Hallucination+symptom+(Jeromy,+Nicole,+Ivan)

5. Do the hallucination symptoms suffered by patients with schizophrenia have a biological root?

Group members: Jerome Lok Sai Hong 08609497t Nicole Lau Ka Yan 08629251t Ivan Tsui Ho Kit 10945501t


 * Introduction** (Jerome Lok Sai Hong 08609497t)

There is a controversial issue that whether the hallucination symptoms suffered by patients with schizophrenia have a biological root. This paper is going to argue this controversial issue, and suggest some ways to improve the symptoms.


 * First of all, what is schizophrenia?**

Schizophrenia is a major psychiatric illness that can have a devastating impact on the lives of both patients and their family members. Feelings of isolation, anxiety, depression, and frustration are common among family members with an ill relative. The hope for both patients and family members are that by learning about schizophrenia and how to cope with the common problems, the strain involved in dealing with the illness can be reduced, and the quality of life can be improved as well (Ciompi, 1980).

Schizophrenia is a complex and confusing illness for mental health professionals, patients, and family members alike. In the popular media (television, radio, newspaper), the word schizophrenia is often used to describe any person with psychotic symptoms, such as hallucinations or delusions. In the view points of medical professionals who treat persons with mental illness, schizophrenia refers to a specific psychotic illness characterized by severe problems in social functioning and self-care skills and difficulty distinguishing reality (Anderasen, 1984). Myths

There are some myths about schizophrenia; firstly, people with schizophrenia are prone to violence. In fact the opposite is more often the case, most people with schizophrenia withdraw from others and prefer to spend more time alone. Yet, there are some patients who become violent when they are suffering from symptom of auditory hallucination (Volavka & Karkowski, 1989). Secondly, drug and alcohol abuse can cause schizophrenia. Despite the similarity between the symptoms of schizophrenia and the negative effects of drugs and alcohol, substance abuse does not cause schizophrenia. Most people who experiences schizophrenia-like symptoms while using drugs or alcohol stop having these symptoms soon after their substance abuse ceases. And research suggests that those people who do develop schizophrenia after substance abuse would probably have developed the illness anyway. Although substance abuse does not cause schizophrenia, it can worsen the symptoms of the illness (Murray, & lewis, 1987). Thirdly, Outdated double-bind theory suggested schizophrenia is due to inconsistent parenting, with conflicting messages or It was caused by parents who were not based on controlled studies.


 * The cause of hallucination symptoms of schizophrenia--biological factor** (Ivan Tsui Ho Kit 10945501t)

There is controversial issue about the causes of schizophrenia, some people believe that psychosocial factors contribute to schizophrenia, oppositely, modern theories of schizophrenia emphasize that the disorder is biological in nature. To explore this controversial issue, firstly, to understand what are dopamine hypothesis and serotonin hypothesis.

Dopamine hypothesis Dopamine is a neurotransmitter in the brain, which is a chemical that allows the passage of signals between two neurons through the progression of nerve impulse across the synapse. At the synaptic terminal, there are dopamine receptors to facilitate the transmission of dopamine from neuron to neuron. In total, five different types of dopamine receptors are known to be located in human brains (Gaur, 2008): • D1 - prefrontal cortex, striatum • D2 - striatum, low concentration in medial temporal structures (hippocampus, entorhinal cortex, amygdala), thalamus, prefrontal cortex • D3 - striatum and ventral striatum • D4 - prefrontal cortex and hippocampus (have not been detected in the striatum) • D5 - hippocampus and entorhinal cortex



The classical "dopamine hypothesis of schizophrenia" namely postulates a hyperactivity of dopaminergic transmission at the dopamine D2 receptor. As a result, excess dopamine is secreted into the synapses in certain neural area of the brain. The increased dopamine produces over-stimulation of the neuron cells and is believed to be responsible for the symptoms of schizophrenia, principally the hallucinations, the delusions and the psychosis.

