Medicine:Management of schizophrenia

From HandWiki
Management of schizophrenia
SpecialtyPsychiatry

The management of schizophrenia usually involves many aspects including psychological, pharmacological, social, educational, and employment-related interventions directed to recovery, and reducing the impact of schizophrenia on quality of life, social functioning, and longevity.[1]

Hospitalization

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 still occur.[2] 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[3] and patient-led support groups. Efforts to avoid repeated hospitalization include the obtaining of community treatment orders which, following judicial approval, coerce the affected individual to receive psychiatric treatment including long-acting injections of anti-psychotic medication. This legal mechanism has been shown to increase the affected patient's time out of the hospital.[4]

Medication

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

The mainstay of treatment for schizophrenia is an antipsychotic medication.[5] Most antipsychotics can take around 7 to 14 days to have their full effect. Medication may improve the positive symptoms of schizophrenia, and social and vocational functioning.[6] However, antipsychotics fail to significantly improve the negative symptoms and cognitive dysfunction.[7][8] There is evidence of clozapine, amisulpride, olanzapine, and risperidone being the most effective medications. However, a high proportion of studies of risperidone were undertaken by its manufacturer, Janssen-Cilag, and should be interpreted with this in mind.[9] In those on antipsychotics, continued use decreases the risk of relapse.[10][11] There is little evidence regarding consistent benefits from their use beyond two or three years.[11]

Treatment of schizophrenia changed dramatically in the mid-1950s with the development and introduction of the first antipsychotic chlorpromazine.[12] Others such as haloperidol and trifluoperazine soon followed.

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 antipsychotics (neuroleptics).[13]

Most people on antipsychotics get side effects. People on typical antipsychotics tend to have a higher rate of extrapyramidal side effects while some atypicals are associated with considerable weight gain, diabetes, and risk of metabolic syndrome; this is most pronounced with olanzapine, while risperidone and quetiapine are also associated with weight gain.[9] Risperidone has a similar rate of extrapyramidal symptoms to haloperidol.[9] The American Psychiatric Association generally recommends that atypicals be used as first line treatment in most patients, but further states that therapy should be individually optimized for each patient.[14]

The response of symptoms to medication is variable; treatment resistant schizophrenia is the failure to respond to two or more antipsychotic medications given in therapeutic doses for six weeks or more.[15] Patients in this category may be prescribed clozapine, a medication that may be more effective at reducing symptoms of schizophrenia, but treatment may come with a higher risk of several potentially lethal side effects including agranulocytosis and myocarditis.[16][17] Clozapine is the only medication proven to be more effective for people who do not respond to other types of antipsychotics.[18] It also appears to reduce suicide in people with schizophrenia. As clozapine suppresses the development of bone marrow, in turn reducing white blood cells which can lead to infection, blood tests are taken for the first six months on this medication.[19] The risk of experiencing agranulocytosis due to clozapine treatment is higher in elderly people, children, and adolescents.[16] The effectiveness in the studies also needs to be interpreted with caution as the studies may have an increased risk of bias.[16]

Add-on agents

Sometimes the use of a second antipsychotic in combination with another is recommended where there has been a poor response. A review of this use found some evidence for an improvement in symptoms but not for relapse or hospitalisation. The use of combination antipsychotics is increasing in spite of limited supporting evidence, with some countries including Finland, France, and the UK recommending its use and others including Canada, Denmark, and Spain in opposition.[20] Anti-inflammatories, anti-depressants, and mood stabilisers are other add-ons used. Other strategies used include ECT, or repetitive transcranial magnetic stimulation (rTMS) but evidence for these is lacking.

Note: Only adjuncts for which at least one double-blind randomized placebo-controlled trial has provided support are listed in this table.

Adjuncts[21][22] Symptoms against which efficacy is known Notable adverse effects seen in clinical trials Highest quality of clinical data available N Notes
Adjuncts to clozapine[23][24]
Antipsychotics
Amisulpride Global Extrapyramidal side effects (e.g. tremor, dystonia, akathisia, etc.), headache, somnolence, insomnia, elevated serum prolactin, etc. 1 DB-RPCTs 16 Not approved for use in the United States of America or Canada. Approved for use in Australia, Europe and several countries in East Asia. Can prolong the QT interval, some in vivo evidence[25] suggests it may have anti-diabetogenic effects and hence may improve metabolic parameters in patients on clozapine.
Aripiprazole Global, esp. negative Akathisia 1 DB-RPCT 61 Can also improve metabolic side effects of clozapine (including body weight). Six studies so far; only one negative.
Risperidone Global Impaired cognitive functioning, prolactin elevation and hyperglycaemia 2 DB-RPCTs, 1 DB-RCT 357 (DB-RPCTs) & 24 (DB-RCT) 11 studies have been conducted, 5 negative. A meta-analysis[23] found no clinically significant difference between risperidone augmentation and placebo augmentation.
Sulpiride Global Increased serum prolactin 1 DB-RPCT 28 Not approved for use in the US, Canada and Australia.
Ziprasidone Global QTc interval prolongation 1 DB-RCT 24 Was compared with risperidone in the one DB-RCT.
Antidepressants
Citalopram Negative symptoms Well tolerated 1 DB-RPCT 61 Can prolong the QT interval and since clozapine can prolong the QT interval too it is advisable to avoid their concurrent use in patients with cardiovascular risk factors.
Fluvoxamine Negative and depressive symptoms Elevated serum levels of clozapine (via inhibition of P450 cytochromes) Open-label studies NA Improved metabolic parameters
Mirtazapine Negative, depressive and cognitive symptoms Weight gain 2 DB-RPCTs (1 negative) 80 5-HT2A/2C/3 & α2 adrenoceptor antagonist
Anticonvulsants
Lamotrigine Negative & depressive symptoms Stevens–Johnson syndrome, toxic epidermal necrolysis, etc. 4 DB-RPCTs (2 negative) 108 Usually a relatively well tolerated anticonvulsant, but because of risk of potentially-fatal dermatologic AEs the dose must be slowly titrated up in order to prevent these AEs. A meta-analysis[23] found that it was ineffective.
Topiramate Negative symptoms Cognitive impairment, sedation, asthenia 2 DB-RPCTs (1 negative) 57 Can cause cognitive impairment and hence should probably be avoided in patients with cognitive impairments.
Valproate Reduced anxiety & depression Weight gain, hair loss One open-label study comparing it with lithium NA Increases the expression of mGluR2 and GAD67 via histone deacetylase (HDAC) inhibition.
Glutamatergic agents[26][27]
CX-516 Global Well tolerated 1 DB-RPCT 18 Statistically significant improvement in total symptoms but no significant improvement in negative and positive symptoms when considered separately.
Memantine Global Well tolerated 1 DB-RPCT 21 Statistically significant improvement in negative and total symptomtology.
Other
Lithium Global Weight gain, hypersalivation 1 DB-RPCT, 1 DB-RCT 10 (DB-RPCT), 20 (DB-RCT) Increased risk of neurological side effects such as neuroleptic malignant syndrome.
E-EPA Global (especially negative and cognitive symptoms) Well tolerated 3 DB-RPCT (1 negative) 131 Ester of the omega-3 fatty acid, eicosapentaenoic acid.
Adjuncts to other antipsychotics
Anti-inflammatory agents[28][29]
Aspirin[30][31] Global (especially positive symptoms) Well tolerated 1 DB-RPCT 70 Increased risk of bleeding, but seems relatively well tolerated.
Celecoxib Global (especially negative symptoms) Well tolerated 3 DB-RPCTs (1 negative) 147 May increased the risk of cardiovascular events (which is particularly worrisome as schizophrenia patients are a higher risk group for cardiovascular events). Case series (N=2) suggests efficacy in augmenting clozapine.
Minocycline[32][33][34][35] Global Well tolerated 4 DB-RPCTs 164 Increased risk of blood dyscarsias.
Omega-3 fatty acids Global Well tolerated 6 DB-RPCTs (1 negative)[36] 362 May have protective effects against depression.
Pregnenolone[37][38][39][40] Global Well tolerated 3 DB-RPCTs 100 Levels of this neurosteroid in the body are elevated by clozapine treatment.
Glutamatergics[26][41]
D-alanine[42][43] Global Well tolerated 1 DB-RPCT 31 A D-amino acid with affinity towards the glycine site on the NMDA receptor.
D-serine Global (especially negative symptoms) Well tolerated 4 DB-RPCTs 183 Affinity towards the glycine site on NMDA receptors. D. Souza 2013,[44] Heresco-Levy 2005,[45] Lane 2005,[46] Lane 2010,[47] Tsai 1999,[48] Weiser 2012[49]
Glycine Global (predominantly positive symptoms) Well tolerated 5 DB-RPCTs 219 Endogenous NMDA receptor ligand.
N-acetylcysteine[50] Global (especially negative symptoms) Well tolerated 3 DB-RPCTs 140 Cystine and glutathione prodrug.[51][52] Cystine increases intracellular glutamate levels via the glutamate-cystine anti porter.

