Management of schizophrenia

Management of schizophrenia usually involved many aspects including psychological, pharmacological, social, educational, and employment-related interventions directed to recovery, reducing the impact of the disease 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 psychiatric treatment for schizophrenia is antipsychotic medication.[5] Medication might improve a number of outcomes found to be important to patients, including positive, acute and psychotic symptoms, and social and vocational functioning.[6] Medication can reduce the "positive" symptoms of psychosis. Most antipsychotics are thought to take around 7 to 14 days to have their main effect. However, these drugs fail to significantly ameliorate the negative symptoms and cognitive dysfunction.[7][8] There is evidence of clozapine, amisulpride, olanzapine and risperidone being the most effective medications, although 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 neuroleptic or antipsychotic drugs.[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]

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,[16] a medication of superior effectiveness but several potentially lethal side effects including agranulocytosis and myocarditis.[17] Clozapine is the only medication proven to be more effective for persons 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]

Adjunctive agents in schizophrenia

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

Adjuncts[20][21] Symptoms against which efficacy is known Notable AEs seen in clinical trials Highest quality of clinical data available N Notes
Adjuncts to Clozapine[22][23]
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 US or Canada. Approved for use in Australia, Europe and several countries in East Asia. Can prolong the QT interval, some in vivo evidence[24] 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[22] 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's 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[22] 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[25][26]
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 ω-3 fatty acid, eicosapentaenoic acid.
Adjuncts to other antipsychotics
Anti-inflammatory agents[27][28]
Aspirin[29] 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[30][31][32][33] Global Well-tolerated 4 DB-RPCTs 164 Increased risk of blood dyscarsias.
ω-3 fatty acids Global Well-tolerated 6 DB-RPCTs (1 negative)[34] 362 May have protective effects against depression.
Pregnenolone[35][36][37][38] Global Well-tolerated 3 DB-RPCTs 100 Levels of this neurosteroid in the body are elevated by clozapine treatment.
Glutamatergics[25][39]
D-alanine[40][41] 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,[42] Heresco-Levy 2005,[43] Lane 2005,[44] Lane 2010,[45] Tsai 1999,[46] Weiser 2012[47]
Glycine Global (predominantly positive symptoms) Well-tolerated 5 DB-RPCTs 219 Endogenous NMDA receptor ligand.
N-acetylcysteine[48] Global (especially negative symptoms) Well-tolerated 3 DB-RPCTs 140 Cystine and glutathione prodrug.[49][50] Cystine increases intracellular glutamate levels via the glutamate-cystine anti porter.

Berk 2008,[51] Berk 2011,[52] Carmeli 2012,[53] Lavoie 2008[54]

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,[44] Lane 2006,[55] Lane 2008,[56] Lane 2010,[45] Tsai 2004[57]
Cholinergics[58][59][60]
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†[61][62][63][64] Cognitive and negative symptoms Well-tolerated 3 DB-RPCTs 120 Agonist at α7 nAChRs; antagonist at 5-HT3. Expensive (>$20 AUD/tablet).
Antidepressants[65]
Escitalopram†[66] 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.[67] Risk of QT interval prolongation is lower than with escitalopram (but still exists).
Mianserin[68] 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.[69][70]
Mirtazapine[68] Cognition,[71][72] negative and positive symptoms†[73] 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.[74]
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[75][76] Weight gain Well-tolerated 1 DB-RPCT 360 Offset antipsychotic drug-induced weight gain. Increased total antioxidant status. May also increase GSH:GSSH (reduced glutathione:oxidized glutathione) ratio.[77]
L-Theanine[78][79][80] 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.[81][82][83][84] 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.[85]
Famotidine†[86] 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,[87] Doruk 2008,[88] Zhang 2001,[89] Zhang 2001,[90] Zhang 2006,[91] Zhang 2011,[92] Zhou 1999[93]
Ondansetron[94] Negative and cognitive symptoms Well-tolerated 3 DB-RPCTs 151 5-HT3 antagonist. May prolong the QT interval. Expensive (>$4 AUD/tablet).
SAM-e[95] Aggression Well-tolerated 1 DB-RPCT 18 Study noted improvement of aggressive behavior and quality of life impairment.
Vitamin C[96][97][98][99] Global Well-tolerated 1 DB-RPCT 40 Improves BPRS scores.

Acronyms used:
DB-RPCT — Double-blind randomised placebo-controlled trial.
DB-RCT — Double-blind randomised controlled trial.
AE — Adverse effect.

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).