There is much strong evidence that supports the dopamine hypothesis. Firstly, psychopharmacological evidence supports the fact that all clinically useful antipsychotic medications are dopamine antagonists. Those drugs that block dopamine are useful to reduce schizophrenic symptoms. Many of them block or bind to the dopamine receptors to decrease dopamine activity, such as chlorpromazine and apomorphine (Gaur, 2008).

One additional evidence that dopamine may be involved in schizophrenia came from Amphetamine users. It is found that Amphetamine stimulates the brain to produce more dopamine and may subsequently trigger symptoms of schizophrenia (Breier, 1996). Lastly, the dopamine hypothesis has also received support from postmortem and PET indications of increased dopamine D2 receptor levels in the brains of schizophrenic patients (Nordström, 1998).

However, there are actually problems with the above evidences. Firstly, Amphetamines only stimulates the positive symptoms of schizophrenia. They do not produce any kind of the negative symptoms. Likewise, anti-psychotic drugs are only affective on the positive symptoms of the disease (Roth, 2003). While there is still some evidence that schizophrenics do possess higher levels of dopamine, however, these increases are only found in the striatum of the brain. Also, there is evidence that the prefrontal cortex produces lower levels of dopamine (Fredrickson, 2007).

Serotonin hypothesis Another neurochemical hypothesis of schizophrenia is the serotonin hypothesis. The recognition of role of serotonin in schizophrenia was largely based on the studies of drugs like lysergic acid diethylamide (LSD) and ecstasy. These drugs both have the effect of blocking the effects of serotonin at specific receptors. The blockage produces mental and perceptual states that resembled schizophrenia (Siegel, 2005). For example, LSD competes for and occupies serotonin's receptor sites with very high potency, resulting in psychosis-like symptoms. It was hypothesized, therefore, that schizophrenia might be caused by a serotonin deficiency.



The strongest evidence of serotonin's role in schizophrenia, by far, is the mechanism of atypical antipsychotic drugs like clozapine and risperidone. These drugs, which have provided dramatic improvements in patients that were resistant to other medications, show a weak direct dopaminergic antagonist effect. (Kaplan & Sadock, 1995). It reveals that the principal mechanism of symptom relief with atypical antipsychotics is from something other than dopamine antagonism. This mechanism is probably serotonin antagonism. This hypothesis was confirmed when they combined typical antipsychotics with a 5-HT2 antagonist such as ritanserin, they resulted in a substantial relief of patients’ negative symptoms of schizophrenia (Kaplan & Sadock, 1995).

One of the major problems with this hypothesis was the recognition that the primary effect of LSD was to produce visual hallucinations, which are relatively rare in schizophrenia, not auditory hallucinations, which are the most popular perceptual deficit in schizophrenia. Additionally, paranoid delusions, conceptual disorganization, and the wide range of cognitive impairments characteristic of schizophrenia: e.g., disturbances in working memory, semantic memory, and executive function, are generally absent during LSD intoxication (Roth, 2000).


 * Functional anatomy of schizophrenia / Abnormalities in Brain Structure**

Schizophrenia is associated with some brain abnormalities as brain scans like magnetic resonance imaging (MRI), PET; SPET; and fMRI show the functional anatomy of schizophrenia in the brain structure. Such abnormalities can cause nerve damage and disconnections in the pathways that carry brain chemicals. For example, in schizophrenia patients that are vulnerable to hallucinations, there are changes in the activity of pathways connecting the frontal and temporal lobes shown by neuroimaging (Mo, 2008). .

The SPET found the hallucination state was associated with greater blood flow in language-related area, significantly in a region approximately corresponding to Broca’s area and as a trend, in the anterior cingulate and left temporal cortices

Above: Decreased brain activity in schizophrenia subjects (S) compared to normal controls(N) in an fMRI study examining executive functioning. Image courtesy of Prof. Philip Ward, NISAD Cognitive Neuroscience Research Panel.

