Mental health breakdown

Chapter 16 Mental Health Breakdown





INTRODUCTION


Biological processes have been suspected to play a role in the aetiology of mental illness since antiquity. Hippocrates, for example, proposed that depression or ‘melancholy’ resulted from a systemic excess of ‘black bile’1. Interest in pursuing possible biological foundations of mental illness increased in the 1950s and 1960s, with a number of independent observations and discoveries related to the development of pharmacological agents targeting disorders such as tuberculosis and hypertension. Fortuitously, these drugs had an effect on either psychotic or depressive symptoms. The resulting use of drugs such as chlorpromazine, imipramine and iproniazid provided further impetus to interest in identifying the neurochemical mechanism of action of these agents, and the development of theories of the biological foundations of psychiatric illness. The modern era of psychopharmacology was thus born, and from the 1960s onwards, significant research effort has been applied to increasing our understanding of the biological substrates and, importantly, treatment of mental disorders.


Mental disorders are often conceptualised, diagnosed and treated at the broad ‘syndrome’ rather than specific ‘disease’ level. Unlike in, say, pneumonia where diagnosis can be confirmed radiologically via a chest X-ray and a specific infectious agent can be identified through bacterial culture, there are no diagnostic tests to confirm a particular discrete mental disorder. Diagnosis is based, in the main, upon assessment of the presence or absence of certain symptoms. It is likely that mental illnesses such as schizophrenia and depression are broad syndromes that encompass a number of related disorders. Therefore, in most of the mental disorders, biological research findings need to be considered and interpreted with some caution. Biological processes in mental illness may be influenced by clinically heterogenous samples. Interpreting grouped data, possibly affected by the presence of several types of a disorder (such as subtypes of depression), needs to proceed with some caution. The presence of a particular biological abnormality does not necessarily confirm that it is pathophysiologically relevant to the disorder in question. It is possible that a biological finding may relate to another physiological disturbance, such as sleep abnormalities or weight loss, or represent the confounding effect of a biological factor known to influence body systems, for example, age, sex, menstrual cycle, and nutritional status. Having acknowledged these caveats, significant advances have been made in the biological understandings of mental illness related to biochemical, genetic, and neurological abnormalities.


This chapter will provide an overview of some of the key pathophysiological findings related to depression and schizophrenia. While biological factors are discussed primarily, it should be noted, and emphasised, that the environment within which a person develops a mental illness is also important. Although the vulnerability to a particular mental illness may be able to be demonstrated biologically, the expression of the illness is very likely multifactorial.



SCHIZOPHRENIA



PATHOPHYSIOLOGIC PROBLEMS RELATED TO SCHIZOPHRENIA


Schizophrenia is a psychotic illness that can affect a person’s functional and cognitive ability, perception and expression of emotion. A psychotic illness is one where the individual’s mental state is disturbed to the extent that they have difficulty distinguishing external reality from their internal perceptions2. Schizophrenia is perhaps best described as a syndrome that is identifiable by a cluster of signs and symptoms, which have diverse pathogenic bases3. The symptoms of schizophrenia can be debilitating in that they affect the person’s ability to think, to concentrate, to relate, and to function in usual day-to-day activities. The symptoms can be divided into two groups: positive and negative. Positive symptoms include disorders of thinking and perception including delusions, hallucinations and bizarre behaviour. Negative symptoms include reduced levels of energy and motivation, attention deficit, blunted affect, passive social withdrawal and impairment in social functioning, loss of motivation, poverty of speech and poor rapport2,4,5.


The criteria for diagnosing schizophrenia include the presence of characteristic symptoms:








The presentation of an acute episode of schizophrenia is often a critical event that requires an immediate and comprehensive response. People with schizophrenia also frequently suffer emotional symptoms, such as depression and anxiety. Suicidal ideation may be present, with 10% of people with schizophrenia completing suicide7.


A number of subtypes of schizophrenia have been identified. The Diagnostic and Statistical Manual of Mental Disorders6 identified five subtypes: paranoid, disorganised, catatonic, undifferentiated and residual. A number of biological researchers use subtypes of type I or positive schizophrenia, which has a preponderance of positive symptoms; and type II or negative schizophrenia, which has a preponderance of negative symptoms2.