Berk 2008,[53] Berk 2011,[54] Carmeli 2012,[55] Lavoie 2008[56]

Sarcosine Global (especially negative symptoms) Well tolerated 3 DB-RPCTs 112 GlyT1 antagonist (i.e. glycine reuptake inhibitor). Also known as N-methylglycine. Lane 2005,[46] Lane 2006,[57] Lane 2008,[58] Lane 2010,[47] Tsai 2004[59]
Cholinergics[60][27][61]
Donepezil Global Well tolerated 6 DB-RPCTs (5 negative; or 12 DB-RPCTs if one includes cross-over trials; 8 negative in total) 378, 474 (including cross-over trials) Possesses antidepressant effects according to one trial.
Galantamine Cognition Well tolerated 5 DB-RPCTs (1 negative) 170 Robust nootropic
Rivastigmine Cognition Well tolerated 3 DB-RPCTs (all 3 negative; 5 trials including cross-over trials; 4 negative) 93, 131 (including cross-over trials) Seems to be a weaker nootropic
Tropisetron†[62][63][64][65] Cognitive and negative symptoms Well tolerated 3 DB-RPCTs 120 Agonist at α7 nAChRs; antagonist at 5-HT3. Expensive (>$20 AUD/tablet).
Antidepressants[66]
Escitalopram†[67] Negative symptoms Well tolerated 1 DB-RPCT 40 May increase risk of QT interval prolongation.
Fluoxetine Negative symptoms Well tolerated 4 DB-RPCTs (3 negative) 136 The safest of antidepressants listed here in overdose.[68] Risk of QT interval prolongation is lower than with escitalopram (but still exists).
Mianserin[69] Negative and cognitive symptoms Well tolerated 2 DB-RPCTs 48 Weight gain, sedation, dry mouth, constipation and dizziness. Blood dyscarsias are a possible adverse effect and both the Australian Medicines Handbook and British National Formulary 65 (BNF 65) recommend regular complete blood counts to be taken.[70][71]
Mirtazapine[69] Cognition,[72][73] negative and positive symptoms†[74] Well tolerated ≥4 DB-RPCTs (one negative) 127 Relatively safe in overdose. Produces significant sedation and weight gain, however, which could potentially add to the adverse effects of atypical antipsychotics. Can reduce antipsychotic-induced akathisia.[75]
Ritanserin Negative symptoms Well tolerated 2 DB-RPCTs 73 5-HT2A/2C antagonist. Not clinically available.
Trazodone Negative symptoms Well tolerated 2 DB-RPCTs 72 5-HT2A antagonist and SSRI. Has sedative effects and hence might exacerbate some of the side effects of atypical antipsychotics.
Other
Alpha-lipoic acid[76][77] Weight gain Well tolerated 1 DB-RPCT 360 Offset antipsychotic drug-induced weight gain. Increased total antioxidant status. May also increase GSH:GSSG (reduced glutathione:oxidized glutathione) ratio.[78]
L-Theanine[79][80][81] Positive, activation, and anxiety symptoms Well tolerated 2 DB-RPCTs 40 Glutamic acid analog. Primary study noted reduction in positive, activation, and anxiety symptoms. Additional studies have noted improvements in attention.[82][83][84][85] Research suggests that theanime has a regulatory effect on the nicotine acetylcholine receptor-dopamine reward pathway, and was shown to reduced dopamine production in the midbrain of mice.[86]
Famotidine†[87] Global Well tolerated 1 DB-RPCT 30 May reduce the absorption of vitamin B12 from the stomach. Might also increase susceptibility to food poisoning.
Ginkgo biloba Tardive dyskinesia, positive symptoms Well tolerated 4 DB-RPCTs 157 Atmaca 2005,[88] Doruk 2008,[89] Zhang 2001,[90] Zhang 2001,[91] Zhang 2006,[92] Zhang 2011,[93] Zhou 1999[94]
Ondansetron[95] Negative and cognitive symptoms Well tolerated 3 DB-RPCTs 151 5-HT3 antagonist. May prolong the QT interval. Expensive (>$4 AUD/tablet).
SAM-e[96] Aggression Well tolerated 1 DB-RPCT 18 Study noted improvement of aggressive behavior and quality of life impairment. while in another study SAM-e has been purported to have a contributory effect on psychosis [97]
Vitamin C[98][99][100][101] Global Well tolerated 1 DB-RPCT 40 Improves BPRS scores.

Acronyms used:
DB-RPCT — Double-blind randomized placebo-controlled trial.
DB-RCT — Double-blind randomized controlled trial.

Note: Global in the context of schizophrenia symptoms here refers to all four symptom clusters.

N refers to the total sample sizes (including placebo groups) of DB-RCTs.

† No secondary sources could be found on the utility of the drug in question, treating the symptom in question (or any symptom in the case of where † has been placed next to the drug's name).

