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This research paper explored the use of medications to treat schizophrenia. I discovered from the literature review that there were different viewpoints about the use of psychiatric medications as well as concepts about the schizophrenia. The topic of psychiatric medication is complex given its usefulness and at the same time having toxic effects. Besides this, there are social, cultural and economic variables that need to be addressed regarding the use of medications and schizophrenia. Still, there is the arena of medication compliance that had been challenging to mental health practitioners for decades. This literature review only skimmed the surface but is rich in its exploration.
Kaplan and Sadock (1991) pointed out that “schizophrenia in the United States and Europe was between .3 and .6 per 1000 persons.” Furthermore, the peak onset for men was between 15 to 25 years of age. For women, the peak age was between 25 and 35 years of age. The authors referred to biological factors that may influence the onset of schizophrenia. The dopamine hypothesis, for example, is described as a “hyperactivity of dopaminergic systems. Dopamine is a chemical messenger that influences the control of movement, emotional response, pleasure and pain.”
Standford (2001) had gathered research from other studies and noted that there were 200,000 new cases of schizophrenia each year in the United States. In addition, there were 300,000 acute schizophrenic episodes each year. Of this, approximately, 75% require hospitalization. Consumers that have a substance abuse disorder and schizophrenia tend to be five times as likely to have psychotic episodes, four times the amount of hospitalizations and four times the likelihood of non-medication compliance. Schizophrenia is divided into positive and negative symptoms. Positive symptoms include delusions, hallucinations, disorganized speech and catatonia. Negative symptoms include affective flattening, poverty of speech, social isolation and anhedonia. Cognitive components can include impairment in attention, memory and abstract thinking. Mood components can include dysphoria, suicidality and hopelessness.
Maxmen (1991) pointed out that antipsychotic medications attempt to block psychosis and include a tranquilizing effect. However, hypnosedatives do not reduce psychosis. Antipsychotics have been shown to act as dopamine antagonists and elevate prolactin levels. Standford, Dreisbach & Gaw (2001) said there were serious side effects from typical antipsychotic medication. Side effects include extrapyramidal symptoms (stiffness, tremor, drooling, acute spasm) pseudo-parkinsonism, akathesia (achy restless feeling, leg shaking or pacing), tardive dyskinesia, ocular gyric and anti-cholinergic effects (dry mouth, constipation, blurred vision, urinary retention and sedation). Some typical antipsychotic medications include haldol, prolixin, mellaril and thorazine. Side effects can be treated with cogentin or benadryl but these medications have side effects. The antipsychotics help to improve the positive symptoms but not the negative symptoms. In contrast, some atypical psychiatric medications include clozapine (clozaril), resperidone (resperdal), olanzapine (zyprexa) and queetiaine (seroquel). These newer medications improve negative symptoms and have significantly less extrapyramidal effects. In addition, there was improvement in positive symptoms and cognitive functioning.
Stahl (2001) called atypical antipsychotics, “hit-and-run” action. In other words, atypical medications block dopamine-2 receptors and then rapidly depart (shorter binding time). Thus, there was reduction or absence of extrapyramidal side effects and tardive dyskinesia. The author pointed out from other studies that resperidone has a strong serotonergic activity and better against negative symptoms than positive symptoms. Resperidone was relatively non-sedating, less extrapyramidal and fewer cases of tardive dyskinesia. In comparison, Olanzepine has a strong serotonergic activity and better against positive symptoms. Both medications help reduce the negative symptoms. However, there were no extrapyramidal with olanzepine but it is sedating and has more side effects than risperidone.
Carman and Vangeneugden (2001) studied 102 psychoaffective patients on risperidone. The mean dosage was 4.7 plus or minus 2.5 mg/day. Most clients were at 6mg per day, which was the safest and effective for schizophrenia and affective disorders. The authors reported that there were significant improvements among these patients and with no increase of extrapyramidal or tardive dyskinesia. Thus, this study further supported the research that risperidone not only reduces schizophrenia but also mood symptoms (manic, mixed and depression). Kim et al. (2002) studied the effects of switching from resperidone to olanzapine with twenty female schizophrenic patients. The patients were experiencing menstrual disturbances, galactorrhea and/or sexual dysfunction. Instruments used were the “Positive and Negative Syndrome Scale, abnormal Involuntary Movement Scale, Simpson-Angus Scale for Extrapyramidal Symptoms and the Dickson-Glazer Sexual Functioning Scale.” In addition, serum prolactin levels (elevated levels cause sexual and reproductive side effects) were examined every two weeks during the eight weeks of taking olanzapine. Past studies, according to the researchers noted, “resperidone causes increased prolactin levels.” Patients taking olanzapine in this study made improvements in menstrual functioning and a decrease in sexual side effects. The authors suggested that olanzapine is a better choice than risperidone for females with schizophrenia.