Nicotine patch

Following an observation that tobacco smoking eases effects of schizophrenia, the nicotine patch has been proposed as a treatment for schizophrenia. [100]

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.[101]

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 [102] 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.[103][104] Nonetheless more recent meta analyses have cast doubt upon the utility of CBT as a treatment for the symptoms of psychosis[105][106][107]

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.[108]

Metacognitive training: In view of a many empirical findings [109] suggesting deficits of metacognition (thinking about one’s thinking, reflecting upon one’s cognitive process) in patients with schizophrenia, metacognitive training (MCT) [109][110] 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),[111] 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.[109][110] Studies confirm the feasibility [112] and lend preliminary support to the efficacy [109][113][114] of the intervention. Recently, an individualized format has been developed which combines the metacognitive approach with methods derived from cognitive-behavioral therapy.[115]

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.[116][117][118] 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.[119][120] There is also some evidence for benefits from social skills training, although there have also been significant negative findings.[121][122] Some studies have explored the possible benefits of music therapy and other creative therapies.[123][124][125]

The Soteria model is alternative to inpatient hospitalization using full non professional care and a minimal medication approach.[126] Although evidence is limited, a review found the programme equally as effective as treatment with medications but due to the limited evidence did not recommend it as a standard treatment.[127] Training in the detection of suble facial expressions has been used to improve facial emotional recognition.[128]

Diet

An unconventional approach is the use of omega-3 fatty acids, with one study finding some benefits from their use as a dietary supplement.[129]

A 2003 review of four randomized controlled trials of EPA (an omega-3 fatty acid) vs. placebo as adjunctive treatment for schizophrenia found that two of the trials detected a significant improvement on positive and negative symptoms, and suggested that EPA may be an effective adjunct to antipsychotics.[130] The most recent meta-analysis (2006) failed however to find a significant effect.[131] A 2007 review found that studies of omega-3 fatty acids in schizophrenia, despite being mostly of high quality, have produced inconsistent results and small effect sizes of doubtful clinical significance.[132] Individualized nutrition interventions and supplementation has been proposed as an adjunct to pharmacological therapy in people with schizophrenia, though this approach has not been evaluated in clinical trials to determine the efficacy of such an approach in improving symptoms.[133]

Other

Transcranial Magnetic Stimulation (TMS) appears to be effecting in alleviating the negative symptoms and cognitive deficits see in schizophrenia, a recent double-blind randomized sham controlled study of deep-TMS add-on treatment noted an 8-point reduction in the Scale for the Assessment of Negative Symptoms (SANS) in patients.[134][135][136][137][138][139][140][141][142]

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,[143] 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.[144] Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.[145]