COURSE OF THE ILLNESS


The course of schizophrenia is often marked by a prodromal phase in which there may be changes in the person’s social behaviour. Some of these changes, particularly those of withdrawal, irritability and anger, moodiness, and loss of interest in appearance and social relationships, may seem to be related to age-specific behaviours in adolescence. Other symptoms during the prodromal phase may include depression, suspiciousness, anxiety, and sleep disturbance. The first episode of schizophrenia usually occurs between the late teens and early thirties. The trajectory of the illness is highly variable. It may be brief (up to 2 years) with remission, or may last much longer with residual symptoms. Around 25% of people with the illness have a full remission following one or more episodes5. Around one third of people with schizophrenia will have a recovery from the acute phase that is marked by fewer relapses and fewer hospitalisations for acute episodes than those who retain residual symptoms. While this group may still require ongoing treatment and support, they will be able to function in the community8. Positive symptoms of delusions and hallucinations and disorders of thinking predominate in the early episodes of the illness, but tend to decrease in intensity over time. Loss of social and work skills, self-care and relationships may feature in the residual phase.


Better outcome is associated with










Relapse following treatment is associated with







PATHOPHYSIOLOGY OF SCHIZOPHRENIA


The early descriptions of schizophrenia by Kraepelin and Bleuler in the early 1900s described it as a biological disorder10. Later theories ventured into psychological and familial explanations, focusing attention on the psychology of the person, or family communication. These explanations have not been supported by scientific studies and recent research has focussed on genetics, brain pathology and brain chemistry.



GENETIC FACTORS


There is evidence that genetic factors play a role in the development of schizophrenia. Twin studies have indicated a clear genetic link. Studies of monozygotic (identical) twins demonstrate a concordance (both twins having the same illness) rate of 40–55%, compared with a concordance rate for dizygotic (non-identical) twins of around 10%11,12. If one parent has schizophrenia, there is a 10% risk that offspring will develop the disorder. This risk rises to around 45% if both parents have the disorder11. If schizophrenia were a purely genetically inherited disorder, the concordance rate for monozygotic twins would be around 100% since they share 100% of their genes with each other. It must be concluded that other factors are implicated in the development of the disorder. The possibility of one gene being responsible for schizophrenia has been ruled out13. Genetic studies of people with schizophrenia and their biological parents indicate that altered calcineurin signalling could contribute to a susceptibility to schizophrenia13. The genetic effect is complex and probably involves multiple genes as well as non-genetic factors. Other illnesses with this pattern of genetic effect include insulin-dependent diabetes mellitus, multiple sclerosis and coronary artery disease14.



BRAIN PATHOLOGY


Schizophrenia has been described as a neurodevelopmental disorder and a number of influences on brain development have been implicated11. No specific brain development problem has been identified, and it is possible that schizophrenia may be the result of the interaction or combined effect of several neurodevelopmental events in utero. Environmental factors that may have contributed to brain pathology include maternal exposure to viral illness, malnutrition, birth difficulty and injury11. Gestational and birth problems have been identified as more frequent in people who develop schizophrenia. People with schizophrenia are more likely to have been born in winter, and influenza epidemics are linked to higher rates of schizophrenia11. Maternal influenza in the third trimester of pregnancy, or very poor maternal nutrition in the first trimester, has been identified as risk factors. It is suspected that these perinatal insults may result in a lack of oxygen to some brain regions, and with that, the hippocampal and parahippocampal areas being implicated5. These areas play a major role in the reception and distribution of sensory stimuli and subsequently the organisation of thinking processes.


Neuroimaging studies of young people newly diagnosed with schizophrenia show a pattern of brain abnormality similar to people who have had schizophrenia for a much longer time, implying that brain changes may relate to the pathophysiology of the diagnosis rather than the effect of having the diagnosis for a long period of time. These abnormalities include enlargement of the ventricles, enlargement of the sulci on the cortex of the brain, reduction in brain size, and reduction in size of specific areas, such as hippocampal and prefrontal areas11,15. The loss of cells over time in early-onset schizophrenia has also been demonstrated. A group of young people with schizophrenia showed progressive loss of brain cells in the parietal lobes, spreading to other areas of the brain over time. The study correlated the greatest loss of cells with the worst symptoms of the disorder11. Velakoulis and colleagues (2000) suggest a model for neurodevelopmental understanding of schizophrenia involving a lesion in the hippocampal area that creates a vulnerability to further injury during the early stages of psychosis that may be linked to stress or marijuana use15.