The Addiction Science Research and Education Center (n.d.) suggested that schizophrenics have an “overactive dopamine system.” When given dopamine antagonists to patients their symptoms decrease by turning down the dopamine activity. Dopamine antagonists are drugs that blind but do not stimulate or attach to the receptors. In contrast, agonists such as amphetamine and levodopa have been shown to exacerbate psychotic symptoms in many patients. Agonists bind to dopamine receptors and stimulate the receptors.
Kaplan and Sadock (1991) suggested that dopamine antagonists were effective in treating agitated patients, “regardless of the diagnosis.” Therefore, dopamine over activity was not exclusively associated with schizophrenia. Other studies, according to Kaplan and Sadock have shown in schizophrenics a “degeneration of the limbic system and basal ganglia. Brain imaging has also shown ventricular enlargement and cortical atrophy in schizophrenic patients.” Furthermore, electrophysiological theorists have suggested that schizophrenics have deficits in attention and sensory filtering. The deficits might explain hypervigilance or agitation in schizophrenia. It has also been suggested that genetics might be associated with a person’s vulnerability. On the other hand, psychosocial factors have been suggested for the onset of schizophrenia. Theories of schizophrenia range from psychoanalytic, learning theories, family theories and social theories, according to Kaplan.
Breggin (1991) asserted in chapter five that biopsychiatry, including medications and electroshock protect parents from dealing with generations of family issues. It is easier for parents to believe that their children have a genetic defect. This helps parents hide their feeling of hopelessness and helplessness. Breggin stated that “one in ten families with a schizophrenic parent will have a schizophrenic offspring.” Breggin challenged the “the specific gene” discovery that was promoted by the media. The author challenged the “human chromosome 5” theory that was found in seven families in England and Iceland. However, past research has shown that a dominant gene for schizophrenia does not exist. “If a dominant gene existed, like Huntington’s chorea then the human chromosome 5 theory would be valid,” according to Breggin. Still, there are researchers trying to find biochemical theories for schizophrenia. A recent theory was that the dopamine neurotransmitter was being over stimulated. The theory was supported on “evidence that neuroleptics suppress dopamine nerve transmission in parts of the higher brain (frontal lobe and emotion-regulating limbic system).” Breggin asserted that neuroleptics inhibit “passion and willpower” in all humans. Although the research shows that schizophrenics have abnormal active dopamine pathways, this still does not demonstrate the cause of schizophrenia. Breggin pointed out that chronic exposure to neuroleptics cause the nerve pathways to become hyperactive, which might influence abnormal activity in the dopamine pathways. In conclusion, Breggin stated that there was no significant evidence for a biology of schizophrenia. Beggin also examined the theory of shrunken brain tissues in schizophrenia. Brain imaging has shown brain shrinkage in schizophrenics but Breggin pointed to research that argued that psychiatric drugs have caused this problem. Beggin concluded in this chapter, that culture has promoted genetic and biochemical theories for schizophrenia. The cultural buzzword is “biochemical imbalance.” The trend to label only dismisses individuals from exploring psychospiritual crisis, personal conflict, rebellion and behavioral deviance. Breggin called this trend the “worse legacy of biological psychiatry.”
Neuroleptics commonly used for schizophrenia are haldol, thorazine, stelazine, vesprin, mellaril, prolixin, navane, trilafon, tindal, taractan, loxitane, moban, serentil, orap, quide, respoise, comapzine, dartal and clozaril, according to Breggin in chapter three (1991). These drugs help reduce positive symptoms of schizophrenia, i.e., hallucinations, delusions, bizarre behavior and incoherence. Breggin referred to neuroleptics as “chemical lobotomy,” a term created by Peter Sterling. Patients are in a helpless position and continue to believe that doctors are the authorities. Also noted by Breggin was a study by Gordon Paul in 1972. Patients in a psychosocial program were too medicated to participate in the rehabilitative program. The patients were changed from medications to a placebo without the staff knowing about this change. Patients that received the placebo had improved. Thus, it was recommended that medications should be discontinued because it interfered with rehabilitation.
In chapter four, Breggin further argued that medications are toxic and associated with the development of tardive dyskinesia and lethargic encephalitis. Tardive dyskinesia is a movement disorder that can affect any of the voluntary muscles. Lethargic encephalitis refers to an apathetic mental state (lack of emotional expression) and an inflammation of the brain. Also, patients can become hyperactive i.e., internal restlessness, irritable and causes pace. This disorder is known as akathisia. Patients can also develop a parkinson like symptoms, i.e., tremor of the extremities, rigidity of movement, shuffling gait and emotional flatting. All of these symptoms can become permanent disorders.