References

  1. ↑ "Psychosis and schizophrenia in adults: treatment and management | Key-priorities-for-implementation | Guidance and guidelines | NICE".
  2. ↑ Becker T, Kilian R (2006). "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 Supplement 113 (429): 9–16. doi:10.1111/j.1600-0447.2005.00711.x. PMID 16445476.
  3. ↑ McGurk, SR; Mueser, KT; Feldman, K; Wolfe, R; Pascaris, A (2007). "Cognitive training for supported employment: 2-3 year outcomes of a randomized controlled trial.". The American Journal of Psychiatry 164 (3): 437–41. doi:10.1176/appi.ajp.164.3.437. PMID 17329468.
  4. ↑ Effects of compulsory treatment orders on time to hospital readmission (2005).
  5. ↑ The Royal College of Psychiatrists & The British Psychological Society (2003). Schizophrenia. Full national clinical guideline on core interventions in primary and secondary care (PDF). London: Gaskell and the British Psychological Society. Retrieved on 2007-05-17.
  6. ↑ "What matters to patients? A systematic review of preferences for medication-associated outcomes in mental disorders". BMJ Open 5 (4): e007848. 2015. doi:10.1136/bmjopen-2015-007848.
  7. ↑ Smith T, Weston C, Lieberman J (August 2010). "Schizophrenia (maintenance treatment)". Am Fam Physician 82 (4): 338–9. PMID 20704164.
  8. ↑ Tandon R, Keshavan MS, Nasrallah HA (March 2008). "Schizophrenia, "Just the Facts": what we know in 2008 part 1: overview" (PDF). Schizophrenia Research 100 (1–3): 4–19. doi:10.1016/j.schres.2008.01.022. PMID 18291627.
  9. 1 2 3 Barry SJE, Gaughan TM, Hunter R (2012). "Schizophrenia". BMJ Clinical Evidence 2012. PMC 3385413. PMID 23870705.
  10. ↑ Leucht S, Tardy M, Komossa K, et al. (June 2012). "Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: a systematic review and meta-analysis". Lancet 379 (9831): 2063–71. doi:10.1016/S0140-6736(12)60239-6. PMID 22560607.
  11. 1 2 Harrow M, Jobe TH (19 March 2013). "Does long-term treatment of dchizophrenia with antipsychotic medications facilitate recovery?". Schizophrenia bulletin 39 (5): 962–5. doi:10.1093/schbul/sbt034. PMC 3756791. PMID 23512950.
  12. ↑ Turner T. (2007). "Unlocking psychosis". Brit J Med 334 (suppl): s7. doi:10.1136/bmj.39034.609074.94. PMID 17204765.
  13. ↑ Ananth J, Parameswaran S, Gunatilake S, Burgoyne K, Sidhom T (2004). "Neuroleptic malignant syndrome and atypical antipsychotic drugs". Journal of Clinical Psychiatry 65 (4): 464–70. doi:10.4088/JCP.v65n0403. PMID 15119907.
  14. ↑ "PsychiatryOnline | APA Practice Guidelines | Practice Guideline for the Treatment of Patients With Schizophrenia Second Edition".
  15. ↑ Semple.David"Oxford Handbook Of Psychiatry". Oxford Press. 2005. p 207.
  16. ↑ Wahlbeck K, Cheine MV, Essali A (2007). Wahlbeck, Kristian, ed. "Clozapine versus typical neuroleptic medication for schizophrenia". Cochrane Database of Systematic Reviews (John Wiley and Sons, Ltd.) (2): CD000059. doi:10.1002/14651858.CD000059. PMID 10796289. ISSN 1464-780X.
  17. ↑ Haas SJ, Hill R, Krum H (2007). "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. doi:10.2165/00002018-200730010-00005. PMID 17194170.
  18. ↑ Lieberman, Jeffrey A.; Stroup, T. Scott; McEvoy, Joseph P.; Swartz, Marvin S.; Rosenheck, Robert A.; Perkins, Diana O.; Keefe, Richard S.E.; Davis, Sonia M.; Davis, Clarence E.; Lebowitz, Barry D.; Severe, Joanne; Hsiao, John K.; Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators (2005). "Effectiveness of Antipsychotic Drugs in Patients with Chronic Schizophrenia". New England Journal of Medicine 353 (12): 1209–23. doi:10.1056/NEJMoa051688. PMID 16172203.
  19. ↑ Kozier, B et al. (2008). Fundamentals Of Nursing, Concepts, Process, and Practice. London: Pearson Education. p. 189.
  20. ↑ Ritsner, MS (2013). Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. ISBN 9789400758056.
  21. ↑ Ritsner, MS (2013). Polypharmacy in Psychiatry Practice, Volume II. Springer Science+Business Media Dordrecht. ISBN 9789400757998.
  22. 1 2 3 Porcelli, S; Balzarro, B; Serretti, A (March 2012). "Clozapine resistance: augmentation strategies". European Neuropsychopharmacology 22 (3): 165–182. doi:10.1016/j.euroneuro.2011.08.005. PMID 21906915.
