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The concept of a cure as such in the treatment of schizophrenia remains controversial, as there is no consensus on the definition of "treatment" in the case of schizophrenia, although some criteria for the remission of symptoms have recently been suggested.[1]

Management of symptoms and improving function is thought to be more achievable than a cure. A recovery model is increasingly adopted, emphasizing hope, empowerment and social inclusion.[2]

Antipsychotics have been a mainstay of therapy since the introduction of chlorpromazine in the mid 1950s, which revolutionized treatment of the illness. However all antipsychotics have a considerable array of side effects, many unpleasant and some harmful or even fatal. Thus their use has attracted much controversy in the five decades they have been prescribed. Older concerns over sedation, tardive dyskinesia and neuroleptic malignant syndrome have been largely replaced with those of drug-related obesity and diabetes.

In many non-Western societies, schizophrenia may only be treated with more informal, community-led methods. The outcome for people diagnosed with schizophrenia in non-Western countries may actually be better than for people in the West.[3] The reasons for this effect are not clear, although cross-cultural studies are being conducted.

Prognosis[]

Numerous international studies have demonstrated favorable long-term outcomes for around half of those diagnosed with schizophrenia, with substantial variation between individuals and regions.[4] One retrospective study found that about a third of people made a full recovery, about a third showed improvement but not a full recovery, and a third remained ill.[5] A clinical study using strict recovery criteria (concurrent remission of positive and negative symptoms and adequate social and vocational functioning continuously for two years) found a recovery rate of 14% within the first five years.[6] A 5-year community study found that 62% showed overall improvement on a composite measure of symptomatic, clinical and functional outcomes.[7] Rates are not always comparable across studies because an exact definition of what constitutes recovery has not been widely accepted, although standardized criteria have been suggested.[1]

The World Health Organization conducted two long-term follow-up studies involving more than 2,000 people suffering from schizophrenia in different countries. These studies found patients have much better long-term outcomes in developing countries (India, Colombia and Nigeria) than in developed countries (USA, UK, Ireland, Denmark, Czech Republic, Slovakia, Japan, and Russia),[8] despite the fact antipsychotic drugs are typically not widely available in poorer countries, raising questions about the effectiveness of such drug-based treatments.

Several factors are associated with a better prognosis: Being female, acute (vs. insidious) onset of symptoms, older age of first episode, predominantly positive (rather than negative) symptoms, presence of mood symptoms and good premorbid functioning.[9][10] Most studies done on this subject, however, are correlational in nature, and a clear cause-and-effect relationship is difficult to establish. Evidence is also consistent that negative attitudes towards individuals with schizophrenia can have a significant adverse impact. In particular, critical comments, hostility, authoritarian and intrusive or controlling attitudes (termed high 'Expressed Emotion' or 'EE' by researchers) from family members have been found to correlate with a higher risk of relapse in schizophrenia across cultures.[11]

Assessment of effectiveness[]

The effectiveness of schizophrenia treatment is often assessed using standardized methods, one of the most common being the positive and negative syndrome scale (PANSS).[12]

Admission to hospital[]

Hospitalization may occur with severe episodes of schizophrenia. This can be voluntary or (if mental health legislation allows it) involuntary (called civil or involuntary commitment). Long-term inpatient stays are now less common due to deinstitutionalization, although can still occur.[13] Following (or in lieu of) a hospital admission, support services available can include drop-in centers, visits from members of a community mental health team or Assertive Community Treatment team, supported employment[14] and patient-led support groups.

Specific treatments[]

Medication[]

The mainstay of psychiatric treatment for schizophrenia is an antipsychotic medication.[15] These can reduce the "positive" symptoms of psychosis. Most antipsychotics take around 7–14 days to have their main effect.

File:Risperdal tablets.jpg

Risperidone (trade name Risperdal) is a common atypical antipsychotic medication.

Treatment was revolutionized in the mid 1950s with the development and introduction of the first antipsychotic chlorpromazine.[16] Others such as haloperidol and trifluoperazine soon followed.