Psychosocial

Psychotherapy is also widely recommended, though not widely used in the treatment of schizophrenia, due to reimbursement problems or lack of training. As a result, treatment is often confined to psychiatric medication.[102]

Cognitive behavioral therapy (CBT) is used to target specific symptoms and improve related issues such as self-esteem and social functioning. Although the results of early trials were inconclusive[103] as the therapy advanced from its initial applications in the mid-1990s, meta-analytic reviews suggested CBT to be an effective treatment for the psychotic symptoms of schizophrenia.[104][105] Nonetheless, more recent meta analyses have cast doubt upon the utility of CBT as a treatment for the symptoms of psychosis[106][107][108]

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, resulting in the improvement of previous deficits in psychomotor speed, verbal memory, nonverbal memory, and executive function, such improvements being related to measurable changes in brain activation as measured by fMRI.[109]

Metacognitive training (MCT): In view of many empirical findings [110] suggesting deficits of metacognition (thinking about one's thinking, reflecting upon one's cognitive process) in patients with schizophrenia, metacognitive training (MCT) [110][111] is increasingly adopted as a complementary treatment approach. MCT aims at sharpening the awareness of patients for a variety of cognitive biases (e.g. jumping to conclusions, attributional biases, over-confidence in errors), which are implicated in the formation and maintenance of schizophrenia positive symptoms (especially delusions),[112] and to ultimately replace these biases with functional cognitive strategies. The training consists of 8 modules and can be obtained cost-free from the internet in 15 languages.[110][111] Studies confirm the training's feasibility [113] and efficacy in ameliorating positive psychosis symptoms.[114][115] Studies of single training module show that this intervention target specific cognitive biases.[116] Recently, an individualized format has been developed which combines the metacognitive approach with methods derived from cognitive-behavioral therapy.[117]

Family Therapy or Education, which addresses the whole family system of an individual with a diagnosis of schizophrenia, may be beneficial, at least if the duration of intervention is longer-term.[118][119][120] A 2010 Cochrane review concluded that many of the clinical trials that studied the effectiveness of family interventions were poorly designed, and may over estimate the effectiveness of the therapy. High-quality randomized controlled trials in this area are required.[120] 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.[121][122] There is also some evidence for benefits from social skills training, although there have also been significant negative findings.[123][14] Some studies have explored the possible benefits of music therapy and other creative therapies.[124][125][126]

The Soteria model is alternative to inpatient hospitalization using full non professional care and a minimal medication approach.[127] Although evidence is limited, a review found the program equally as effective as treatment with medications but due to the limited evidence did not recommend it as a standard treatment.[128] Training in the detection of subtle facial expressions has been used to improve facial emotional recognition.[129]

Avatar Therapy, developed by Professor Julian Leff, was developed to help patients deal with the impact of auditory hallucinations. A 2020 Cochrane review however failed to find any consistent effects in the reviewed studies.[130]

Supplements

Disruption of the gut microbiota has been linked to inflammation, and disorders of the central nervous system. This includes schizophrenia, and probiotic supplementation has been proposed to improve its symptoms. A review found no evidence to support this but it concludes that probiotics may be of benefit in regulating bowel movements and lessening the metabolic effects of antipsychotics.[131]

A review explains the need for an optimal level of vitamin D and omega-3 fatty acids for the proper synthesis and control of the neurotransmitter serotonin. Serotonin regulates executive function, sensory gating, and social behavior – all of which are commonly impaired in schizophrenia. The model proposed suggests that supplementation would help in preventing and treating these brain dysfunctions.[132] Another review finds that omega-3 fatty acids and vitamin D are among the nutritional factors known to have a beneficial effect on mental health.[133] A Cochrane review found evidence to suggest that the use of omega-3 fatty acids in the prodromal stage may prevent the transition to psychosis but the evidence was poor quality and further studies were called for.[134]

Traditional Chinese medicine

Acupuncture is a procedure generally known to be safe and with few adverse effects. A Cochrane review found limited evidence for its possible antipsychotic effects in the treatment of schizophrenia and called for more studies.[135] Another review found limited evidence for its use as an add-on therapy for the relief of symptoms but positive results were found for the treatment of sleep disorders that often accompany schizophrenia.[136]

Wendan decoction is a classic herbal treatment in traditional Chinese medicine used for symptoms of psychosis, and other conditions. Wendan decoction is safe, accessible, and inexpensive, and a Cochrane review was carried out for its possible effects on schizophrenia symptoms. Limited evidence was found for its positive antipsychotic effects in the short term, and it was associated with fewer adverse effects. Used as an add-on to an antipsychotic, wider positive effects were found. Larger studies of improved quality were called for.[137][138]

Other

Various brain stimulation techniques have been used to treat the positive symptoms of schizophrenia, in particular auditory verbal hallucinations (AVHs), and investigations are ongoing.[139] Most studies focus on transcranial direct-current stimulation (tDCM), and repetitive transcranial magnetic stimulation (rTMS).[140] Transcranial magnetic stimulation is low-cost, noninvasive, and almost free of side-effects making it a good therapeutic choice with promising outcomes.[139] Low-frequency TMS of the left temporoparietal cortex (the region containing Broca's area) can reduce auditory hallucinations.[139] rTMS seems to be the most effective treatment for those with persistent AVHs, as an add-on therapy.[140] AVHs are not resolved in up to 30 per cent of those on antipsychotics and a further percentage still experience only a partial response.[140] Techniques based on focused ultrasound for deep brain stimulation could provide insight for the treatment of AVHs.[140]

An established brain stimulation treatment is electroconvulsive therapy. This 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,[141] 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.[142] Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.[143]

A study in 2014 conducted by an Australian researcher indicated that the pericarp powder of Garcinia mangostana L. have the ability to reduce oxidative stress as an effective treatment for schizophrenia. This process includes increasing glutathione S-transferase levels which enhances mitochondrial activity over a period of 180 days under a sustained intake of 1000 mg/day.[144][145]

There may be some benefit in trying several treatment modalities at the same time, especially those that could be classed as lifestyle interventions.[146] Nidotherapy is suggested to be a cost-effective social prescribing intervention using efforts to change the environment to improve functional ability.[147]

Peer support in which people with experiential knowledge of mental illness provide knowledge, experience, emotional, social or practical help to each other is considered an important aspect of coping with schizophrenia and other serious mental health conditions. A 2019 Cochrane reviews of evidence for peer-support interventions compared to supportive or psychosocial interventions were unable to support or refute the effectiveness of peer-support due to limited data.[148]

