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Psychotic Disorders: Biological & Psychological Theories Research Paper

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Introduction

Psychotic disorders are severe mental disorders that are characterized by extreme impairment of a person’s ability to think clearly, respond emotionally, communicate effectively, understand reality, and behave appropriately (AACAP, 2008). According to the DSM-IV-TR, there are nine formal psychotic disorders: schizophrenia; schizoaffective disorder; schizophreniform disorder; brief psychotic disorder; delusional; shared psychotic disorder (Folie a Deux); substance-induced psychosis; psychosis due to a general medical condition and psychosis due to other miscellaneous conditions.

Psychotic symptoms accompany various mental illnesses such as depression, bipolar disorder (manic-depression), schizophrenia, and some forms of alcohol and drug abuse. Psychotic symptoms interfere with a person’s daily functioning and can be quite debilitating. Psychotic symptoms include delusions and hallucinations. Delusion refers to a false, fixed, odd, or unusual belief firmly held by the patient that is not ordinarily accepted by other members of the person’s culture or subculture. There are delusions of paranoia (others are plotting against them), grandiose delusions (exaggerated ideas of one’s importance or identity), and somatic delusions (a healthy person believing that they have a terminal illness).

The other psychotic symptom of hallucination can be described as a sensory perception (seeing, hearing, feeling, and smelling) in the absence of an outside stimulus. For example, with auditory hallucinations, the person hears voices when there is no one talking. Treatment for psychotic disorders varies by disorder. It might involve drugs to control symptoms and talk therapy. A hospitalization is an option for serious cases where a person might be dangerous to himself or others.

The word psychosis was first used by Ernst von Feuchtersleben in 1845 to distinguish psychotic disorders from neurological ones. The word has its root in the green words as psyche (soul) and -osis (diseased or abnormal condition. It was used to distinguish disorders that were thought to be disorders of the mind, as opposed to neurosis, which was thought to stem from a disorder of the nervous system.

Biological and Psychological Theories of Psychotic Disorders

Psychiatry, the field of treating psychotic disorders, is based firmly within both the biological and social sciences and draws from developmental and cognitive psychology. The 1990s were described as the decade of the brain due to rapid development in the knowledge of the neurosciences. During the same period, a high level of research has taken place in the fields of genetics, neuroanatomy, neuropsychology, and pharmacology.

Of greatest influence on the treatment of psychosis was the neurological work of John Hughlings Jackson (1835-1911) and his colleague William Gowers (1845-1915) at the National Hospital for Neurology, London. Jackson outlined the organization of the nervous system as occurring at different levels in an ascending hierarchy. He regarded the highest cerebral functions, which were to do with consciousness and thought, as no more than developed elaborations of the most basic sensory and motor reflexes. These higher levels overrode the lower ones and were thus the first to be lost in disease, reducing individuals to lower levels of the organization.

In his view, such a deficit could lead to epileptic attacks, or to a range of neuropsychiatric symptoms, even outbursts of mania, since “the increased action [results from] what, metaphorically speaking, is loss of control of lower centres by the higher centres.”

Genetically speaking, it has been found that people may have psychotic experiences through biochemical abnormalities (Read et al., 2004). The dopamine hypothesis – the theory that schizophrenia may result from an overproduction of the neurotransmitter dopamine – has been extensively researched over the last 20 years. This theory is based on two observations: some neuroleptic or antipsychotic drugs affect the chemical dopamine and can induce Parkinsonism related to low dopamine levels; drugs such as amphetamines, which increase dopamine production, can also produce psychotic disorders (Kuipers and Bebbington, 1997).

But the theory has its limitations. It does not explain why there is only gradual improvement despite the fast action of the drug on dopamine in the brain. Researchers are now investigating the possible role of neurotransmitters like serotonin and noradrenalin in causing psychotic disorders leading to a diagnosis of bipolar disorder (Read et al., 2004). Studies comparing identical and non-identical twins and adoption studies indicate that there may be a genetic factor to psychotic disorders (Kuipers and Bebbington, 1997). The closer a person is related to a person with psychotic disorder, the greater the risk of him getting it.

The best estimate is that the risk of being given a diagnosis of schizophrenia is 46 percent for the child of two parents with the diagnosis, 13 percent for the child of one parent with the diagnosis, and 9 percent for siblings (IP-NHS, 2008). This is compared to the overall risk of 1 percent for the general population. Similar findings have been reported for a genetic contribution to bipolar disorder. It is clear that psychotic disorders do have a genetic factor in their occurrence.