  23. ↑ Sommer, IE; Begemann, MJ; Temmerman, A; Leucht, S (September 2012). "Pharmacological Augmentation Strategies for Schizophrenia Patients With Insufficient Response to Clozapine: A Quantitative Literature Review" (PDF). Schizophrenia Bulletin 38 (5): 1003–1011. doi:10.1093/schbul/sbr004. PMC 3446238. PMID 21422107.
  24. ↑ Roix, JJ; DeCrescenzo, GA; Cheung, PH; Ciallella, JR; Sulpice, T; Saha, S; Halse, R (April 2012). "Effect of the antipsychotic agent amisulpride on glucose lowering and insulin secretion". Diabetes, Obesity & Metabolism 14 (4): 329–334. doi:10.1111/j.1463-1326.2011.01529.x. PMID 22059694.
  25. 1 2 Singh, SP; Singh, V (October 2011). "Meta-Analysis of the Efficacy of Adjunctive NMDA Receptor Modulators in Chronic Schizophrenia". CNS Drugs 25 (10): 859–885. doi:10.2165/11586650-000000000-00000. PMID 21936588.
  26. ↑ Choi, KH; Wykes, T; Kurtz, MM (September 2013). "Adjunctive pharmacotherapy for cognitive deficits in schizophrenia: meta-analytical investigation of efficacy". The British Journal of Psychiatry 203 (3): 172–178. doi:10.1192/bjp.bp.111.107359. PMID 23999481.
  27. ↑ Keller, WR; Kum, LM; Wehring, HJ; Koola, MM; Buchanan, RW; Kelly, DL (April 2013). "A review of anti-inflammatory agents for symptoms of schizophrenia". Journal of Psychopharmacology 27 (4): 337–342. doi:10.1177/0269881112467089. PMID 23151612.
  28. ↑ Sommer, I. E.; Van Westrhenen, R.; Begemann, M. J. H.; De Witte, L. D.; Leucht, S.; Kahn, R. S. (2013). "Efficacy of Anti-inflammatory Agents to Improve Symptoms in Patients with Schizophrenia: An Update". Schizophrenia Bulletin 40 (1): 181–191. doi:10.1093/schbul/sbt139. PMC 3885306. PMID 24106335.
  29. ↑ Laan, W.; Grobbee, D. E.; Selten, J. P.; Heijnen, C. J.; Kahn, R. S.; Burger, H. (2010). "Adjuvant Aspirin Therapy Reduces Symptoms of Schizophrenia Spectrum Disorders". The Journal of Clinical Psychiatry 71 (5): 520–527. doi:10.4088/JCP.09m05117yel. PMID 20492850.
  30. ↑ Liu, F.; Guo, X.; Wu, R.; Ou, J.; Zheng, Y.; Zhang, B.; Xie, L.; Zhang, L.; Yang, L.; Yang, S.; Yang, J.; Ruan, Y.; Zeng, Y.; Xu, X.; Zhao, J. (2014). "Minocycline supplementation for treatment of negative symptoms in early-phase schizophrenia: A double blind, randomized, controlled trial". Schizophrenia Research 153 (1–3): 169–76. doi:10.1016/j.schres.2014.01.011. PMID 24503176.
  31. ↑ Khodaie-Ardakani, M. R.; Mirshafiee, O.; Farokhnia, M.; Tajdini, M.; Hosseini, S. M. R.; Modabbernia, A.; Rezaei, F.; Salehi, B.; Yekehtaz, H.; Ashrafi, M.; Tabrizi, M.; Akhondzadeh, S. (2014). "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. doi:10.1016/j.psychres.2013.12.051. PMID 24480077.
  32. ↑ Chaudhry, I. B.; Hallak, J.; Husain, N.; Minhas, F.; Stirling, J.; Richardson, P.; Dursun, S.; Dunn, G.; Deakin, B. (2012). "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): 1185–1193. doi:10.1177/0269881112444941. PMID 22526685.
  33. ↑ Levkovitz, Y.; Mendlovich, S.; Riwkes, S.; Braw, Y.; Levkovitch-Verbin, H.; Gal, G.; Fennig, S.; Treves, I.; Kron, S. (2010). "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): 138–149. doi:10.4088/JCP.08m04666yel. PMID 19895780.
  34. ↑ Irving, CB; Mumby-Croft, R; Joy, LA (July 2006). "Polyunsaturated fatty acid supplementation for schizophrenia(Review)". Cochrane Database of Systematic Reviews (3): CD001257. doi:10.1002/14651858.CD001257.pub2. PMID 16855961.
  35. ↑ Ritsner, M. S.; Gibel, A.; Shleifer, T.; Boguslavsky, I.; Zayed, A.; Maayan, R.; Weizman, A.; Lerner, V. (2010). "Pregnenolone and Dehydroepiandrosterone as an Adjunctive Treatment in Schizophrenia and Schizoaffective Disorder". The Journal of Clinical Psychiatry 71 (10): 1351–1362. doi:10.4088/JCP.09m05031yel. PMID 20584515.
  36. ↑ Marx, C. E.; Keefe, R. S. E.; Buchanan, R. W.; Hamer, R. M.; Kilts, J. D.; Bradford, D. W.; Strauss, J. L.; Naylor, J. C.; Payne, V. M.; Lieberman, J. A.; Savitz, A. J.; Leimone, L. A.; Dunn, L.; Porcu, P.; Morrow, A. L.; Shampine, L. J. (2009). "Proof-of-Concept Trial with the Neurosteroid Pregnenolone Targeting Cognitive and Negative Symptoms in Schizophrenia". Neuropsychopharmacology 34 (8): 1885–1903. doi:10.1038/npp.2009.26. PMC 3427920. PMID 19339966.