VULNERABILITY-STRESS MODELS


The biological defects related to genetic factors, brain pathology and biochemical changes, while showing consistent and strong association with schizophrenia, are not a sufficient condition for the occurrence of the disorder16. The occurrence of a particular mental disorder in a particular individual needs to be understood by the presence of interacting biological, psychological, and social factors. The vulnerability-stress model is based on the understanding that a certain percentage of the population will, because of particular genetic and brain development factors, be vulnerable to schizophrenia. In certain psychological and environmental conditions, this vulnerability will be expressed as an episode of schizophrenia. Having a vulnerability to schizophrenia does not necessarily imply that the person will develop an episode of the disorder. Whether or not the person will experience the disorder, and whether or not the person will suffer relapses of the disorder, is dependent upon





These three factors interact, thus providing a model for aetiology of schizophrenia that recognises biological, psychological and sociological influences5,16.




NURSING IMPLICATIONS


The diagnosis of schizophrenia is made by careful and comprehensive psychological and biological assessment including assessment of presenting problems, history of the illness, premorbid personality and functioning, corroborating information, family history, and observation. The presence of delusions, hallucinations, disorganised speech and behaviour are characteristic symptoms of acute psychosis that may indicate a schizophrenic process. Positive symptoms tend to fluctuate over time and the client may be unwilling to discuss delusional material until there is a level of trust. The negative symptoms of loss of interest, withdrawal, anergia, poverty of speech, poor self-care and a blunted emotional response may be observed. The person presenting with a range of symptoms indicative of schizophrenia may also present with high levels of anxiety, depression, or aggressive responses related to delusional material. There is a high level of substance misuse and dependency in people presenting with schizophrenia8.





TREATMENT


Treatment for schizophrenia involves a combination of pharmacological and psychotherapeutic interventions5,18. Early treatment of schizophrenia is important. The duration of untreated psychosis has been associated with cognitive deterioration. Early treatment may increase the likelihood of symptomatic relief, reduce cognitive deficits19, and decrease the adverse effects on family and social networks20. The place of treatment needs to be assessed in light of the person’s safety, the ability of the family to provide containment and support, and the availability of community mental health services. Hospitalisation should be considered if there is any concern for the safety of the person, family and community.



PHARMACOLOGY


Drugs, which aim to reduce the symptoms of schizophrenia, are called antipsychotics. Traditional antipsychotic drugs, such as chlorpromazine, haloperidol and trifluoperazine, block D2 receptors and have an effect on positive symptoms, but little effect on the negative symptoms that can have a significant impact on the person’s quality of life and functional status. These drugs may also produce sedation, emotional settling, and psychomotor slowing. In addition, these drugs have a range of peripheral and central nervous system side effects that range from minor effects, such as constipation and dry mouth, to chronic movement disorders and life-threatening neuroleptic malignant syndrome2.


Atypical antipsychotic drugs such as olanzapine, risperidone, and quetiapine are much better tolerated, although patients taking these drugs still need monitoring for neuroleptic malignant syndrome, extrapyramidal and a range of other side effects, including significant weight gain. In addition, atypical antipsychotics have been significantly associated with the onset of diabetes mellitus21. This group of drugs is called atypical because of their difference from the earlier antipsychotic agents. The atypical antipsychotic agents differ in terms of their neurotransmitter and neuroreceptor activity and their effect on negative symptoms. These drugs have less effect on D2 receptors, but antagonise other dopamine and serotonin receptor sites. They are being increasingly favoured in clinical practice. First-episode psychosis is usually treated with one of the atypical antipsychotic drugs. Monitoring of effectiveness includes observation of both positive and negative symptoms. An anxiolytic, such as diazepam, can be added in the short term to reduce distress levels of anxiety, agitation and insomnia. Monitoring for side effects includes observation for signs of dystonia (impaired muscle tone, often in the head, neck and tongue) shaking, stiffness and restlessness. Physical observations should include temperature, blood pressure and pulse as medication may alter cardiovascular function or have toxic effects. In the longer term, maintenance doses of atypical antipsychotics can be used, with continued monitoring. Clozapine may be effective when other treatments have failed. The use of clozapine is limited to registered centres, and in addition to the previously mentioned adverse effects, there is need to monitor for the severe adverse effects of neutropenia, agranulocytosis, and myocarditis2,20.