References

  1. ↑ "Psychosis and schizophrenia in adults: treatment and management | Key-priorities-for-implementation | Guidance and guidelines". The United Kingdom National Institute for Health and Care Excellence (NICE). http://www.nice.org.uk/guidance/CG178/chapter/Key-priorities-for-implementation. 
  2. ↑ "Psychiatric services for people with severe mental illness across western Europe: what can be generalized from current knowledge about differences in provision, costs and outcomes of mental health care?". Acta Psychiatrica Scandinavica. Supplementum 113 (429): 9–16. 2006. doi:10.1111/j.1600-0447.2005.00711.x. PMID 16445476. 
  3. ↑ "Cognitive training for supported employment: 2-3 year outcomes of a randomized controlled trial". The American Journal of Psychiatry 164 (3): 437–41. March 2007. doi:10.1176/appi.ajp.164.3.437. PMID 17329468. 
  4. ↑ "Effects of compulsory treatment orders on time to hospital readmission". Psychiatric Services (Washington, D.C.) 56 (7): 867–9. July 2005. doi:10.1176/appi.ps.56.7.867. PMID 16020822. 
  5. ↑ National Collaborating Centre for Mental Health; National Institute for Clinical Excellence (2003). Schizophrenia : full national clinical guideline on core interventions in primary and secondary care. London: Gaskell, Royal College of Psychiatrists. ISBN 978-1-901242-97-3. http://www.nice.org.uk/download.aspx?o=289559. 
  6. ↑ "What matters to patients? A systematic review of preferences for medication-associated outcomes in mental disorders". BMJ Open 5 (4): e007848. April 2015. doi:10.1136/bmjopen-2015-007848. PMID 25854979. 
  7. ↑ "Schizophrenia (maintenance treatment)". American Family Physician 82 (4): 338–9. August 2010. PMID 20704164. 
  8. ↑ "Schizophrenia, "Just the Facts": what we know in 2008 part 1: overview". Schizophrenia Research 100 (1–3): 4–19. March 2008. doi:10.1016/j.schres.2008.01.022. PMID 18291627. 
  9. ↑ 9.0 9.1 9.2 "Schizophrenia". BMJ Clinical Evidence 2012. June 2012. PMID 23870705. PMC 3385413. http://www.clinicalevidence.bmj.com/x/systematic-review/1007/archive/06/2012.html. 
  10. ↑ "Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: a systematic review and meta-analysis". Lancet 379 (9831): 2063–71. June 2012. doi:10.1016/S0140-6736(12)60239-6. PMID 22560607. 
  11. ↑ 11.0 11.1 "Does long-term treatment of schizophrenia with antipsychotic medications facilitate recovery?". Schizophrenia Bulletin 39 (5): 962–5. September 2013. doi:10.1093/schbul/sbt034. PMID 23512950. 
  12. ↑ "Chlorpromazine: unlocking psychosis". BMJ 334 Suppl 1: s7. January 2007. doi:10.1136/bmj.39034.609074.94. PMID 17204765. 
  13. ↑ "Neuroleptic malignant syndrome and atypical antipsychotic drugs". The Journal of Clinical Psychiatry 65 (4): 464–70. April 2004. doi:10.4088/JCP.v65n0403. PMID 15119907. 
  14. ↑ 14.0 14.1 "Practice Guideline for the Treatment of Patients With Schizophrenia". American Journal of Psychiatry (American Psychological Association (APA)) 161 (2 supplement). February 2004. http://psychiatryonline.org/content.aspx?bookID=28&sectionID=1665359#46267. 
  15. ↑ Oxford Handbook of Psychiatry. Oxford University Press. July 2019. p. 207. ISBN 978-0-19-251496-7. 
  16. ↑ 16.0 16.1 16.2 "Clozapine versus typical neuroleptic medication for schizophrenia". The Cochrane Database of Systematic Reviews (1): CD000059. January 2009. doi:10.1002/14651858.cd000059.pub2. PMID 19160174. 
  17. ↑ "Clozapine-associated myocarditis: a review of 116 cases of suspected myocarditis associated with the use of clozapine in Australia during 1993-2003". Drug Safety 30 (1): 47–57. 2007. doi:10.2165/00002018-200730010-00005. PMID 17194170. 
  18. ↑ "Effectiveness of antipsychotic drugs in patients with chronic schizophrenia". The New England Journal of Medicine 353 (12): 1209–23. September 2005. doi:10.1056/NEJMoa051688. PMID 16172203. 
  19. ↑ "Chapter 10: Mental health". Fundamentals of Nursing: Concepts, Process and Practice (1st adaptation ed.). Harlow, England: Pearson Education. 2008. p. 189. ISBN 978-0-13-197653-5. https://books.google.com/books?id=_0_pRyy9McQC&q=clozapine&pg=PA189. 
  20. ↑ "Antipsychotic combinations for schizophrenia". The Cochrane Database of Systematic Reviews 6: CD009005. June 2017. doi:10.1002/14651858.CD009005.pub2. PMID 28658515. 
  21. ↑ Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. 2013. doi:10.1007/978-94-007-5805-6. ISBN 9789400758056. 
  22. ↑ Polypharmacy in Psychiatry Practice, Volume II. Springer Science+Business Media Dordrecht. 2013. doi:10.1007/978-94-007-5799-8. ISBN 9789400757998. 
  23. ↑ 23.0 23.1 23.2 "Clozapine resistance: augmentation strategies". European Neuropsychopharmacology 22 (3): 165–82. March 2012. doi:10.1016/j.euroneuro.2011.08.005. PMID 21906915. 
  24. ↑ "Pharmacological augmentation strategies for schizophrenia patients with insufficient response to clozapine: a quantitative literature review". Schizophrenia Bulletin 38 (5): 1003–11. September 2012. doi:10.1093/schbul/sbr004. PMID 21422107. 
  25. ↑ "Effect of the antipsychotic agent amisulpride on glucose lowering and insulin secretion". Diabetes, Obesity & Metabolism 14 (4): 329–34. April 2012. doi:10.1111/j.1463-1326.2011.01529.x. PMID 22059694. 
  26. ↑ 26.0 26.1 "Meta-analysis of the efficacy of adjunctive NMDA receptor modulators in chronic schizophrenia". CNS Drugs 25 (10): 859–85. October 2011. doi:10.2165/11586650-000000000-00000. PMID 21936588. 
  27. ↑ 27.0 27.1 "Adjunctive pharmacotherapy for cognitive deficits in schizophrenia: meta-analytical investigation of efficacy". The British Journal of Psychiatry 203 (3): 172–8. September 2013. doi:10.1192/bjp.bp.111.107359. PMID 23999481. 
  28. ↑ "A review of anti-inflammatory agents for symptoms of schizophrenia". Journal of Psychopharmacology 27 (4): 337–42. April 2013. doi:10.1177/0269881112467089. PMID 23151612. 
  29. ↑ "Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update". Schizophrenia Bulletin 40 (1): 181–91. January 2014. doi:10.1093/schbul/sbt139. PMID 24106335. 
  30. ↑ "Adjuvant aspirin therapy reduces symptoms of schizophrenia spectrum disorders: results from a randomized, double-blind, placebo-controlled trial". The Journal of Clinical Psychiatry 71 (5): 520–7. May 2010. doi:10.4088/JCP.09m05117yel. PMID 20492850. https://research.rug.nl/en/publications/adjuvant-aspirin-therapy-reduces-symptoms-of-schizophrenia-spectrum-disorders(5644f8cd-b8ea-4ecc-9755-0f7c9ed86d02).html. 
  31. ↑ "Acetylsalicylic acid (aspirin) for schizophrenia". The Cochrane Database of Systematic Reviews 8: CD012116. August 2019. doi:10.1002/14651858.CD012116.pub2. PMID 31425623. 