Though expensive, the newer atypical antipsychotic drugs are usually preferred for initial treatment over the older typical antipsychotics; they are often better tolerated and associated with lower rates of tardive dyskinesia, although they are more likely to induce weight gain and obesity-related diseases.[17] Of the atypical antipsychotics, olanzapine and clozapine are the most likely to induce weight gain.[18] The effect is more pronounced if high doses of olanzapine are used.[19] Smaller amounts of weight gain are induced by risperidone and quetiapine. Ziprasidone and aripiprazole are considered to be weight neutral antipsychotics.

It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome, a rare but serious and potentially fatal neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs.[20]

The two classes of antipsychotics are generally thought equally effective for the treatment of the positive symptoms. Some researchers have suggested that the atypicals offer additional benefit for the negative symptoms and cognitive deficits associated with schizophrenia, although the clinical significance of these effects has yet to be established. Recent reviews have refuted the claim that atypical antipsychotics have fewer extrapyramidal side effects than typical antipsychotics, especially when the latter are used in low doses or when low potency antipsychotics are chosen.[21]

Response of symptoms to mediation is variable; "Treatment-resistant schizophrenia" is a term used for the failure of symptoms to respond satisfactorily to at least two different antipsychotics.[22] Patients in this category may be prescribed clozapine,[23] a medication of superior effectiveness but several potentially lethal side effects including agranulocytosis and myocarditis.[24] For other patients who are unwilling or unable to take medication regularly, long-acting depot preparations of antipsychotics may be given every two weeks to achieve control. America and Australia are two countries with laws allowing the forced administration of this type of medication on those who refuse but are otherwise stable and living in the community.

Nevertheless, some findings indicate that, in the long term, many schizophrenic individuals function better without antipsychotic medicine.[25] In a 2007 study, only 28% of patients who were not being treated medicinally showed signs of psychotic activity, while 64% of those on antipsychotics had psychotic activity. The authors of the study cautioned that some of this gap may be accounted for by the increased likelihood of symptomatic patients to be placed on antipsychotic medicine, but also noted that some of the difference held even when on-antipsychotic and off-medicine patients of similar prognosis were compared. [26]

"LY2109823"[]

A new schizophrenia drug "LY219873" yielded promising results, as it targets in the brainglutamate receptors rather than dopamine and had few side effects. The Nature Medicine study, by drug firm Eli Lilly found it promising and Dr.Sandeep Patil's team proved that LY2140023 appear to work as antipsychotics when tested upon rodents.[27]

Nicotine patch[]

Following an observation that tobacco smoking eases effects of schizophrenia, Dr. Tony George from the Yale School of Medicine proposed nicotine patch as a treatment for schizophrenia.[28]

Psychological and social interventions[]

Psychotherapy is also widely recommended and used in the treatment of schizophrenia, although services may often be confined to pharmacotherapy because of reimbursement problems or lack of training.[29]

Cognitive behavioral therapy (CBT) is used to reduce symptoms and improve related issues such as self-esteem, social functioning, and insight. Although the results of early trials were inconclusive,[30] more recent reviews suggest that CBT can be an effective treatment for the psychotic symptoms of schizophrenia.[31] Another approach is cognitive remediation therapy, a technique aimed at remediating the neurocognitive deficits sometimes present in schizophrenia. Based on techniques of neuropsychological rehabilitation, early evidence has shown it to be cognitively effective, with some improvements related to measurable changes in brain activation as measured by fMRI.[32] A similar approach known as cognitive enhancement therapy, which focuses on social cognition as well as neurocognition, has shown efficacy.[33]

Family Therapy or Education, which addresses the whole family system of an individual with a diagnosis of schizophrenia, has been consistently found to be beneficial, at least if the duration of intervention is longer-term.[34][35][36] Aside from therapy, the impact of schizophrenia on families and the burden on careers has been recognized, with the increasing availability of self-help books on the subject.[37][38] There is also some evidence for benefits from social skills training, although there have also been significant negative findings.[39][40] Some studies have explored the possible benefits of music therapy and other creative therapies.[41][42][43]

Other[]

Electroconvulsive therapy is not considered a first line treatment but may be prescribed in cases where other treatments have failed. It is more effective where symptoms of catatonia are present,[44] and is recommended for use under NICE guidelines in the UK for catatonia if previously effective, though there is no recommendation for use for schizophrenia otherwise.[45] Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.[46]