  37. ↑ Wong, P.; Chang, C. C. R.; Marx, C. E.; Caron, M. G.; Wetsel, W. C.; Zhang, X. (2012). Hashimoto, Kenji, ed. "Pregnenolone Rescues Schizophrenia-Like Behavior in Dopamine Transporter Knockout Mice". PLoS ONE 7 (12): e51455. doi:10.1371/journal.pone.0051455. PMC 3519851. PMID 23240026.
  38. ↑ Marx, C. E.; Stevens, R. D.; Shampine, L. J.; Uzunova, V.; Trost, W. T.; Butterfield, M. I.; Massing, M. W.; Hamer, R. M.; Morrow, A. L.; Lieberman, J. A. (2005). "Neuroactive Steroids are Altered in Schizophrenia and Bipolar Disorder: Relevance to Pathophysiology and Therapeutics". Neuropsychopharmacology. doi:10.1038/sj.npp.1300952.
  39. ↑ Javitt, D. C.; Zukin, S. R.; Heresco-Levy, U.; Umbricht, D. (2012). "Has an Angel Shown the Way? Etiological and Therapeutic Implications of the PCP/NMDA Model of Schizophrenia". Schizophrenia Bulletin 38 (5): 958–966. doi:10.1093/schbul/sbs069. PMC 3446214. PMID 22987851.
  40. ↑ Hatano, T.; Ohnuma, T.; Sakai, Y.; Shibata, N.; Maeshima, H.; Hanzawa, R.; Suzuki, T.; Arai, H. (2010). "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. doi:10.1016/j.psychres.2010.02.014. PMID 20226539.
  41. ↑ Tsai, G. E.; Yang, P.; Chang, Y. C.; Chong, M. Y. (2006). "D-Alanine Added to Antipsychotics for the Treatment of Schizophrenia". Biological Psychiatry 59 (3): 230–234. doi:10.1016/j.biopsych.2005.06.032. PMID 16154544.
  42. ↑ d'Souza, D. C.; Radhakrishnan, R.; Perry, E.; Bhakta, S.; Singh, N. M.; Yadav, R.; Abi-Saab, D.; Pittman, B.; Chaturvedi, S. K.; Sharma, M. P.; Bell, M.; Andrade, C. (2012). "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. doi:10.1038/npp.2012.208. PMC 3547200. PMID 23093223.
  43. ↑ Heresco-Levy, U.; Javitt, D. C.; Ebstein, R.; Vass, A.; Lichtenberg, P.; Bar, G.; Catinari, S.; Ermilov, M. (2005). "D-serine efficacy as add-on pharmacotherapy to risperidone and olanzapine for treatment-refractory schizophrenia". Biological Psychiatry 57 (6): 577–585. doi:10.1016/j.biopsych.2004.12.037. PMID 15780844.
  44. 1 2 Lane, H. Y.; Chang, Y. C.; Liu, Y. C.; Chiu, C. C.; Tsai, G. E. (2005). "Sarcosine or D-Serine Add-on Treatment for Acute Exacerbation of Schizophrenia". Archives of General Psychiatry 62 (11): 1196–1204. doi:10.1001/archpsyc.62.11.1196. PMID 16275807.
  45. 1 2 Lane, H. Y.; Lin, C. H.; Huang, Y. J.; Liao, C. H.; Chang, Y. C.; Tsai, G. E. (2009). "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): 451–460. doi:10.1017/S1461145709990939. PMID 19887019.
  46. ↑ Tsai, G. E.; Yang, P.; Chung, L. C.; Tsai, I. C.; Tsai, C. W.; Coyle, J. T. (1999). "D-serine added to clozapine for the treatment of schizophrenia". The American Journal of Psychiatry 156 (11): 1822–1825. PMID 10553752.
  47. ↑ Weiser, M.; Heresco-Levy, U.; Davidson, M.; Javitt, D. C.; Werbeloff, N.; Gershon, A. A.; Abramovich, Y.; Amital, D.; Doron, A.; Konas, S.; Levkovitz, Y.; Liba, D.; Teitelbaum, A.; Mashiach, M.; Zimmerman, Y. (2012). "A Multicenter, Add-On Randomized Controlled Trial of Low-Dosed-Serine for Negative and Cognitive Symptoms of Schizophrenia". The Journal of Clinical Psychiatry 73 (6): e728. doi:10.4088/JCP.11m07031.
  48. ↑ Dean, O.; Giorlando, F.; Berk, M. (2011). "N-acetylcysteine in psychiatry: Current therapeutic evidence and potential mechanisms of action". Journal of psychiatry & neuroscience : JPN 36 (2): 78–86. doi:10.1503/jpn.100057. PMC 3044191. PMID 21118657.
  49. ↑ Aoyama, K.; Watabe, M.; Nakaki, T. (2008). "Regulation of Neuronal Glutathione Synthesis". Journal of Pharmacological Sciences 108 (3): 227–238. doi:10.1254/jphs.08R01CR. PMID 19008644.
  50. ↑ Jain, A.; Mårtensson, J.; Stole, E.; Auld, P. A.; Meister, A. (1991). "Glutathione deficiency leads to mitochondrial damage in brain". Proceedings of the National Academy of Sciences of the United States of America 88 (5): 1913–1917. doi:10.1073/pnas.88.5.1913. PMC 51136. PMID 2000395.
  51. ↑ Berk, M.; Copolov, D.; Dean, O.; Lu, K.; Jeavons, S.; Schapkaitz, I.; Anderson-Hunt, M.; Judd, F.; Katz, F.; Katz, P.; Ording-Jespersen, S.; Little, J.; Conus, P.; Cuenod, M.; Do, K. Q.; Bush, A. I. (2008). "N-Acetyl Cysteine as a Glutathione Precursor for Schizophrenia—A Double-Blind, Randomized, Placebo-Controlled Trial". Biological Psychiatry 64 (5): 361–368. doi:10.1016/j.biopsych.2008.03.004. PMID 18436195.