  32. ↑ "Minocycline supplementation for treatment of negative symptoms in early-phase schizophrenia: a double blind, randomized, controlled trial". Schizophrenia Research 153 (1–3): 169–76. March 2014. doi:10.1016/j.schres.2014.01.011. PMID 24503176. 
  33. ↑ "Minocycline add-on to risperidone for treatment of negative symptoms in patients with stable schizophrenia: randomized double-blind placebo-controlled study". Psychiatry Research 215 (3): 540–6. March 2014. doi:10.1016/j.psychres.2013.12.051. PMID 24480077. 
  34. ↑ "Minocycline benefits negative symptoms in early schizophrenia: a randomised double-blind placebo-controlled clinical trial in patients on standard treatment". Journal of Psychopharmacology 26 (9): 1185–93. September 2012. doi:10.1177/0269881112444941. PMID 22526685. 
  35. ↑ "A double-blind, randomized study of minocycline for the treatment of negative and cognitive symptoms in early-phase schizophrenia". The Journal of Clinical Psychiatry 71 (2): 138–49. February 2010. doi:10.4088/JCP.08m04666yel. PMID 19895780. 
  36. ↑ "Polyunsaturated fatty acid supplementation for schizophrenia". The Cochrane Database of Systematic Reviews (3): CD001257. July 2006. doi:10.1002/14651858.CD001257.pub2. PMID 16855961. 
  37. ↑ "Pregnenolone and dehydroepiandrosterone as an adjunctive treatment in schizophrenia and schizoaffective disorder: an 8-week, double-blind, randomized, controlled, 2-center, parallel-group trial". The Journal of Clinical Psychiatry 71 (10): 1351–62. October 2010. doi:10.4088/JCP.09m05031yel. PMID 20584515. 
  38. ↑ "Proof-of-concept trial with the neurosteroid pregnenolone targeting cognitive and negative symptoms in schizophrenia". Neuropsychopharmacology 34 (8): 1885–903. July 2009. doi:10.1038/npp.2009.26. PMID 19339966. 
  39. ↑ "Pregnenolone rescues schizophrenia-like behavior in dopamine transporter knockout mice". PLOS ONE 7 (12): e51455. 2012. doi:10.1371/journal.pone.0051455. PMID 23240026. Bibcode: 2012PLoSO...751455W. 
  40. ↑ "Neuroactive steroids are altered in schizophrenia and bipolar disorder: relevance to pathophysiology and therapeutics". Neuropsychopharmacology 31 (6): 1249–63. June 2006. doi:10.1038/sj.npp.1300952. PMID 16319920. 
  41. ↑ "Has an angel shown the way? Etiological and therapeutic implications of the PCP/NMDA model of schizophrenia". Schizophrenia Bulletin 38 (5): 958–66. September 2012. doi:10.1093/schbul/sbs069. PMID 22987851. 
  42. ↑ "Plasma alanine levels increase in patients with schizophrenia as their clinical symptoms improve-Results from the Juntendo University Schizophrenia Projects (JUSP)". Psychiatry Research 177 (1–2): 27–31. May 2010. doi:10.1016/j.psychres.2010.02.014. PMID 20226539. 
  43. ↑ "D-alanine added to antipsychotics for the treatment of schizophrenia". Biological Psychiatry 59 (3): 230–4. February 2006. doi:10.1016/j.biopsych.2005.06.032. PMID 16154544. 
  44. ↑ "Feasibility, safety, and efficacy of the combination of D-serine and computerized cognitive retraining in schizophrenia: an international collaborative pilot study". Neuropsychopharmacology 38 (3): 492–503. February 2013. doi:10.1038/npp.2012.208. PMID 23093223. 
  45. ↑ "D-serine efficacy as add-on pharmacotherapy to risperidone and olanzapine for treatment-refractory schizophrenia". Biological Psychiatry 57 (6): 577–85. March 2005. doi:10.1016/j.biopsych.2004.12.037. PMID 15780844. 
  46. ↑ 46.0 46.1 "Sarcosine or D-serine add-on treatment for acute exacerbation of schizophrenia: a randomized, double-blind, placebo-controlled study". Archives of General Psychiatry 62 (11): 1196–204. November 2005. doi:10.1001/archpsyc.62.11.1196. PMID 16275807. 
  47. ↑ 47.0 47.1 "A randomized, double-blind, placebo-controlled comparison study of sarcosine (N-methylglycine) and D-serine add-on treatment for schizophrenia". The International Journal of Neuropsychopharmacology 13 (4): 451–60. May 2010. doi:10.1017/S1461145709990939. PMID 19887019. 
  48. ↑ "D-serine added to clozapine for the treatment of schizophrenia". The American Journal of Psychiatry 156 (11): 1822–5. November 1999. doi:10.1176/ajp.156.11.1822. PMID 10553752. 
  49. ↑ "A multicenter, add-on randomized controlled trial of low-dose d-serine for negative and cognitive symptoms of schizophrenia". The Journal of Clinical Psychiatry 73 (6): e728-34. June 2012. doi:10.4088/JCP.11m07031. PMID 22795211. 
  50. ↑ "N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action". Journal of Psychiatry & Neuroscience 36 (2): 78–86. March 2011. doi:10.1503/jpn.100057. PMID 21118657. 
  51. ↑ "Regulation of neuronal glutathione synthesis". Journal of Pharmacological Sciences 108 (3): 227–38. November 2008. doi:10.1254/jphs.08R01CR. PMID 19008644. 
  52. ↑ "Glutathione deficiency leads to mitochondrial damage in brain". Proceedings of the National Academy of Sciences of the United States of America 88 (5): 1913–7. March 1991. doi:10.1073/pnas.88.5.1913. PMID 2000395. Bibcode: 1991PNAS...88.1913J. 
  53. ↑ "N-acetyl cysteine as a glutathione precursor for schizophrenia--a double-blind, randomized, placebo-controlled trial". Biological Psychiatry 64 (5): 361–8. September 2008. doi:10.1016/j.biopsych.2008.03.004. PMID 18436195. 
  54. ↑ "Qualitative methods in early-phase drug trials: broadening the scope of data and methods from an RCT of N-acetylcysteine in schizophrenia". The Journal of Clinical Psychiatry 72 (7): 909–13. July 2011. doi:10.4088/JCP.09m05741yel. PMID 20868637. 
  55. ↑ "Glutathione precursor N-acetyl-cysteine modulates EEG synchronization in schizophrenia patients: a double-blind, randomized, placebo-controlled trial". PLOS ONE 7 (2): e29341. 2012. doi:10.1371/journal.pone.0029341. PMID 22383949. Bibcode: 2012PLoSO...729341C. 
  56. ↑ "Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients". Neuropsychopharmacology 33 (9): 2187–99. August 2008. doi:10.1038/sj.npp.1301624. PMID 18004285. 
  57. ↑ "Glycine transporter I inhibitor, N-methylglycine (sarcosine), added to clozapine for the treatment of schizophrenia". Biological Psychiatry 60 (6): 645–9. September 2006. doi:10.1016/j.biopsych.2006.04.005. PMID 16780811. 
  58. ↑ "Sarcosine (N-methylglycine) treatment for acute schizophrenia: a randomized, double-blind study". Biological Psychiatry 63 (1): 9–12. January 2008. doi:10.1016/j.biopsych.2007.04.038. PMID 17659263. 
  59. ↑ "Glycine transporter I inhibitor, N-methylglycine (sarcosine), added to antipsychotics for the treatment of schizophrenia". Biological Psychiatry 55 (5): 452–6. March 2004. doi:10.1016/j.biopsych.2003.09.012. PMID 15023571. 