Citrome et al. (2001) studied the effects of clozapine, olanzapine, risperidone and haloperidol with 157 schizophrenic inpatients. These medications are the most widely antipsychotics on the market. The researchers were interested in knowing what medications would reduce hostility. Hostility from the schizophrenic inpatients were mainly verbal rather than physical. Outcome measures were gathered from the hostility item on the “Positive and Negative Syndrome Scale (PANSS) and the sedation item on the Nurses Observation Scale for Inpatient Observation (NOSIE).” The results showed that clozapine had an “advantage” over the reduction of hostility compared to the other medications. Furthermore, the anti-hostility effect was shown to be independent of the drug’s effects on other psychotic symptoms and sedation. However, clozapine was not superior to olanzapine as measured on the PANSS. Also, neither risperidone nor olanzapine showed superiority over haloperidol for reduction of hostility. One limitation of the study was that most patients were verbally hostile. Thus, the research has to be cautious about generalizing the results to physically assaultive psychotic patients. Another limitation, according to the researches was the limited use of scales to analyze a complex behavior.
I would use a general framework to make a mental health assessment. The general framework includes: 1) Referral source; 2) demographic data; 3) presenting problem and why now; 4) pertinent historical information, including family history, 5) psychiatric hospitalizations and crisis visits; 6) current and past medications, including psychiatric medications; 7) side effects from medications; 8) medical problems; 9) primary doctor and mental health practitioner; 10) living situation and education; 11) history of suicidal and homicidal thoughts/acts; 12) involvement in the justice system; 13) substance use, abuse or dependence; 14) mental health examine; 15) individual and/or family strengths; 16) supporters in the community; and 17) possible disturbances in work, social relations, self-care and social isolation.
Besides history taking, the mental health exam is a crucial part of the assessment. There are many factors to exam but that would be a paper in itself. I tried to highlight some of the features to look for during an interview. The mental health exam would include: 1) I would assess for appearance (hygiene); 2) behavior toward the interviewer (friendly, angry, guarded); 3) motor activity (restless, slow, lack of energy); 4) speech (pressured, loud, soft, poverty); 5) affect and mood (depressed, elated, irritable, constricted, blunted), thought process and content, (vague, suicidal, homicidal, ruminates, loose associations, tangential, auditory hallucinations, paranoid, delusions, bizarre behavior); 6) memory and intellect (oriented, fund of knowledge, short and long term memory); and 7) insight and judgment (self awareness, coping skills, strengths, wellness recovery processes).
After history taking (listening to the client’s story) and the mental health examine, an assessment with rule outs can be hypothesized. Given that this paper is on schizophrenia, the DSM-IV-R is used to find clustered symptoms, features and characteristics of schizophrenia. Under schizophrenia there is the paranoid type, disorganized type, catatonic type, undifferentiated type and residual type. In addition, there is schizoaffective disorder (schizophrenia and a mood disorder). Still, other psychotic disorders can be influenced by medical conditions and/or substance induced. Furthermore, psychotic disorder not otherwise specified is used when there is inadequate information to make a specific diagnosis.
This scenario, for example, showed that the client had bizarre paranoid thoughts, voices telling him that people are after him, disorganized speech, disheveled, guarded, irritable and at times verbally threatening, denied suicidal thoughts, constricted facial affect, poor judgment and not able to provide for himself. The best fitting diagnosis would be either schizophrenia, paranoid type or psychotic disorder NOS. Rule outs would be substance abuse, schizoaffective disorder, bipolar disorder with psychotic features, medical conditions and organic brain syndrome. So, what medications would be the most advantageous at this time?
Hyman (1991) pointed out that the old antipsychotics are either low-potency or high potency medications. The low-potency drugs are more sedating, anticholinergic and cause hypotension. In contrast, the high potency drugs are more likely to cause extrapyramindal symptoms. With the newer atypical medications, I would suggest that olanzapine would be the best fit given that it has a sedating effect. This client is frightened, paranoid and irritable. An immediate choice of medications might be ativan to help with the immediate situation. In this situation, my opinion would be to have the client 5150 as gravely disabled. Psychiatry emergency services could do a tox screen for substances. If, for example, this client was negative for substances, had a long history of schizophrenia and it was discovered that he had not taken his medications for 6 months, then the issue is at what dose to start in acute situations and then for long term (decrease dosage). The best fitting diagnosis at this time would be schizophrenia, paranoid type. The atypical antipsychotic medications would be the first choice. Depending on the client’s baseline (paranoid and irritable features), olzanipine might be the first choice given that it has a sedating effect and no EPS or DT side effects. Another decision is the client’s support system and supporters. Some paranoid schizophrenics have difficulty following through with medication compliance. This may rule out the use of clozipne and other atypical antipsychotics and instead injections of prolixin would be the first choice until medication compliance could be established.