  52. ↑ Berk, M.; Munib, A.; Dean, O.; Malhi, G. S.; Kohlmann, K.; Schapkaitz, I.; Jeavons, S.; Katz, F.; Anderson-Hunt, M.; Conus, P.; Hanna, B.; Otmar, R. E.; Ng, F.; Copolov, D. L.; Bush, A. I. (2011). "Qualitative Methods in Early-Phase Drug Trials". The Journal of Clinical Psychiatry 72 (7): 909–913. doi:10.4088/JCP.09m05741yel. PMID 20868637.
  53. ↑ Carmeli, C.; Knyazeva, M. G.; Cuénod, M.; Do, K. Q. (2012). Burne, Thomas, ed. "Glutathione Precursor N-Acetyl-Cysteine Modulates EEG Synchronization in Schizophrenia Patients: A Double-Blind, Randomized, Placebo-Controlled Trial". PLoS ONE 7 (2): e29341. doi:10.1371/journal.pone.0029341. PMC 3285150. PMID 22383949.
  54. ↑ Lavoie, S.; Murray, M. M.; Deppen, P.; Knyazeva, M. G.; Berk, M.; Boulat, O.; Bovet, P.; Bush, A. I.; Conus, P.; Copolov, D.; Fornari, E.; Meuli, R.; Solida, A.; Vianin, P.; Cuénod, M.; Buclin, T.; Do, K. Q. (2007). "Glutathione Precursor, N-Acetyl-Cysteine, Improves Mismatch Negativity in Schizophrenia Patients". Neuropsychopharmacology 33 (9): 2187–2199. doi:10.1038/sj.npp.1301624. PMID 18004285.
  55. ↑ Lane, H. Y.; Huang, C. L.; Wu, P. L.; Liu, Y. C.; Chang, Y. C.; Lin, P. Y.; Chen, P. W.; Tsai, G. (2006). "Glycine Transporter I Inhibitor, N-methylglycine (Sarcosine), Added to Clozapine for the Treatment of Schizophrenia". Biological Psychiatry 60 (6): 645–649. doi:10.1016/j.biopsych.2006.04.005. PMID 16780811.
  56. ↑ Lane, H. Y.; Liu, Y. C.; Huang, C. L.; Chang, Y. C.; Liau, C. H.; Perng, C. H.; Tsai, G. E. (2008). "Sarcosine (N-Methylglycine) Treatment for Acute Schizophrenia: A Randomized, Double-Blind Study". Biological Psychiatry 63 (1): 9–12. doi:10.1016/j.biopsych.2007.04.038. PMID 17659263.
  57. ↑ Tsai, G.; Lane, H. Y.; Yang, P.; Chong, M. Y.; Lange, N. (2004). "Glycine transporter I inhibitor, N-Methylglycine (sarcosine), added to antipsychotics for the treatment of schizophrenia". Biological Psychiatry 55 (5): 452–456. doi:10.1016/j.biopsych.2003.09.012. PMID 15023571.
  58. ↑ Singh, J; Kour, K; Jayaram, MB (January 2012). "Acetylcholinesterase inhibitors for schizophrenia". Cochrane Database of Systematic Reviews 1: CD007967. doi:10.1002/14651858.CD007967.pub2. PMID 22258978.
  59. ↑ Choi, KH; Wykes, T; Kurtz, MM (September 2013). "Adjunctive pharmacotherapy for cognitive deficits in schizophrenia: meta-analytical investigation of efficacy". The British Journal of Psychiatry 203 (3): 172–178. doi:10.1192/bjp.bp.111.107359. PMID 23999481.
  60. ↑ Ribeiz, SR; Bassitt, DP; Arrais, JA; Avila, R; Steffens, DC; Bottino, CM (April 2010). "Cholinesterase Inhibitors as Adjunctive Therapy in Patients with Schizophrenia and Schizoaffective Disorder A Review and Meta-Analysis of the Literature". CNS Drugs 24 (4): 303–317. doi:10.2165/11530260-000000000-00000. PMID 20297855.
  61. ↑ Koike, K; Hashimoto, K; Takai, N; Shimizu, E; Komatsu, N; Watanabe, H; Nakazato, M; Okamura, N; Stevens, KE; Freedman, R; Iyo, M (July 2005). "Tropisetron improves deficits in auditory P50 suppression in schizophrenia". Schizophrenia Research 76 (1): 67–72. doi:10.1016/j.schres.2004.12.016. PMID 15927799.
  62. ↑ Shiina, A; Shirayama, Y; Niitsu, T; Hashimoto, T; Yoshida, T; Hasegawa, T; Haraguchi, T; Kanahara, N; Shiraishi, T; Fujisaki, M; Fukami, G; Nakazato, M; Iyo, M; Hashimoto, K (June 2010). "A randomised, double-blind, placebo-controlled trial of tropisetron in patients with schizophrenia" (PDF). Annals of General Psychiatry 9 (1): 27. doi:10.1186/1744-859X-9-27. PMC 2901366. PMID 20573264.
  63. ↑ Zhang, XY; Liu, L; Liu, S; Hong, X; Chen da, C; Xiu, MH; Yang, FD; Zhang, Z; Zhang, X; Kosten, TA; Kosten, TR (September 2012). "Short-Term Tropisetron Treatment and Cognitive and P50 Auditory Gating Deficits in Schizophrenia". The American Journal of Psychiatry 169 (9): 974–981. doi:10.1176/appi.ajp.2012.11081289. PMID 22952075.
  64. ↑ Noroozian, M; Ghasemi, S; Hosseini, SM; Modabbernia, A; Khodaie-Ardakani, MR; Mirshafiee, O; Farokhnia, M; Tajdini, M; Rezaei, F; Salehi, B; Ashrafi, M; Yekehtaz, H; Tabrizi, M; Akhondzadeh, S (Aug 2013). "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. doi:10.1007/s00213-013-3064-2. PMID 23515583.