  60. ↑ "Acetylcholinesterase inhibitors for schizophrenia". The Cochrane Database of Systematic Reviews 1: CD007967. January 2012. doi:10.1002/14651858.CD007967.pub2. PMID 22258978. 
  61. ↑ "Cholinesterase inhibitors as adjunctive therapy in patients with schizophrenia and schizoaffective disorder: a review and meta-analysis of the literature". CNS Drugs 24 (4): 303–17. April 2010. doi:10.2165/11530260-000000000-00000. PMID 20297855. 
  62. ↑ "Tropisetron improves deficits in auditory P50 suppression in schizophrenia". Schizophrenia Research 76 (1): 67–72. July 2005. doi:10.1016/j.schres.2004.12.016. PMID 15927799. 
  63. ↑ "A randomised, double-blind, placebo-controlled trial of tropisetron in patients with schizophrenia". Annals of General Psychiatry 9 (1): 27. June 2010. doi:10.1186/1744-859X-9-27. PMID 20573264. 
  64. ↑ "Short-term tropisetron treatment and cognitive and P50 auditory gating deficits in schizophrenia". The American Journal of Psychiatry 169 (9): 974–81. September 2012. doi:10.1176/appi.ajp.2012.11081289. PMID 22952075. 
  65. ↑ "A placebo-controlled study of tropisetron added to risperidone for the treatment of negative symptoms in chronic and stable schizophrenia". Psychopharmacology 228 (4): 595–602. August 2013. doi:10.1007/s00213-013-3064-2. PMID 23515583. 
  66. ↑ "Efficacy of antidepressants in treating the negative symptoms of chronic schizophrenia: meta-analysis". The British Journal of Psychiatry 197 (3): 174–9. September 2010. doi:10.1192/bjp.bp.109.067710. PMID 20807960. 
  67. ↑ "Escitalopram in the treatment of negative symptoms in patients with chronic schizophrenia: a randomized double-blind placebo-controlled trial". Psychiatry Research 179 (1): 19–23. August 2010. doi:10.1016/j.psychres.2010.04.035. PMID 20472299. 
  68. ↑ "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type". Journal of Medical Toxicology 4 (4): 238–50. December 2008. doi:10.1007/BF03161207. PMID 19031375. 
  69. ↑ 69.0 69.1 "Alpha-2 receptor antagonist add-on therapy in the treatment of schizophrenia; a meta-analysis". Schizophrenia Research 134 (2–3): 202–6. February 2012. doi:10.1016/j.schres.2011.11.030. PMID 22169246. 
  70. ↑ Rossi, S, ed (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3. 
  71. ↑ Joint Formulary Committee (2013). British National Formulary (BNF) (65 ed.). London, UK: Pharmaceutical Press. p. 247. ISBN 978-0-85711-084-8. https://archive.org/details/bnf65britishnati0000unse/page/247. 
  72. ↑ Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. 2013. doi:10.1007/978-94-007-5805-6. ISBN 9789400758056. 
  73. ↑ "Meta-Analysis of Efficacy of Mirtazapine as an Adjunctive Treatment of Negative Symptoms in Schizophrenia". Clinical Schizophrenia & Related Psychoses 9 (2): 88–95. March 2013. doi:10.3371/CSRP.VIRE.030813. PMID 23491969. 
  74. ↑ "More evidence on proneurocognitive effects of add-on mirtazapine in schizophrenia". Progress in Neuro-Psychopharmacology & Biological Psychiatry 35 (4): 1080–6. June 2011. doi:10.1016/j.pnpbp.2011.03.004. PMID 21402120. 
  75. ↑ "Akathisia and second-generation antipsychotic drugs". Current Opinion in Psychiatry 22 (3): 293–99. May 2009. doi:10.1097/YCO.0b013e32832a16da. PMID 19378382. 
  76. ↑ "Effects of alpha-lipoic Acid on body weight in obese subjects". The American Journal of Medicine 124 (1): 85.e1–8. January 2011. doi:10.1016/j.amjmed.2010.08.005. PMID 21187189. 
  77. ↑ "A preliminary investigation of alpha-lipoic acid treatment of antipsychotic drug-induced weight gain in patients with schizophrenia". Journal of Clinical Psychopharmacology 28 (2): 138–46. April 2008. doi:10.1097/JCP.0b013e31816777f7. PMID 18344723. 
  78. ↑ "Restoration of blood total glutathione status and lymphocyte function following alpha-lipoic acid supplementation in patients with HIV infection". Journal of Alternative and Complementary Medicine 14 (2): 139–46. March 2008. doi:10.1089/acm.2006.6397. PMID 18315507. 
  79. ↑ "L-theanine relieves positive, activation, and anxiety symptoms in patients with schizophrenia and schizoaffective disorder: an 8-week, randomized, double-blind, placebo-controlled, 2-center study". The Journal of Clinical Psychiatry 72 (1): 34–42. January 2011. doi:10.4088/JCP.09m05324gre. PMID 21208586. 
  80. ↑ "Serum levels of brain-derived neurotrophic factor and cortisol to sulfate of dehydroepiandrosterone molar ratio associated with clinical response to L-theanine as augmentation of antipsychotic therapy in schizophrenia and schizoaffective disorder patients". Clinical Neuropharmacology 34 (4): 155–60. 2011. doi:10.1097/WNF.0b013e318220d8c6. PMID 21617527. 
  81. ↑ "Neurobiological effects of the green tea constituent theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders". Nutritional Neuroscience 17 (4): 145–55. July 2014. doi:10.1179/1476830513Y.0000000079. PMID 23883567. https://zenodo.org/record/995651. 
  82. ↑ "L-theanine and caffeine in combination affect human cognition as evidenced by oscillatory alpha-band activity and attention task performance". The Journal of Nutrition 138 (8): 1572S–1577S. August 2008. doi:10.1093/jn/138.8.1572S. PMID 18641209. 
  83. ↑ "A combination of green tea extract and l-theanine improves memory and attention in subjects with mild cognitive impairment: a double-blind placebo-controlled study". Journal of Medicinal Food 14 (4): 334–43. April 2011. doi:10.1089/jmf.2009.1374. PMID 21303262. 
  84. ↑ "Assessing the effects of caffeine and theanine on the maintenance of vigilance during a sustained attention task". Neuropharmacology 62 (7): 2320–7. June 2012. doi:10.1016/j.neuropharm.2012.01.020. PMID 22326943. 
  85. ↑ "L-theanine, a natural constituent in tea, and its effect on mental state". Asia Pacific Journal of Clinical Nutrition 17 Suppl 1: 167–8. 2008. PMID 18296328. 
  86. ↑ "L-theanine inhibits nicotine-induced dependence via regulation of the nicotine acetylcholine receptor-dopamine reward pathway". Science China Life Sciences 55 (12): 1064–74. December 2012. doi:10.1007/s11427-012-4401-0. PMID 23233221. 
  87. ↑ "A randomized clinical trial of histamine 2 receptor antagonism in treatment-resistant schizophrenia". Journal of Clinical Psychopharmacology 33 (4): 472–8. August 2013. doi:10.1097/JCP.0b013e3182970490. PMID 23764683. 
  88. ↑ "The effect of extract of ginkgo biloba addition to olanzapine on therapeutic effect and antioxidant enzyme levels in patients with schizophrenia". Psychiatry and Clinical Neurosciences 59 (6): 652–6. December 2005. doi:10.1111/j.1440-1819.2005.01432.x. PMID 16401239. 
