder may be more appropriate. Additionally, if the active phase of psychosis includes depressive symptoms, a diagnosis of schizoaffective disorder may be warranted (APA, 2013).

Schizoaffective Disorder is similar to schizophrenia and symptoms include hallucinations, delusions, disorganized thought, and negative symptoms. In addition to the psychotic features present, individuals with schizoaffective disorder also exhibit features of depressive disorders and bipolar disorders. Coding for schizoaffective disorder is based on the mood episodes exhibited. 295.70 (F25.0) Schizoaffective Disorder, Bipolar type indicated there is a manic phase to the mood disturbances indicative of bipolar disorder. In 295.70 (F25.1) Schizoaffective Disorder, Depressive type, the individual experiences mood symptoms congruent with major depressive disorder (APA, 2013).

298.8 (F23) Brief Psychotic Disorder is characterized by the presence of delusions, hallucinations, disorganized speech and grossly disorganized or catatonic behavior. Symptoms last for at minimum, one day and at maximum, one month. Typically the onset is sudden and an individual goes from a non-psychotic to a psychotic state within two weeks. The differentiation between Brief psychotic disorder and other forms of psychotic disorder focuses on the length of time and onset of the symptoms. If the symptoms last longer that one month, the diagnosis of schizophrenipform disorder is more appropriate. Additionally, individuals who experience brief psychotic disorder do not meet the full DSM criteria for schizophrenia and show no disturbance in mood or affect. Individuals who experience brief psychotic disorder do not often show negative symptom that are common in schizophrenia. If mood congruent symptoms are present, schizoaffective disorder is a more appropriate diagnosis (APA, 2013).

The exact cause of schizophrenia is still unknown. It is believed that there is genetic, biological, and environmental links that correspond with the disorder and provide risk factors. Schizophrenia shows a genetic component and runs within families. Having a first degree relative with schizophrenia increases a person’s likelihood to develop the disorder themselves. Environmental factors such as exposure to prenatal viruses, malnutrition, and complications during birth also increase the risk of schizophrenia (NIMH, 2009). According to the diathesis stress model, individuals inherit a high or low genetic risk for schizophrenia. Varying psychosocial factors throughout the lifespan such as stressors and experiences influence the trajectory and development of the disorder (U.S. Department of Health and Human Services, 1999).

Several genes have been linked to schizophrenia and individuals with schizophrenia have a higher rate of gene mutation than healthy individuals. Brain physiology also differs in individuals with schizophrenia. Ventricles in the center of the brain are often larger in schizophrenic patients and individuals have decreased amounts of gray matter than healthy individuals. Genes that code for the chemicals associated with the development of higher brain function, neurotransmitters such as dopamine and glutamine are also effected which cause changes to the neuropathways that develop during puberty (NIMH, 2009).

Individuals with schizophrenia who receive treatment have a better outcome than individuals who do not. One halt to two thirds of individuals who receive treatment recover or show significant improvement over time (U.S. Department of Health and Human Services, 1999). Treatment for schizophrenia includes both psycho-pharmisudical and psychotherapeutic interventions that focus on eliminating the symptoms and developing coping strategies.

During the 1950’s antipsychotics were developed to treat schizophrenic symptoms. This first generation of antipsychotics consisted of medications including Chlorpromazine (Thorazine), Haloperidol (Haldol), Perphenazine (Etrafon, Trilafon), Fluphenazine (Prolixin), and Clozapine (Clozaril). Each individual responds to treatment differently, however Clozapine appeared to be most effective in the most varied cases. Clozapine also had a side effect that reduced white blood cell count requiring patients using the medication to receive blood screening every two weeks (NIMH, 2009).

During the 1990’s a second generation of antipsychotics were developed that had reduces side-effects. These include Risperidone (Risperdal), Olanzapine (Zyprexa), Quetiapine (Seroquel), Ziprasidone (Geodon), Aripiprazole (Abilify), Paliperidone (Invega); which are more commonly prescribed today. Side effects to antipsychotics may include drowsiness, dizziness, blurred vision, rapid heartbeat, sensitivity to the sun, and skin rashes. In women, menstrual problems may occur. Additional side effects may be physical in nature and long term use of antipsychotics may cause loss of neuromuscular control. Once a compatible antipsychotic is found patients may see improvements in as little a few days, with an overall reduction in psychotic symptoms in as little as six weeks (NIMH, 2009).

In addition to pharmisudical treatment, psychotherapy is important to an individual’s recovery.  Therapy provides prosocial, interpersonal, vocational skills, and education that helps prevent relapse of symptoms. Family and community based therapy helps to build a support system that also helps improve the individual’s prognosis. Psychosocial and Cognitive Behavioral Therapy address the disruptive thoughts and perceptions that are symptomatic of schizophrenia. CBT helps develop coping skills that allow the individual to test the legitimacy of their delusions or hallucinations and implement healthy behavioral alternative to actin on such thoughts. Prosocial components address areas of daily self-care, occupational, and educational skills that help schizophrenic patients live healthy and functioning lives (U.S. Department of Health and Human Services, 1999, & NIMH, 2009).

Schizophrenia effects men and woman and displays cultural equality, however not all symptoms manifest the same. Misdiagnosis can occur if the culture to which a patient differs from that of the diagnosing clinician.  Many cultural sub groups participate in religious experiences where hearing voices or seeing vision is acceptable. In other cultures, affect and avoidance can be misinterpreted as paranoia or other negative symptoms. It is important to understand the culture from which an individual comes from to determine if the symptoms are due to psychosis or cultural misinterpretation (U.S. Department of Health and Human Services, 1999, & NIMH, 2009).

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References

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). Washington, DC: Author. ISBN: 9780890425558.

National Institute of Mental Health. (2009). Schizophrenia. Retrieved from http://www.nimh.nih.gov/health/topics/schizophrenia/index.shtml

U.S. Department of Health and Human Services. (1999). Mental health: A report of the surgeon general. Retrieved from http://profiles.nlm.nih.gov/ps/access/NNBBHS.pdf