  65. ↑ Singh, SP; Singh, V; Kar, N; Chan, K (September 2010). "Efficacy of antidepressants in treating the negative symptoms of chronic schizophrenia: meta-analysis". The British Journal of Psychiatry 197 (3): 174–179. doi:10.1192/bjp.bp.109.067710. PMID 20807960.
  66. ↑ Iancu, I; Tschernihovsky, E; Bodner, E; Piconne, AS; Lowengrub, K (August 2010). "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. doi:10.1016/j.psychres.2010.04.035. PMID 20472299.
  67. ↑ White, N; Litovitz, T; Clancy, C (December 2008). "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type" (PDF). Journal of Medical Toxicology 4 (4): 238–250. doi:10.1007/BF03161207. PMC 3550116. PMID 19031375.
  68. 1 2 Hecht, EM; Landy, DC (February 2012). "Alpha-2 receptor antagonist add-on therapy in the treatment of schizophrenia; a meta-analysis". Schizophrenia Research 134 (2-3): 202–206. doi:10.1016/j.schres.2011.11.030. PMID 22169246.
  69. ↑ Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3.
  70. ↑ Joint Formulary Committee (2013). British National Formulary (BNF) (65 ed.). London, UK: Pharmaceutical Press. p. 247. ISBN 978-0-85711-084-8.
  71. ↑ Ritsner, MS (2013). Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. ISBN 9789400758056.
  72. ↑ Vidal, C; Reese, C; Fischer, BA; Chiapelli, J; Himelhoch, S (March 2013). "Meta-Analysis of Efficacy of Mirtazapine as an Adjunctive Treatment of Negative Symptoms in Schizophrenia". Clinical Schizophrenia & Related Psychoses (Walsh Medical Media) 1: 1–24. doi:10.3371/CSRP.VIRE.030813. ISSN 1935-1232. PMID 23491969.
  73. ↑ Stenberg, JH; Terevnikov, V; Joffe, M; Tiihonen, J; Tchoukhine, E; Burkin, M; Joffe, G (June 2011). "More evidence on proneurocognitive effects of add-on mirtazapine in schizophrenia". Progress in Neuro-Psychopharmacology and Biological Psychiatry 35 (4): 1080–1086. doi:10.1016/j.pnpbp.2011.03.004. PMID 21402120.
  74. ↑ Kumar, R; Sachdev, PS (May 2009). "Akathisia and Second-generation Antipsychotic Drugs". Current Opinion in Psychiatry 22 (3): 293–299. doi:10.1097/YCO.0b013e32832a16da. PMID 19378382.
  75. ↑ Koh, E. H.; Lee, W. J.; Lee, S. A.; Kim, E. H.; Cho, E. H.; Jeong, E.; Kim, D. W.; Kim, M. S.; Park, J. Y.; Park, K. G.; Lee, H. J.; Lee, I. K.; Lim, S.; Jang, H. C.; Lee, K. H.; Lee, K. U. (2011). "Effects of Alpha-Lipoic Acid on Body Weight in Obese Subjects". The American Journal of Medicine 124: 85.e1. doi:10.1016/j.amjmed.2010.08.005.
  76. ↑ Kim, E.; Park, D. W.; Choi, S. H.; Kim, J. J.; Cho, H. S. (2008). "A Preliminary Investigation of α-Lipoic Acid Treatment of Antipsychotic Drug-Induced Weight Gain in Patients with Schizophrenia". Journal of Clinical Psychopharmacology 28 (2): 138–146. doi:10.1097/JCP.0b013e31816777f7. PMID 18344723.
  77. ↑ Jariwalla, R. J.; Lalezari, J.; Cenko, D.; Mansour, S. E.; Kumar, A.; Gangapurkar, B.; Nakamura, D. (2008). "Restoration of Blood Total Glutathione Status and Lymphocyte Function Followingα-Lipoic Acid Supplementation in Patients with HIV Infection". The Journal of Alternative and Complementary Medicine 14 (2): 139–146. doi:10.1089/acm.2006.6397. PMID 18315507.
  78. ↑ Ritsner, M. S.; Miodownik, C.; Ratner, Y.; Shleifer, T.; Mar, M.; Pintov, L.; Lerner, V. (2011). "L-Theanine Relieves Positive, Activation, and Anxiety Symptoms in Patients with Schizophrenia and Schizoaffective Disorder". The Journal of Clinical Psychiatry 72 (1): 34–42. doi:10.4088/JCP.09m05324gre. PMID 21208586.
  79. ↑ Miodownik, C.; Maayan, R.; Ratner, Y.; Lerner, V.; Pintov, L.; Mar, M.; Weizman, A.; Ritsner, M. S. (2011). "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): 155–160. doi:10.1097/WNF.0b013e318220d8c6. PMID 21617527.
  80. ↑ Lardner, A. L. (2013). "Neurobiological effects of the green tea constituent theanine and its potential role in the treatment of psychiatric and neurodegenerative disorders". Nutritional Neuroscience 17: 140123093232009. doi:10.1179/1476830513Y.0000000079.
  81. ↑ Kelly, S. P.; Gomez-Ramirez, M.; Montesi, J. L.; Foxe, J. J. (2008). "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. PMID 18641209.