On the neurological side, patterns of blood flow and patterns of electrical activity in the brain have been examined. It has been found that different types of psychotic experiences are associated with different patterns of activity. In particular, low levels of activity in the frontal lobes of the brain have been observed in people experiencing ‘negative symptoms’ (Lee et al., 2004). It is also possible that life experiences, psychological trauma, severe distress, and psychotic experiences may themselves leave physical traces on the brain, as well as the other way round.

Psychotic disorders are associated with cognitive abilities. People with psychotic disorders have a problem understanding other people’s way of thinking. They have unusual beliefs that make them jump to conclusions. They tend to be paranoid about everything in life. They sometimes hear voices they are not able to identify or comprehend. Sometimes, they also exhibit incoherent speech or ‘thought disorder.’ These psychotic disorders are thus obviously related to cognitive psychology (Read et al., 2004).

Psychological approaches to psychotic experiences focus on the patterns of thought that are associated with them. This pattern of thinking is related to specific brain activity, and hence all psychological theories of psychotic disorders can be said to have a biological basis (IP-NHS, 2008). Recently blood flow and electrical activity in the brain are being studied using brain scanning techniques, and in the context of psychotic disorders, it has been found that there are two kinds of phenomena: cognitive deficits and temporary deficits (Kuipers and Bebbington, 1997).

According to the cognitive deficit theory, psychotic disorders are caused by brain damage or biological problems, or environmental problems. Cognitive ‘deficits’ refer to deficits in cognitive processes such as perception, memory, and attention. According to the temporary ‘deficits’ theory, psychotic disorders can also result from depression, demoralization, or poor motivation. This is because depressed people tend to observe, recall and interpret negative information more than people who are not depressed (Kuipers and Bebbington, 1997).

These are just cognitive biases that differ from person to person and are not associated with brain damage. Childhood trauma can also cause such temporary deficits leading to psychotic disorders (IP-NHS, 2008). Life events such as bereavements, abuse, and assault can also lead to the same (IP-NHS, 2008).

Most cognitive research into psychotic experiences has focused on people with a broad diagnosis of schizophrenia. It has been found that schizophrenic people tend to There is good evidence that schizophrenic people have difficulty concentrating on a task. Due to their psychotic disorders, they are easily distracted. Moreover, people with psychotic disorders lack social skills. Ordinary social behavior depends on understanding other people’s views, actions and words.

When psychotic disorders interfere with these skills, they face problems in their social skills. The ‘Theory of Mind’ uses this fact to explain reduced levels of emotional expression during episodes of psychotic experiences, disorganized speech, hearing voices, and unusual beliefs (Kuipers and Bebbington, 1997).

These deficits in social skills are found in people recovering from psychotic disorders, in children of schizophrenic people, and people having a high level of risk for psychotic disorders. However, they are greatest in the case of people who actually experience psychotic disorders (IP- NHS, 2008). These findings have to lead to three conclusions: deficits in information processing make people more open to psychotic disorders; this vulnerability can make it more difficult for such people to cope with stressful events; emotional stress can lead to cognitive deficits, which in turn can lead to further problems and the development of psychotic disorders (IP-NHS, 2008).

Psychotic disorders cause delusions or hallucinations. The two most common kinds of unusual belief that people report are the fear that people are trying to harm or kill them (persecutory delusions) and the belief that they have special powers or abilities or that they are famous or powerful (grandiose delusions) (Read et al., 2004). Studies suggest that these unusual beliefs are associated with specific biases in reasoning about social situations.

There is scientific evidence that people who experience paranoia have a general tendency to blame other people for things that go wrong in their lives. Some researchers have argued that these kinds of beliefs have a defensive function and protect the individual from low self-esteem (Read et al., 2004). Most people often experience an ‘inner voice’ during textual thinking. These inner voices happen when it is difficult to distinguish their inner speech from an external source.

Some of this evidence has emerged from physiological studies such as brain scanning experiments (Kuipers and Bebbington, 1997). Other psychological experiments show that some people who hear voices experience difficulty when they are asked to distinguish between their thoughts and words were spoken to them. Incoherent speech is another psychotic disorder that indicates difficulty in adjusting speech to the needs of the hearer (IP-NHS, 2008).

Mania is a term used to describe a complex cluster of psychotic ‘symptoms,’ which includes grandiose delusions, increased activity, incoherent speech, and, in most cases, a paradoxical combination of both positive emotions (euphoria) and negative emotions (depression and irritability). Recent studies show that both paranoia and mania might play a role in protecting self-esteem (IP-NHS, 2008). Some researchers think that the increased energy and activity seen in people experiencing mania may sometimes be caused by disruption of the physiological mechanisms that control the sleep-wake cycle.