  89. ↑ "A placebo-controlled study of extract of ginkgo biloba added to clozapine in patients with treatment-resistant schizophrenia". International Clinical Psychopharmacology 23 (4): 223–7. July 2008. doi:10.1097/YIC.0b013e3282fcff2f. PMID 18545061. 
  90. ↑ "The effect of extract of ginkgo biloba added to haloperidol on superoxide dismutase in inpatients with chronic schizophrenia". Journal of Clinical Psychopharmacology 21 (1): 85–8. February 2001. doi:10.1097/00004714-200102000-00015. PMID 11199954. 
  91. ↑ "A double-blind, placebo-controlled trial of extract of Ginkgo biloba added to haloperidol in treatment-resistant patients with schizophrenia". The Journal of Clinical Psychiatry 62 (11): 878–83. November 2001. doi:10.4088/JCP.v62n1107. PMID 11775047. 
  92. ↑ "The effects of Ginkgo biloba extract added to haloperidol on peripheral T cell subsets in drug-free schizophrenia: a double-blind, placebo-controlled trial". Psychopharmacology 188 (1): 12–7. September 2006. doi:10.1007/s00213-006-0476-2. PMID 16906395. 
  93. ↑ "Extract of Ginkgo biloba treatment for tardive dyskinesia in schizophrenia: a randomized, double-blind, placebo-controlled trial". The Journal of Clinical Psychiatry 72 (5): 615–21. May 2011. doi:10.4088/JCP.09m05125yel. PMID 20868638. 
  94. ↑ "The effects of classic antipsychotic haloperidol plus the extract of ginkgo biloba on superoxide dismutase in patients with chronic refractory schizophrenia". Chinese Medical Journal 112 (12): 1093–6. December 1999. PMID 11721446. 
  95. ↑ "The role of ondansetron in the treatment of schizophrenia". The Annals of Pharmacotherapy 44 (7–8): 1301–6. July–August 2010. doi:10.1345/aph.1P008. PMID 20516364. 
  96. ↑ "Improvement of aggressive behavior and quality of life impairment following S-adenosyl-methionine (SAM-e) augmentation in schizophrenia". European Neuropsychopharmacology 19 (1): 14–22. January 2009. doi:10.1016/j.euroneuro.2008.08.004. PMID 18824331. 
  97. ↑ "S-adenosyl methionine and DNA methyltransferase-1 mRNA overexpression in psychosis". NeuroReport 18 (1): 57–60. January 2007. doi:10.1097/WNR.0b013e32800fefd7. PMID 17259861. 
  98. ↑ "Supplementation of vitamin C with atypical antipsychotics reduces oxidative stress and improves the outcome of schizophrenia". Psychopharmacology 182 (4): 494–8. November 2005. doi:10.1007/s00213-005-0117-1. PMID 16133138. 
  99. ↑ "Effects of vitamin C and vitamin D administration on mood and distress in acutely hospitalized patients". The American Journal of Clinical Nutrition 98 (3): 705–11. September 2013. doi:10.3945/ajcn.112.056366. PMID 23885048. 
  100. ↑ "Vitamin C provision improves mood in acutely hospitalized patients". Nutrition 27 (5): 530–3. May 2011. doi:10.1016/j.nut.2010.05.016. PMID 20688474. 
  101. ↑ "Effects of high-dose B vitamin complex with vitamin C and minerals on subjective mood and performance in healthy males". Psychopharmacology 211 (1): 55–68. July 2010. doi:10.1007/s00213-010-1870-3. PMID 20454891. 
  102. ↑ "Psychosocial Treatment Often Missing From Schizophrenia Regimens". Psychiatric News 40 (22): 24–37. 18 November 2005. doi:10.1176/pn.40.22.0024b. 
  103. ↑ "Cognitive behaviour therapy for schizophrenia". The Cochrane Database of Systematic Reviews (4): CD000524. October 2004. doi:10.1002/14651858.CD000524.pub2. PMID 15495000.  (Retracted)
  104. ↑ "Cognitive behavior therapy for schizophrenia: effect sizes, clinical models, and methodological rigor". Schizophrenia Bulletin 34 (3): 523–37. May 2008. doi:10.1093/schbul/sbm114. PMID 17962231. 
  105. ↑ "The effect of cognitive behavioral treatment on the positive symptoms of schizophrenia spectrum disorders: a meta-analysis". Schizophrenia Research 77 (1): 1–9. September 2005. doi:10.1016/j.schres.2005.02.018. PMID 16005380. 
  106. ↑ "Cognitive behavioural therapy for major psychiatric disorder: does it really work? A meta-analytical review of well-controlled trials". Psychological Medicine 40 (1): 9–24. January 2010. doi:10.1017/s003329170900590x. PMID 19476688. 
  107. ↑ Newton‐Howes, Giles and Rebecca Wood. "Cognitive behavioural therapy and the psychopathology of schizophrenia: Systematic review and meta‐analysis." Psychology and Psychotherapy: Theory, Research and Practice (2011).
  108. ↑ "WITHDRAWN: Cognitive behaviour therapy versus other psychosocial treatments for schizophrenia". The Cochrane Database of Systematic Reviews (4): CD000524. April 2011. doi:10.1002/14651858.cd000524.pub3. PMID 21491377. 
  109. ↑ "Effects on the brain of a psychological treatment: cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia". The British Journal of Psychiatry 181: 144–52. August 2002. doi:10.1192/bjp.181.2.144. PMID 12151286. 
  110. ↑ 110.0 110.1 110.2 "Metacognitive training in schizophrenia: from basic research to knowledge translation and intervention". Current Opinion in Psychiatry 20 (6): 619–25. November 2007. doi:10.1097/YCO.0b013e3282f0b8ed. PMID 17921766. 
  111. ↑ 111.0 111.1 Metacognitive skill training for patients with schizophrenia (MCT). Hamburg: VanHam Campus. 2005. http://www3.telus.net/Todd_S_Woodward/MKT_Manual_%28eng%29_18_4_06.pdf. Retrieved 1 April 2011. 
  112. ↑ "Explaining delusions: a cognitive perspective". Trends in Cognitive Sciences 10 (5): 219–26. May 2006. doi:10.1016/j.tics.2006.03.004. PMID 16600666. 
  113. ↑ "Metacognitive training for schizophrenia patients (MCT): A pilot study on feasibility, treatment adherence, and subjective efficacy". German Journal of Psychiatry 10: 69–78. 2007. http://www.gjpsy.uni-goettingen.de/gjp-article-moritz3.pdf. Retrieved 2011-04-01. 
  114. ↑ "The effectiveness of metacognitive training for patients with schizophrenia: a narrative systematic review of studies published between 2009 and 2015" (in pl). Psychiatria Polska 50 (4): 787–803. 2016. doi:10.12740/pp/59113. PMID 27847929. 
  115. ↑ "Acceptance and Efficacy of Metacognitive Training (MCT) on Positive Symptoms and Delusions in Patients With Schizophrenia: A Meta-analysis Taking Into Account Important Moderators". Schizophrenia Bulletin 42 (4): 952–62. July 2016. doi:10.1093/schbul/sbv225. PMID 26748396. 
  116. ↑ "Do specific metacognitive training modules lead to specific cognitive changes among patients diagnosed with schizophrenia? A single module effectiveness pilot study". Psychosis 9 (3): 254–259. 2017-07-03. doi:10.1080/17522439.2017.1300186. ISSN 1752-2439. 
  117. ↑ Moritz S, Veckenstedt R, Randjbar S, Vitzthum F (in press). "Individualized metacognitive therapy for people with schizophrenia psychosis (MCT+)", Springer, Heidelberg. [clarification needed]