Downloaded from http://schizophreniabulletin.oxfordjournals.org/ at The Hong Kong Polytechnic University on November 19, 2011



Neuroimaging techniques reveal reduced volume and loss of tissue in the brains of schizophrenic patients. Many of them have a reduced volume of gray matter in the brain, especially in the temporal and frontal lobes. Recently some neuroscientists have detected gray matter loss of up to 25% in people with schizophrenia. The damage starts in the parietal or outer regions of the brain but can spreads to the rest of the brain in a five year span. Patients with the worst brain tissue loss would have the worst symptoms, including hallucinations, delusions, hearing voices, etc. (Torrey, 2011).

Also, reductions in volume of the prefrontal cortex are observed in many schizophrenic patients. Deterioration can damage nerve cells and weaken the function of attention, reasoning, and meaningful speech. Impairment in the left side of the cortex is also associated with auditory hallucinations (Wible, 1995). On the other hand, schizophrenic patients are reported loss of volume in limbic system, which contain hypothalamus, amygdala, and hippocampus. Activities in the limbic area in general are related to emotions and memory, and abnormalities there would be lined to positive symptoms, including delusions and hallucinations, and also with disordered thinking (Torrey, 1974).


 * Stress-Vulnerability Model** (Nicole Lau Ka Yan 08629251t)

Although some scientists believe that the illness is biological in nature, another perspective shows evidence to argue that certain psychosocial factors determine the severity of schizophrenia. Although the tension and problems of family did not cause schizophrenia, there is an evidence to say that expressed emotion in the family increase relapse rate of schizophrenia into psychosis or hallucination again. In fact, family plays a key role in helping patient cope more effectively with the illness (Nuechterlein & dawson, 1984).

According to the Stress-Vulnerability Model of Schizophrenia, the severity and course of schizophrenic symptoms are determined by three different factors: biological vulnerability, stress, and patient coping skills.

Biological vulnerability refers to the biological predisposition to experience the symptoms of schizophrenia, such as an imbalance in brain chemistry caused by genetic factors, exposure to early biological risks, or both. If the person does not have this vulnerability, he or she will not develop the symptoms of schizophrenia. Among individuals who have schizophrenia, there appears to be a correlation between the degree of biological vulnerability and the severity of symptoms and course of illness(McNeil, 1987).

Stress refers to negative aspects of the environment in which patients currently live. Research has shown that several types of stress can have a negative effect on persons with schizophrenia. Significant life events, such as the death of someone close, loss of a job, or change in residence can be stressful and lead to relapses in some patients. Living in an environment in which there is a great deal of conflict, criticism, or negativity between the patient and others (either family members or professional staff) can be stressful to patients and increase their risk of relapse. Also, an environment that either places heavy demands on the patient or that lacks structure can be stressful and worsen symptoms of schizophrenia (McFarlane, et al., 2003).

Coping skills refers to patient’s ability to handle stress effectively and thereby to reduce the negative effects of stress. Effective social skills enable patients to resolve interpersonal conflicts thus lowering stress in relationships (Lefley, & Jahnson, 1990).

Therefore, the majority of scientists believed that the interaction between biological vulnerability, stress, and coping skills influences the severity of symptoms and the patient’s risk of relapse and rehospitalization. The stress-vulnerability model, as illustrated in Figure 1.1. of schizophrenia provides a framework for understanding the factors that influence the course and severity of schizophrenia, the stress-vulnerability model is also helpful in guiding the treatment of the illness (Nuechterlein & Dawson, 1984).

The Stress-Vulnerability model of Schizophrenia



The symptoms of schizophrenia-- hallucination (Nicole Lau Ka Yan 08629251t) The symptoms of schizophrenia can be divided into five broad categories: positive symptoms, i.e. hallucination, delusions; negative symptoms i.e. social withdrawal; mood problems i.e. reduced emotional expressiveness (blunt affect), disturbances in thinking; and behavioral disturbance.