Thus, there are both psychological theories and biological theories to explain various psychotic disorders. Many psychologists believe that psychotic experiences often result from a combination of biological and psychological processes.

The mode of action of the medications used to treat psychotic disorders

The first two drugs introduced in the treatment of psychotic disorders were reserpine (Serpasil) and Chlorpromazine (Thorazine) (Brick and Erickson, 1999). The most common method of treating schizophrenia is neuroleptic medication, more or less combined with rehabilitative measures. The popularity of neuroleptics is easy to understand. They are relatively easy to administer to large numbers of patients, including outpatients (Alanen, 1997).

This medication, together with the progress of rehabilitative activities, made it possible gradually to shift the focus of schizophrenia treatment from inpatient to outpatient care in the 1960s. The effectiveness of neuroleptic treatment in relieving psychotic symptoms has been verified conclusively. As early as 1969, Cole and Davis’ reviewed a hundred studies in which their effectiveness in schizophrenia was compared with placebo groups, using double-blind procedures. In 86 of the studies, the medication alleviated the psychotic symptoms more effectively than did placebos (Alanen, 1997).

The multiple center research organized in the United States by the National Institute of Mental Health and headed by Cole yielded the most conclusive results: the condition of 70% of the patients improved essentially within six weeks, while the corresponding figure in the placebo group was only 25% ( Cole & Davis, 1969). Neuroleptics are effective in the case of several psychotic disorders, and their effect tends to be the more pronounced, the more distressed and restless the patient is. They do not cure schizophrenia, but they have a clearly favorable alleviating and antipsychotic effect (Cole & Davis, 1969).

They act most effectively on the positive symptoms (thought disorders, hallucinations, delusions), and they also help the patient to control such symptoms in the long term. Their effect on the negative symptoms (isolation, passivity, affective blunting), however, is less obvious. Especially in acute states, they often help to eliminate the symptoms completely. In chronic cases, the effect is less spectacular, and sufficiently long follow-up studies–see chapter two–indicate that the number of patients who have become permanently cured of their psychotic symptoms has not changed markedly since the introduction of neuroleptics. However, with the help of these drugs, the symptoms of the chronic patients are now less severe, reducing the need for inpatient treatment.

The effective–mechanism of most neuroleptics–especially the phenothiazine and butyrophenone derivatives–on psychoses is due to their blocking the transmission of nerve impulses between brain cells by means of the dopamine 2 (D2) transmitter (Snyder, 1981).

Positron emission tomography (PET) studies have shown that relatively low closes of neuroleptics are enough to do this. A higher dosage increases the number of adverse side effects. Because of the difference between the time-course of receptor occupancy and the time-course of antipsychotic effect, researchers (Wiesel, 1994) have postulated that the antipsychotic effect of neuroleptics is not exclusively due to the blocking of dopamine functions but includes more complex interactions among several different neuronal systems.

One may suppose that the adjustment “on a low flame” of central nervous system functions, associated with the neuroleptic effect, may also have psychological influences that help the patient’s ego to resume the internal psychic balance. Clozapine holds a special position among neuroleptics. Its effect on the blocking of dopamine two receptors is only about half that recorded for other neuroleptics, but its alleviating effect on the symptoms of chronic patients, in particular, is, nevertheless, better.

This has been tentatively ascribed to the more extensive action of clozapine on the functions of other transmitters, but we do not know for certain what mechanisms are involved in it. Serotonin (5-HT2) antagonists, as well as blocking effects of dopamine 4 (D4) receptors, have been proposed as plausible possibilities (Lieberman, 1993). The use of clozapine is restricted by potentially fatal consequences due to severe leukopenia (Idänpään- Heikkilä et al., 1977). The risk of hematological changes is present in about 1% of all cases (Alvir et al., 1993) and is greatest in the first several weeks to three months of treatment. Recently, a number of compounds currently in development–such as risperidone–with combined serotonin (5-HT2) and D2 antagonist properties have demonstrated impressive antipsychotic efficacy (Lieberman, 1993).

The attitude of psychiatrists towards neuroleptic medication is mostly related to their theory of schizophrenia: some consider neuroleptics a necessary basic medication that should be administered regularly and continuously, while others see neuroleptics as important agents to be used with moderation to support psychotherapeutically and psychosocially oriented therapy. Of the other psychoactive drugs used in the treatment of schizophrenia, benzodiazepine derivatives are the most common (Alanen, 1999).