DEPRESSION


Depression represents a significant public health issue. The World Health Organization’s (WHO) recent Global Burden of Disease study has estimated that by 2020, depression will contribute the largest share of disability in the developing world, and the second largest share of disability worldwide24,25. The incidence of depressive disorders is relatively similar worldwide in terms of distribution and impact at individual and community levels26.


Depression causes significant distress and suffering, and can lead to impairment in educational, social, family, interpersonal and employment functioning. There is a well established link between depression and suicide, and it is a grim fact that each year upwards of 2,300 Australians27 and 500 New Zealanders28 die by suicide. Rates of suicide in Australia and New Zealand are similar and rank high in comparison to international rates28. The direct cost of treating depression in the Australian context is estimated to be in the region of $500 million annually, of which approximately $60 million is spent on pharmaceuticals. The true cost of depression to individuals and the community defies quantification27.


In Australia, depression has been identified as a National Health Priority Area, and the National Action Plan for Depression has been developed to provide a strategic direction for the prevention, early intervention, assessment and treatment of depression29. These initiatives aim to elevate depression to the ranks of heart disease and cancer in terms of community awareness and government commitment to prevention and treatment.



PREVALENCE, NATURAL HISTORY AND COURSE OF DEPRESSION


Depression is disconcertingly prevalent in the community, an observation that has been confirmed by the findings of a number of large-scale epidemiological studies conducted internationally. In Australia, the National Survey of Mental Health and Wellbeing estimated that some 5.8% of the adult population (or approximately 778,000 adults) had an identifiable depressive disorder in the 12 months prior to the survey30. The National Co-morbidity Survey, a second large survey of the epidemiology of mental disorders in the USA, found the overall lifetime rate of major depressive episode to be 17.1% (12.7% among males, and 21.3% among females)31.


Differences in the prevalence rates reported between epidemiological studies are likely to be accounted for by differing methodologies employed in each study, for example the use of different survey questionnaires. However, it can be stated with some confidence that between 5 and 10% of the adult population will experience a major depressive episode in a 12-month period26.


Depression frequently co-occurs with other mental disorders, for example anxiety symptoms or disorders occur in approximately 30% of patients with depression, and approximately 30% of people with depression experience panic attacks32. There are a number of medical illnesses where depression is a frequent concomitant condition, or where there seems to be evidence of the primary medical illness precipitating depression – either through a biologically mediated process and/or due to the stress associated with chronic, disabling or life-threatening illness. The incidence of depression among medically ill populations has been found to be as high as 15%33. Medical illnesses or syndromes where there is evidence of an association with depression include, but are not limited to, the list in Table 16.1.


TABLE 16.1 SOME MEDICAL ILLNESSES OR SYNDROMES ASSOCIATED WITH DEPRESSION
























Cancer Migraine
Myocardial infarction Multiple sclerosis
Cerebrovascular accident Parkinson’s disease
Diabetes Rheumatoid arthritis
HIV/AIDS Systemic lupus erythematosus
Epilepsy Chronic fatigue syndrome
Dementia Pain

The average age of onset of major depressive disorder is in the late 20s; however, depression can occur at any age34, with depression in the elderly and childhood depression being common and sometimes under-recognised by health professionals35,36. The onset of symptoms of major depression can be insidious, with symptoms increasing in frequency and severity over several weeks or months, or onset can be sudden. The duration of an episode of major depression is variable, lasting from weeks to years. Left untreated an episode of major depression can last for six to nine months34,37.


While many people experience only a single episode of major depression and recover fully, approximately 50–85% of people will experience subsequent episodes of major depression38. Approximately 20% of people who experience a major depressive episode will experience a relapse within 12 months39, an important consideration for planning preventative treatment, such as maintenance antidepressant medication or ‘booster sessions’ where psychological treatment has been used.

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Dec 22, 2016 | Posted by in NURSING | Comments Off on Mental health breakdown

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