The major positive symptom of schizophrenia is auditory hallucination (AH). Hallucination is a precept in the absence of an external stimulus, and AH occurs in 70-80 % of all patients (Blom et.al., 2011). A video called Yi Huan Yi Zhen, the interviewee in the video illustrated the experience of suffering auditory hallucination of schizophrenia.

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Patients perceive external person(s) talk(s) to them, these may involve single and/or multiple voices, who may be known and/or unknown, speaking sequentially, and which may give commands, comments, insults, or encouragement (Jones, 2008), and often produce distress, functional disability and behavioral dys-control (Shergill, Murray & McGuire, 1998). Hugdahal (2009), states the processes of auditory hallucination in schizophrenia, process of auditory hallucination as failure of top-down control of bottom- up perceptual processes, this point of view see auditory hallucinations as bottom-up driven perceptual phenomena originating from the left temporal lobe that are out of control due to failure of top-down inhibition, and the failure of inhibitory control is mediated through impaired functioning of the prefrontal and anterior cingulate cortex since these brain regions are critically involved in cognitive control processes (Braver, Cohen & barch, 2002).



Fig. 3. Outline of a cortical network involved in auditory hallucinations (AH) in patients that are seen as bottom-up perceptual misrepresentations, attention shift/enhancement, and failure of prefrontal inhibitory control function. The model emphasizes the involvement of the middle and superior temporal gyri in the peri-Sylvian region (1) for the generation of AH, prefrontal cortex (2) for top-down inhibitory control, and parietal cortex (3) for attention focus.

Hugdahl, K. (2009). ‘‘Hearing voices’’: Auditory hallucinations as failure of top-down control of bottom-up perceptual processes. Scandinavian Journal of Psychology, 50, 553–560. DOI: 10.1111/j.1467-9450.2009.00775.

Auditory Hallucination

Fig. 1. SPM(T)’s for the conjunction analysis revealing brain regions significantly activated during the experience ofAVH in both psychotic and nonpsychotic individuals with AVH. (A) Areas significantly activated within a priori hypothesized regions. (B) Areas significantly activated within all gray matter voxels in the brain Thresholded at P5.05 False Discovery Rate (FDR) corrected for multiple comparisons. Abbreviations: SPM(T)’s, spatial parametric mapping T-values; AVH, auditory verbal hallucinations. Diederen, K. M.J., Daalman, K., Weijer, A. D. de., Neggers, S. F.W., Gaste, W. van, Blom J. D., Kahn. R. S., and Sommer, I. E.C.. ( 2011). Auditory Hallucinations Elicit Similar Brain Activation in Psychotic and Nonpsychotic Individuals. Schizophrenia Bulletin doi:10.1093/schbul/sbr033.

Downloaded from http://schizophreniabulletin.oxfordjournals.org/ at The Hong Kong Polytechnic University on November 19, 2011


 * Schizophrenia affect the well-being of a society (Nicole Lau Ka Yan 08629251t)**

Some people claim that hallucination symptoms suffered by patient with schizophrenia affect the well-being of a society, when patients with schizophrenia experience auditory hallucinations, their voices may command them to harm themselves or others. Such voices are often very distressing, and some patients are unable to resist complying with the commands (Mackinnon, Copolov, & Trauer, 2004). Thus, treatments are needed to decrease the degree of symptoms which patients suffering from hallucination so as to minimize the rate of their harmful behavior to themselves or to others.

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 * Treatment** (Nicole Lau Ka Yan 08629251t)

Research evidences shows that psychopharmacological approaches and psychological approaches are effective for symptoms reduction, and / or relapse prevention. The aims of treatment are to reduce biological vulnerability; reduce environmental stress; and improves coping skills.

Psychopharmacological approaches Although there is no cure for the biological vulnerability that causes the symptoms of schizophrenia, antipsychotic medications can reduce both symptoms and the risk of relapses.