The most typical indication for the use of benzodiazepines is the need for additional rapid tranquillization along with neuroleptic medication. Antidepressive drugs are also occasionally used to treat depressive conditions associated with psychoses. However, it is believed that psychotherapeutic work with the patient is generally a better alternative in these cases than antidepressive medication.

The treatment process for a patient with a psychotic disorder and how decisions are made regarding treatment. When and if pharmacological treatment was warranted.

Psychotherapeutic community treatment, family therapy, and individual therapy should be seen as complementary modes of treatment, used either separately or in combination, as indicated by the case-specific needs. For many patients, community treatment and family therapy are important prerequisites for successful individual treatment, both through their increased motivation to study their problems and through a sufficient loosening of inner psychological resources bound into symbiotic interfamilial relationships.

When a person exhibits psychotic disorders, he should be taken to the therapist. The therapist focuses on alleviating the symptoms, preventing recurrences, and improving functioning (Micucci, 1998). The therapist also serves as a consultant to the family to help them identify ways in which they may facilitate the patient’s progress. The patient may be given medication to relieve the psychotic symptoms and family therapy to help the family members reduce their isolation from one another and from their community (Martindale, 2000). Patients with acute psychotic attacks may need hospitalization for evaluation and safety concerns.

If symptoms are only minimally impairing the patient’s function and a specific stressor is identified, removing the stressor should suffice. In the event that symptoms are disabling, an antipsychotic agent should be used for the minimal duration (Martindale, 2000). If adverse effects are intolerable, the use of atypical antipsychotics may be helpful. A case series suggests that rapid tranquilization with olanzapine can achieve symptom relief in acute psychosis (Martindale, 2000). After the acute episode is resolved, individual, family and group therapy may be considered to help cope with stressors, resolve conflict, and improve self-esteem and self-confidence.

Bibliography

Brick, John; Erickson, K. Carlton (1999). Drugs, the Brain, and Behavior: The Pharmacology of Abuse and Dependence. Haworth Medical Press. New York.

AACAP(American Academy of Child and Adolescent Psychiatry) (2008). Glossary of Symptoms and Illnesses. Psychosis. Web.

Micucci, A. Joseph (1998). The Adolescent in Family Therapy: Breaking the Cycle of Conflict and Control. Guildford Press. New York.

Martindale, Brian (2000). Psychosis: Psychological Approaches and Their Effectiveness. RCPsych Publications.

Alanen, O. Yrjö (1997). Schizophrenia: Its Origins and Need-Adapted Treatment. Karnac Books. London.

Alvir J. M. J.; Lieberman J. A.; Safferman A. Z., et al. (1993). “Clozapineinduced agranulocytosis: incidence and risk factors in the United States”. New England Journal of Medicine. 329:162-167.

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Cole J. O., & Davis J. M. ( 1969). ” Antipsychotic drugs”. In: L. Bellak & L. Loeb (Eds.), The Schizophrenic Syndrome (pp. 478-568). New York: Grune & Stratton.

Idänpään-Heikkilä J., Alhava E.,; Olkinuora M. et al. (1977). “A granulocytosis during treatment with clozapine”. European Journal of Clinical Pharmacology, 11: 193-198.

Lieberman J. A. (1993). Understanding the mechanism of action of atypical antipsychotic drugs. A review of compounds in use and development. British Journal of Psychiatry, 163 (Suppl. 22): 7-18.

Snyder S. H. (1981). “Dopamine receptors, neuroleptics, and schizophrenias”. American Journal of Psychiatry, 138: 460-464.

Wiesel F.-A. (1994). “Neuroleptic treatment of patients with schizophrenia. Mechanisms of action and clinical significance”. British Journal of Psychiatry, 164 (Suppl. 23): 65-70.

Lee, H. K.; Farrow, T. F. D.; Spence, S. A. and Woodruff, P. W. R. (2004). Social cognition, brain networks and schizophrenia. Psychological Medicine. Volume 34. Issue 03. 391-400. Cambridge University Press.

Kuipers, Elizabeth and Bebbington, Paul (1997). Living with Mental Illness: A book for relatives and friends. Souvenir Press.

IP- NHS (Institute of Psychiatry- National Health Services) (2008). Causes of schizophrenia and psychosis. Web.

Read, John; Mosher, R. Loren and Bentall, P. Richard. Models of Madness: Psychological, Social and Biological Approaches to Schizophrenia. Brunner-Routledge Publishers. New York. 2004.

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