Alternative approaches[]

Service-user led movements have become integral to the recovery process in Europe and America; groups such as the Hearing Voices Network and the Paranoia Network have developed a self-help approach that aims to provide support and assistance outside the traditional medical model adopted by mainstream psychiatry. By avoiding framing personal experience in terms of criteria for mental illness or mental health, they aim to destigmatize the experience and encourage individual responsibility and a positive self-image. Partnerships between hospitals and consumer-run groups are becoming more common, with services working toward remediating social withdrawal, building social skills and reducing rehospitalization.[47]

The Soteria model is an alternative treatment to institutionalization and early use of antipsychotics.[48] It is described as a milieu-therapeutic recovery method, characterized by its founder as "the 24 hour a day application of interpersonal phenomenologic interventions by a nonprofessional staff, usually without neuroleptic drug treatment, in the context of a small, homelike, quiet, supportive, protective, and tolerant social environment."[49] Soteria or Soteria-based houses are currently run in Sweden,[50] Germany,[51][52][53] Switzerland,[54] and Hungary.[55] The Soteria house in Berne, Switzerland is associated with a psychiatrist who teaches at the University of Berne, and has been featured in the Schweizerische Aertzezeitung, the Bulletin of Swiss Physicians.[56]

The biologically based branch of alternative medicine that deals with schizophrenia is known as orthomolecular psychiatry. Some scientists claim that schizophrenia can be treated effectively with nutrients like niacin, vitamin C and B6, omega-3 EFAs (fish oil) along with various minerals and amino acids.[57][58] The body's adverse reactions to gluten and other allergens are implicated in some alternative theories as the cause of some cases. This theory—discussed by one author in three British journals in the 1970s[59]—is unproven. A 2006 literature review suggests that gluten may be a factor for a subset of patients with schizophrenia, but further study is needed to confirm the association between gluten and schizophrenia.[60]

An unconventional approach is the use of omega-3 fatty acids, with one study finding some benefits from their use as a dietary supplement.[61]

Sodium - a once trialed approach[]

In the test tube, sodium converts d2high (the psychotic state of the receptor) to d2low [62]. While stable schizophrenics show no difference in the sodium content of their CSF [63], subjects who are in need of hospitalisation benefit significantly from the addition of sodium valpoarate until they become stable (after a month) [64] and chronic schizophrenics often have hyponatremia [65].

Several of the body's natural salts increase sodium naturally[66]. As one, AVP (Arginine Vasopressin) is inhibited by caffeine [67]. Schizophrenics on caffeine can show worse symptoms [68], including positive symptoms[69](although there are conflicting results).

In the clinical setting, while still being treated with antipsychotics, negative and residual symptoms were greatly improved by l-arginine (in the case of negative symptoms) and modestly improved in the case of residual symptoms - perhaps only a modest improvement was necessary for antipsychotic treated residual symptoms ... This study references four other studies on l-arginine and schizophrenia[70] - the article points out that some patients experienced unusual electrolyte or fluid measures. Responders to a blog say they had bad experiences with l-arginine [71]

A more recent article says: "It is concluded from our study that nitric oxide produces conflicting results on various models of psychosis. L-arginine might be useful as an antipsychotic without causing extrapyramidal symptoms" [72] (Amphetamine was used to simulate psychosis.)

However, plasma AVP levels may vary in hyponatremia, yet serum sodium levels are the same[73] and seem predetermined.

Although sodium may have helped the exacerbated schizophrenics mentioned before - and perhaps only because of a calming influence in exacerbation, it is not a cure for chronic schizophrenia as, if it was, the saline solutions used in experiments would have been noted to improve it. Sodium levels are caused by prenatal factors[74].

(An early edition of American Journal of Insanity tested infusion of salt solution in schizophrenics and found positive results: "Comparing these percentages with those recorded in Table I, I am led to infer that common salt in the blood of catatonic patients as well as those with other clinical forms of dementia precox might be deficient and that the infusion ...of the physiological salt solution would meet this deficiency, though the results might be transitory," said the author [75] - yet this result is before the use of antipsychotics. If the permanence of the dopamine receptor broken G link is due to arrestins, a news article in Schizophrenia forum says antipsychotics hinder arrestins from binding [76][77]; so lifestyle choices may now have a marginal effect. Bearing in mind that the broken G protein link was observed in schizophrenics on medication; it is hope lifting to see that on medication the caudate is larger in schizophrenics (less vasoconstriction) than in schizotypal people).