Effective pharmacological treatment of schizophrenia has been available since 1950s.The discovery of the effects of antipsychotic medications on schizophrenia was accidental. In the early 1950s, a number of different scientists were in the process of trying to develop more effective medications for the treatment of hypertension. One of these newly invented medications was the drug Thorazine (chemical name chlorpromazine). When this drug was administered to animals in laboratory tests, its effects on blood pressure were disappointing. However, the scientists observed that Thorazine appeared to have a mildly tranquilizing effect (The term major tranquilizer was first used to describe antipsychotic medications, including what later came to be known as Thorazine.), and began to explore the possibility that it might have other beneficial effects. This drug was given to patients with schizophrenia, it resulted in dramatic reductions in psychotic symptoms such as hallucinations and delusions. In some cases, these symptoms were completely eliminated. Thorazine was first given to patients with schizophrenia not in carefully controlled drug studies, but rather in open drug trials.with the success of Thorazine, scientists began to develop other antipsychotic medications with similar clinical effects (Mueser, & Gingerich, 1994). The effects of antipsychotic medications on schizophrenia focus on symptom reduction e.g. hallucination and relapse prevention (Davis et.al.,1991).

There are two categories of antipsychotic medication, one is Dopamine D2 antagoists, another one is mixed neuroreceptor antagonists. The potency level refers to that the higher the potency, the lower the dosage is needed.

The antipsychotics are divided into traditional antipsychotic and atypical antipsychotic.

“Traditional antipsychotic” (neuroleptic), now refers to first-generation antipsychotics. For examples, haldol (Haloperidol), stelazine (Trifluoperazine).

“Atypical antipsychotic” refers to second gneration antipsychotics, i.e. clozaril (Clozapine), risperdal (Risperidone), olanzapine (Zyprexa). This new generation antipsychotic medications are believed to operate by different mechanisms of action than traditional antipsychotics as stated previously (Geddes et.al., 2000).

SCHULTZ, S. H., NORTH, S. W., and SHIELDS, C. G., (2007). Schizophrenia: A Review. American Family Physician. Vol 75 (12), 1821-1829.

There are huge evidences show that drug treatment is effective to reduce or diminish symptoms of schizophrenia.

Yet, there are adverse effects when taking these antipsychotic medications. The first-generation antipsychotics (i.e. Haloperidol, Trifluoperazine) confer an increased risk of extrapyramidal side (EPS) side effects, such as dystonic reactions (i.e. fixed upper gaze, neck twisting, facial muscle spasms), parkinsonian symptoms (i.e. rigidity, bradykinesia, shuffling gait, termor), and akathsia (i.e. inability to sit still, restlessness, tapping of feet). Tardive dyskinesia, which is a chronic disorder of the nervous system characterized by involuntary jerking movements (primarily of the face, tongue, and jaw), often is considered an extrapyramidal side effect, and the tardive dyskinesia is a common late side effect of prolonged treatment with antipsychotics. It is the most concerning side effects as it does not diminish the chronicity and severity if it does present(Correll et, al. 2004). It is important to notice that the first-generation antipsychotic may induce medication side effects such as acute dystonic reaction. The most common method to reduce such a medication side effects is to prescribe additional medications (anticholinergic medications), i.e. Cogentin, Artane either by oral route or injection to reduce the activity of choline chemical in the brain (Tammenmaa, et.al., 2004).



SCHULTZ, S. H., NORTH, S. W., and SHIELDS, C. G., (2007). Schizophrenia: A Review. American Family Physician.Vol 75 (12), 1821-1829.