  118. ↑ "Family psychoeducation and schizophrenia: a review of the literature". Journal of Marital and Family Therapy 29 (2): 223–45. April 2003. doi:10.1111/j.1752-0606.2003.tb01202.x. PMID 12728780. 
  119. ↑ "New challenges in family interventions for schizophrenia". Expert Review of Neurotherapeutics 7 (1): 33–43. January 2007. doi:10.1586/14737175.7.1.33. PMID 17187495. 
  120. ↑ 120.0 120.1 "Family intervention for schizophrenia". The Cochrane Database of Systematic Reviews (12): CD000088. December 2010. doi:10.1002/14651858.CD000088.pub2. PMID 21154340. 
  121. ↑ Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. Oxford, England: Oneworld Pub.. 2004. ISBN 978-1-85168-344-4. https://archive.org/details/copingwithschizo00jone. 
  122. ↑ Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th ed.). HarperCollins. 2006. ISBN 978-0-06-084259-8. 
  123. ↑ "Recent advances in social skills training for schizophrenia". Schizophrenia Bulletin 32 Suppl 1 (Suppl 1): S12-23. October 2006. doi:10.1093/schbul/sbl023. PMID 16885207. 
  124. ↑ "Music therapy for in-patients with schizophrenia: exploratory randomised controlled trial". The British Journal of Psychiatry 189 (5): 405–9. November 2006. doi:10.1192/bjp.bp.105.015073. PMID 17077429. 
  125. ↑ "Art therapy for schizophrenia or schizophrenia-like illnesses". The Cochrane Database of Systematic Reviews (4): CD003728. October 2005. doi:10.1002/14651858.CD003728.pub2. PMID 16235338. 
  126. ↑ "Drama therapy for schizophrenia or schizophrenia-like illnesses". The Cochrane Database of Systematic Reviews (1): CD005378. January 2007. doi:10.1002/14651858.CD005378.pub2. PMID 17253555. 
  127. ↑ "Soteria and other alternatives to acute psychiatric hospitalization: a personal and professional review". The Journal of Nervous and Mental Disease 187 (3): 142–9. March 1999. doi:10.1097/00005053-199903000-00003. PMID 10086470. 
  128. ↑ "A systematic review of the Soteria paradigm for the treatment of people diagnosed with schizophrenia". Schizophrenia Bulletin 34 (1): 181–92. January 2008. doi:10.1093/schbul/sbm047. PMID 17573357. 
  129. ↑ Handbook of Schizophrenia Spectrum Disorders, Volume III: Therapeutic Approaches, Comorbidity, and Outcomes. Springer. 2011. p. 189. ISBN 9789400708341. https://books.google.com/books?id=SJLrIa7yFBgC&pg=PA189. 
  130. ↑ "Avatar Therapy for people with schizophrenia or related disorders". The Cochrane Database of Systematic Reviews 5: CD011898. May 2020. doi:10.1002/14651858.CD011898.pub2. PMID 32413166. 
  131. ↑ "A Systematic Review of the Effect of Probiotic Supplementation on Schizophrenia Symptoms". Neuropsychobiology 78 (1): 1–6. 2019. doi:10.1159/000498862. PMID 30947230. 
  132. ↑ "Vitamin D and the omega-3 fatty acids control serotonin synthesis and action, part 2: relevance for ADHD, bipolar disorder, schizophrenia, and impulsive behavior". FASEB Journal 29 (6): 2207–22. June 2015. doi:10.1096/fj.14-268342. PMID 25713056. 
  133. ↑ "Nutritional Factors Affecting Mental Health". Clinical Nutrition Research 5 (3): 143–52. July 2016. doi:10.7762/cnr.2016.5.3.143. PMID 27482518. 
  134. ↑ "Interventions for prodromal stage of psychosis". The Cochrane Database of Systematic Reviews 2019 (11). November 2019. doi:10.1002/14651858.CD012236.pub2. PMID 31689359. 
  135. ↑ "Acupuncture for schizophrenia". The Cochrane Database of Systematic Reviews (10): CD005475. October 2014. doi:10.1002/14651858.CD005475.pub2. PMID 25330045. 
  136. ↑ "Acupuncture as Add-On Treatment of the Positive, Negative, and Cognitive Symptoms of Patients with Schizophrenia: A Systematic Review". Medicines 5 (2): 29. March 2018. doi:10.3390/medicines5020029. PMID 29601477. 
  137. ↑ "Wendan decoction (Traditional Chinese medicine) for schizophrenia". The Cochrane Database of Systematic Reviews 6: CD012217. June 2017. doi:10.1002/14651858.CD012217.pub2. PMID 28657646. 
  138. ↑ "Summary of a Cochrane review: Wendan decoction traditional Chinese medicine for schizophrenia". European Journal of Integrative Medicine 15: 81–82. October 2017. doi:10.1016/j.eujim.2017.09.009. PMID 29062436. 
  139. ↑ 139.0 139.1 139.2 "A Neurophysiological Perspective on a Preventive Treatment against Schizophrenia Using Transcranial Electric Stimulation of the Corticothalamic Pathway". Brain Sciences 7 (4): 34. March 2017. doi:10.3390/brainsci7040034. PMID 28350371. 
  140. ↑ 140.0 140.1 140.2 140.3 "Auditory verbal hallucinations in schizophrenia: current perspectives in brain stimulation treatments". Neuropsychiatric Disease and Treatment 15: 2105–2117. 2019. doi:10.2147/NDT.S168801. PMID 31413576. 
  141. ↑ "Clinical and cost-effectiveness of electroconvulsive therapy for depressive illness, schizophrenia, catatonia and mania: systematic reviews and economic modelling studies". Health Technology Assessment 9 (9): 1–156, iii-iv. March 2005. doi:10.3310/hta9090. PMID 15774232. 
  142. ↑ National Institute for Health and Clinical Excellence (April 2003). "The clinical effectiveness and cost effectiveness of electroconvulsive Therapy (ECT) for depressive illness, schizophrenia, catatonia and mania". National Institute for Health and Clinical Excellence. http://www.nice.org.uk/page.aspx?o=TA059. 
  143. ↑ "Psychosurgery: past, present, and future". Brain Research. Brain Research Reviews 48 (3): 409–19. June 2005. doi:10.1016/j.brainresrev.2004.09.002. PMID 15914249. 
  144. ↑ Laupu WK (2014). The efficacy of Garcinia mangostana L. (mangosteen) pericarp as an adjunctive to second-generation antipsychotics for the treatment of schizophrenia: a double blind, randomised, placebo-controlled trial (phd). James Cook University. 40097. Retrieved April 24, 2017.
  145. ↑ "Interpreting outcomes from the supplementation of mangosteen rind powder capsules in schizophrenia and schizoaffective disorders". British Journal of Medical and Health Research 3 (9). September 2016. http://www.bjmhr.com/show_author_index_script.php?volume=3&issue=9&month=September&user=334#. Retrieved April 24, 2017. 
  146. ↑ "Recovery from schizophrenia: An autoethnography". Deviant Behavior 39 (3): 380–399. 2018. doi:10.1080/01639625.2017.1286174. 
  147. ↑ "Nidotherapy: a cost-effective systematic environmental intervention". World Psychiatry 18 (2): 144–145. June 2019. doi:10.1002/wps.20622. PMID 31059613. 
  148. ↑ "Peer support for people with schizophrenia or other serious mental illness". The Cochrane Database of Systematic Reviews 4: CD010880. April 2019. doi:10.1002/14651858.CD010880.pub2. PMID 30946482. 




Retrieved from "https://handwiki.org/wiki/index.php?title=Medicine:Management_of_schizophrenia&oldid=3416749"