See also[]


References[]

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  62. Philip Seeman's article SYNAPSE 49:209 –215 (2003) "Dopamine Displaces [3H]Domperidone From High-Affinity Sites of the Dopamine D2 Receptor, But Not [3H]Raclopride or [3H]Spiperone in Isotonic Medium: Implications for Human Positron Emission Tomography" PHILIP SEEMAN, TERESA TALLERICO, AND FRANCOISE KO1, they point out that in the petri dish brain samples with d2high, are converted to d2low by NaCl. Even with the benefits of this new method, Dr Seeman recommended future experiments to be done in hypotonic medium to halt the conversion to d2low.
  63. SODIUM OF CEREBROSPINAL POTASSIUM AND CONTENT FLUID COLLECTED FROM PATIENTS WITH CHRONIC SCHIZOPHRENIC REACTIONS’by TURGUT ZILELI, M.D., LORING FO CHAPMAN, PH.D.,HAROLD C. WOLFF, M.D. Am J Psychiatry 118:449-450, November 1961
  64. Sodium Valproate as an Adjunctive Drug in Treatment of Schizophrenia Victoria Omranifard MD, Afsaneh Karbasi Amel MD , Siamak Amanat MD Iranian Journal of Psychiatry and Behavioral Sciences(IJPBS) , Volume 1, Number 1, Spring and Summer 2007: 12-15
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  71. http://www.schizophrenia.com/sznews/archives/005764.html as at 25-07-08
  72. (http://cat.inist.fr/?aModele=afficheN&cpsidt=13460412 as at 01-05-08) "Role of nitric oxide in experimental models of psychosis in rats" GUPTA M; BALAKRISHNAN S.; PANDHI P; Methods and findings in experimental and clinical pharmacology 2001, vol. 23, no9, pp. 497-500.
  73. Nobutoshi Kawai,U , Atsuomi Babab, Toshihito Suzuki, Hiroyasu Shiraishi Roles of arginine vasopressin and atrial natriuretic peptide in polydipsia-hyponatremia of schizophrenic patients Psychiatry Research 101 Ž2001. p43
  74. Shengbiao Wang, Jiexiong Chen, Nathash Kallichanda, Arm Azim, Glenda Calvario and Michael G. Ross Prolonged Prenatal Hypernatremia Alters Neuroendocrine and Electrolyte Homeostasis in Neonatal Sheep Experimental Biology and Medicine 228:41-45 (2003)
  75. NOBORU ISHIDA, RESULTS PRODUCED iN DEMENTIA PR)ECOX OR SO-CALLED ENDOGENOUS DEMENTIA BY THE INFUSION OF SODIUM CHLORIDE SOLUTION.American Journal of Insanity 73:541-547, January 1917
  76. http://www.schizophreniaforum.org/new/detail.asp?id=1459 as at 14-12-08
  77. Masri B, Salahpour A, Didriksen M, Ghisi V, Beaulieu JM, Gainetdinov RR, Caron MG. Antagonism of dopamine D2 receptor/beta-arrestin 2 interaction is a common property of clinically effective antipsychotics. Proc Natl Acad Sci U S A. 2008 Sep 9;105(36):13656-61. Epub 2008 Sep 3.

Further reading[]

Key texts[]

Books[]

  • Martindale, B.V., Mueser, K.T., Kuipers, E., Sensky, T., & Green, L. (2003). Psychological treatments for schizophrenia. In S.R. Hirsch & D. Weinberger (Eds.), Schizophrenia (2nd Edition). Oxford, England: Blackwell Scientific Publications (pp. 657-687)

Papers[]

  • Brenner, H. D., & Pfammatter, M. (2000). Psychological therapy in schizophrenia: What is the evidence? : Acta Psychiatrica Scandinavica Vol 102(Suppl407) Dec 2000, 74-77.

Additional material[]

Books[]

Papers[]

External links[]



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