New antipsychotics(i.e. Risperidone, Olanzapine, Clozapine) that confer less risk of EPS side effects than the traditional antipsychotics. Yet, the most concerning adverse effects of the atypical antipsychotic is the causation of weight gain and diabetes-related conditions. A retrospective cohort studies indicated that both Risperidone (Risperdal) and Olanzapine (Zyprexa) were associated with weight gain, but only olanzapine was shown to be associated with development of diabetes. Although Clozapine does not cause the extrapyramidal side effects of traditional antipsychotics, such as tremors and akathisia, the most concerned adverse effect is granulocytopenia—a reduction in the number of granulocytes (a type of white cell) in the blood. Patients must have a baseline white blood cell (WBC) differential count before initiating therapy. Preform regular WBC counts during treatment and after 4 weeks after discontinuation (Leucht et.al., 2003; Farwell et.al., 2004; Marder, 2004).



SCHULTZ, S. H., NORTH, S. W., and SHIELDS, C. G., (2007). Schizophrenia: A Review. American Family Physician.Vol 75 (12), 1821-1829.



SCHULTZ, S. H., NORTH, S. W., and SHIELDS, C. G., (2007). Schizophrenia: A Review. American Family Physician.Vol 75 (12), 1821-1829.

It is important that medication adherence and symptoms monitored on a regular basis are important, so that medication can be adjusted if changes in symptoms are detected.

Although antipsychotic medications are main focus of current treatment approached to schizophrenia and psychotic symptoms, there are some disadvantages to such treatments including side-effects, non-response and non-compliance. Researches also indicated that it is more effective to treat schizophrenia with a combination of antipsychotic medication and psychosocial intervention, compared with medication alone. Adding a psychosocial intervention to antipsychotic medication reduces treatment discontinuation among people with early-stage schizophrenia. Combined treatment also reduces rates of relapse, readmission and non-adherence, and improves patient insight and social functioning (Uxley et.al., 2000).

Cognitive behavioral therapy (CBT) interventions have been considered to be an alternative way to treat symptoms of schizophrenia. Rector and Beck (2001) indicates that he aim of CBT is that via modification of cognitive appraisal, by focusing on the characteristics of the voice, encourages the patient to accept the voices as self-generated. Oya et. al. (2011) indicates CBT is a useful alternative to medication for auditory hallucination in schizophrenia patient. This study aims to prepare program for patients with schizophrenia coping with auditory hallucination. 12 male inpatients aged between 18 and 55 years diagnosed with schizophrenia were recruited, the experimental group (7 patients) received routine care plus group CBT and the control group (5 patients) received routine care alone. The group treatment program was conducted for 9-10 sessions twice a week. Measurement was done in pre-treatment, post-treatment, and at the 1-year follow-up. The results indicated that there was a significant reduction in the severity and frequency of hallucination, delusions, distress and occupation with auditory hallucinations in the CBT group after treatment.
 * Psychosocial intervention**

Another study by Kumari (2011) also indicated that reduction of functional magnetic resonance imaging response during angry expressions correlated directly with symptom improvement. This study provides the first evidence that cognitive behavior therapy for schizophrenia attenuates brain responses to threatening stimuli and suggests that cognitive behavior therapy for schizophrenia may mediate symptom reduction by promoting processing of threats in a less distressing way.



Figure 1 (A and D) Areas of reduced brain activity following CBT for psychosis + TAU (CBTp) (but not following TAU alone) to fearful and angry facial expressions (voxel threshold P50.005 uncorrected) in axial views with associated MNI z co-ordinates. Left hemisphere is shown on the left. (B) Mean functional MRI response in the left inferior frontal–insula cluster in each group at baseline and follow-up to fearful expressions. (C) Mean functional MRI response in the left inferior frontal cluster in each group at baseline and follow-up to angry expressions. (E) Scatter plot of decreases in activity from baseline to follow-up in the left inferior frontal region during angry expressions against the change in symptoms from baseline to follow-up across the whole sample.

Functional MRI of cognitive therapy for psychosis Brain 2011: 134; 2396–2407 | 2403.In Kumari. V., Fannon. D., Peters. E. R., ffytche. D. H., Sumich. A. L., Premkumar. P., Anilkumar. A. P., Andrew, C. Phillips, M. L., Williams, S. C. R. and Kuipers, E. (2011). Neural changes following cognitive behavior therapy for psychosis: a longitudinal study Brain,134; 2396–2407.