Another major challenge with mental disabilities is non-medication compliance. Chen (1991) suggested that noncompliance includes more than taking medications. It also involves keeping appointments and following up on aftercare referrals. From the review of the literature, Chen suggested that there are four methods to improve compliance. This included: Scheduling appointments before being released from the hospital, shortening the waiting period for appointments, using letters and phone calls to remind clients about their appointments, and offering education concerning medications and treatments.
Green (1988) found that 92% of
hospitalized patients where noncompliant with medication. The
most significant factor was 76% being noncompliant with aftercare
Diagnosis included scizoaffective, bipolar, and major depression.
The author suggested that an affective component might increase the
of hospitalization. In addition, Green suggested that an emphasis
on outpatient services should reduce the recidivism.
Draine and Solomon (1994) were interested in variables associated with medication compliance, the relationships among social relations, social activity, social networking and psychiatric symptoms. The authors found that more positive attitudes about compliance were related with older age, less psychiatric symptoms, and a variety of daily activities with others. The size of the social network was not significant; however, the increased social activities were significant. One explanation was that increased social activities improved client’s social skills and confidence, which may contribute to more positive attitudes toward medication compliance.
Swartz et al. (1998) studied the effects of substance abuse and medication noncompliance with the severe mental health clients. The results showed that the combination of substance abuse and medication noncompliance were associated with violent behavior that occurred within 4 months before hospitalization. African Americans in high crime areas were significant. This suggested that the living environment also contributed to the risk of violent behavior.
Mulaik (1992) studied factors identified by patients, family members, and nurses regarding medication noncompliance. The results had shown that most patients perceived that they did not need medication or needed less than prescribed. Most patients denied that they had a “mental illness.” One explanation by the author was that when patients feel better from taking medications, they rationalize that they no longer need it or need less. Another interesting finding was that these patients had only vague ideas of their behavioral symptoms before psychiatric hospitalization. Also, most families were not aware of the early symptoms. One explanation for being unaware of behavioral changes is due to mental illness being stigmatized in this country. One other barrier to noncompliance as reported by family members and nurses were alcohol and substance use. The author recommended that patients and family members need more knowledge of mental illness, emotional support, how to identify patient stressors, and dual diagnosis treatment.
Dow, Verdi and Sacco (1991) had studied psychiatric inpatients abilities to communicate about medications. The study consisted of two groups; a medication communication skills program and a medication education program. The medication communication skills program taught how to improve eye contact, voice volume, non-verbal behavior, making specific requests, and using resources to open other forms of communication with physicians. The medication education program taught clients about their medications, i.e., side effects, therapeutic effects, dosage, and precautions. The results showed that both groups had improved in their knowledge of medications. There were no significant differences between the two groups. However, clients in the medication communication skills program were more assertive, showed greater social skills, and asked more relevant questions. The significant differential improvements in the doctor-patient communication produced a meaningful change in the doctor-patient relationship. The authors suggested that a focused communication skills program might improve communication about medications and thereby increase patient involvement in treatment, knowledge in about medications, and following the medication regimen.
Kuipers, Bell, Davidhizar, Cosgray and Fawley (1994) studied the chronically mentally ill patients’ knowledge and attitudes about medication compliance. The study included patients in a state hospital. The results showed no statistically significant difference between structured and unstructured medication education. The study suggested that other factors might relate to knowledge and attitudes about medication compliance. This may include special learning problems, the lack of control over medications, dependence, lack of a support system, substance abuse, family income, literacy, homelessness, unsafe conditions, and unable to negotiate needs. The authors suggested that educational plans need to be “individualized, evaluated, and modified.”
Medications have advanced as demonstrated with the newer atypical antipsychotics on the market. There are less side effects and marked improvements with the negative symptoms of schizophrenia. However, some mental health practitioners have argued that all antipsychotic medications are toxic and cause serious side effects. Still others have linked antipsychotic medications to warehousing of the mentally ill. Yet others have argued that the pharmaceutical industry is only interested in making profits over the health of the mentally ill.
From the literature that I read, it appeared that the atypical antipsychotic medications are a significant improvement over the older generation of psychiatric medications. However, Breggin’s point of view has merit that there is an overuse of psychiatric medications in Western culture. In addition, multinational corporations promote the Western disease model that in part is driven by economic incentives. Breggin’s use of the word “chemical lobotomy” makes sense and fits into many arenas. I would suggest that the best combination for wellness recovery of schizophrenia is minimal use of medications (moving away from cocktails) with the hope of tapering medications, participation in supportive therapy, encouraging social interaction and activities, consumer led support groups and promoting community support.
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