Downloaded from http://brain.oxfordjournals.org/ at Hong Kong Polytechnic University on November 19, 2011

Reduce environmental stress is also important. Stress resulting from tense family relationships can be lowered by strategies of family interventions, such as developing specific and realistic expectations on patient’s behavior and improving both communication skills and problem solving skills. In-home crisis intervention prevents treatment drop-out rates. Eventually, reduces relapse rates, improve symptoms, and functioning (Pharoah et.al., 2003).

Improving coping skills is also helpful by teaching patients more effective coping techniques, so that they are better able to handle everyday types of stress. Intensive Psychiatric Rehabilitation Treatment, which is a program that teaches living, job, and social skills to patients, has resulted in improvements in functioning. Social skills training has improved independent living skills, their skills for interacting with others; supported employment programs have shown improvements in the number of hours worked and total wages earned, and stress reduction techniques to cope with problems of anxiety (Joy &et.al., 2000).

Other kinds of treatment Other evidences have been evaluated the effects on treating schizophrenia includes Traditional Chinese medicine; Acupuncture; Electroconvulsive therapy.

Study concluded that Chinese herbal medicines, given in a Western biomedical context, may be beneficial for people with schizophrenia when combined with antipsychotics. Traditional Chinese medicine is also under-evaluated, but results from one pioneering study that attempted to evaluate TCM should encourage further trials (Rathbone et al., 2005).

Researchers found insufficient evidence to recommend the use of acupuncture for people with schizophrenia. The numbers of participants and the blinding of acupuncture were both inadequate, and more comprehensive and better designed studies are needed to determine the effects of acupuncture for schizophrenia (Rathblone & Xia, 2005).

The evidence in this review of Tharyan (2005) suggests that Electroconvulsive therapy (ECT) for schizophrenia, combined with treatment with antipsychotic drugs, may be considered an option for people with schizophrenia, particularly when rapid global improvement and reduction of symptoms is desired. This is also the case for those with schizophrenia who show limited response to medication alone. Even though this initial beneficial effect may not last beyond the short term, there is no clear evidence to refute its use for people with schizophrenia. The research base for the use of ECT in people with schizophrenia continues to expand, but even after more than five decades of clinical use, there remain many unanswered questions regarding its role in the management of people with schizophrenia.


 * Conclusion (Nicole Lau Ka Yan 08629251t)**

The cause of schizophrenia is not well known. However, the dopamine hypothesis and serotonin hypothesis explain the illness is biological in nature, and involves some types of disturbance in the brain, and the profound effects of antipsychotic medications on the symptoms of schizophrenia proved the illness is related to disordered brain functioning. The majority of scientists believed that the interaction between biological vulnerability, stress, and coping skills would influences the severity of symptoms and the patient’s risk of relapse and rehospitalization. The stress-vulnerability model of schizophrenia provides a framework for understanding the factors that influence the course and severity of schizophrenia, and it provides a supplementary explanation of that there is an element of interaction between biological basis with the psychosocial factors that give the content of the hallucination,, i.e. give rise to some sort of hallucination, and the content of the hallucination come from the environment, or other psychosocial stress. The effects of antipsychotic medications on schizophrenia focus on symptom reduction e.g. hallucination and relapse prevention. Yet, there are adverse effects when taking these antipsychotic medications. Whereas evidences show that adding a psychosocial intervention to antipsychotic medication reduces treatment discontinuation among people with early-stage schizophrenia, and combined treatment also reduces rates of relapse, readmission and non-adherence, and improves patient insight and social functioning. Psychosocial interventions include cognitive behavioral therapy; environmental stress reduction; coping skills improvement. Other interventions such as Traditional Chinese medicine; acupuncture; and electroconvulsive therapy have been studied, but some kinds of these interventions need further studied to determine the effectiveness.


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