  82. ↑ Park, S. K.; Jung, I. C.; Lee, W. K.; Lee, Y. S.; Park, H. K.; Go, H. J.; Kim, K.; Lim, N. K.; Hong, J. T.; Ly, S. Y.; Rho, S. S. (2011). "A Combination of Green Tea Extract andl-Theanine Improves Memory and Attention in Subjects with Mild Cognitive Impairment: A Double-Blind Placebo-Controlled Study". Journal of Medicinal Food 14 (4): 334–343. doi:10.1089/jmf.2009.1374. PMID 21303262.
  83. ↑ Foxe, J. J.; Morie, K. P.; Laud, P. J.; Rowson, M. J.; De Bruin, E. A.; Kelly, S. P. (2012). "Assessing the effects of caffeine and theanine on the maintenance of vigilance during a sustained attention task". Neuropharmacology 62 (7): 2320–2327. doi:10.1016/j.neuropharm.2012.01.020. PMID 22326943.
  84. ↑ Nobre, A. C.; Rao, A.; Owen, G. N. (2008). "L-theanine, a natural constituent in tea, and its effect on mental state". Asia Pacific journal of clinical nutrition. 17 Suppl 1: 167–168. PMID 18296328.
  85. ↑ Di, X.; Yan, J.; Zhao, Y.; Chang, Y.; Zhao, B. (2012). "L-theanine inhibits nicotine-induced dependence via regulation of the nicotine acetylcholine receptor-dopamine reward pathway". Science China Life Sciences 55 (12): 1064–1074. doi:10.1007/s11427-012-4401-0. PMID 23233221.
  86. ↑ Meskanen, K; Ekelund, H; Laitinenm, J; Neuvonen, PJ; Haukka, J; Panula P; Ekelund, J (August 2013). "A randomized clinical trial of histamine 2 receptor antagonism in treatment-resistant schizophrenia". Journal of Clinical Psychopharmacology 33 (4): 472–478. doi:10.1097/JCP.0b013e3182970490. PMID 23764683.
  87. ↑ Atmaca, M.; Tezcan, E.; Kuloglu, M.; Ustundag, B.; Kirtas, O. (2005). "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): 652–656. doi:10.1111/j.1440-1819.2005.01432.x. PMID 16401239.
  88. ↑ Doruk, A.; Uzun, Ö.; Ozşahin, A. (2008). "A placebo-controlled study of extract of ginkgo biloba added to clozapine in patients with treatment-resistant schizophrenia". International Clinical Psychopharmacology 23 (4): 223–227. doi:10.1097/YIC.0b013e3282fcff2f. PMID 18545061.
  89. ↑ Zhang, X. Y.; Zhou, D. F.; Su, J. M.; Zhang, P. Y. (2001). "The effect of extract of ginkgo biloba added to haloperidol on superoxide dismutase in inpatients with chronic schizophrenia". Journal of Clinical Psychopharmacology 21 (1): 85–88. doi:10.1097/00004714-200102000-00015. PMID 11199954.
  90. ↑ Zhang, X. Y.; Zhou, D. F.; Zhang, P. Y.; Wu, G. Y.; Su, J. M.; Cao, L. Y. (2001). "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): 878–883. doi:10.4088/JCP.v62n1107. PMID 11775047.
  91. ↑ Zhang, X. Y.; Zhou, D. F.; Cao, L. Y.; Wu, G. Y. (2006). "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): 12–17. doi:10.1007/s00213-006-0476-2. PMID 16906395.
  92. ↑ Zhang, W. F.; Tan, Y. L.; Zhang, X. Y.; Chan, R. C. K.; Wu, H. R.; Zhou, D. F. (2011). "Extract ofGinkgo bilobaTreatment for Tardive Dyskinesia in Schizophrenia". The Journal of Clinical Psychiatry 72 (5): 615–621. doi:10.4088/JCP.09m05125yel. PMID 20868638.
  93. ↑ Zhou, D.; Zhang, X.; Su, J.; Nan, Z.; Cui, Y.; Liu, J.; Guan, Z.; Zhang, P.; Shen, Y. (1999). "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): 1093–1096. PMID 11721446.
  94. ↑ Bennett, AC; Vila, TM (July–August 2010). "The role of ondansetron in the treatment of schizophrenia". Annals of Pharmacotherapy 44 (7-8): 1301–1306. doi:10.1345/aph.1P008. PMID 20516364.
  95. ↑ Strous, R. D.; Ritsner, M. S.; Adler, S.; Ratner, Y.; Maayan, R.; Kotler, M.; Lachman, H.; Weizman, A. (2009). "Improvement of aggressive behavior and quality of life impairment following S-Adenosyl-Methionine (SAM-e) augmentation in schizophrenia". European Neuropsychopharmacology 19 (1): 14–22. doi:10.1016/j.euroneuro.2008.08.004. PMID 18824331.
  96. ↑ Dakhale, G. N.; Khanzode, S. D.; Khanzode, S. S.; Saoji, A. (2005). "Supplementation of vitamin C with atypical antipsychotics reduces oxidative stress and improves the outcome of schizophrenia". Psychopharmacology 182 (4): 494–498. doi:10.1007/s00213-005-0117-1. PMID 16133138.
  97. ↑ Wang, Y.; Liu, X. J.; Robitaille, L.; Eintracht, S.; MacNamara, E.; Hoffer, L. J. (2013). "Effects of vitamin C and vitamin D administration on mood and distress in acutely hospitalized patients". American Journal of Clinical Nutrition 98 (3): 705–711. doi:10.3945/ajcn.112.056366. PMID 23885048.
  98. ↑ Zhang, M.; Robitaille, L.; Eintracht, S.; Hoffer, L. J. (2011). "Vitamin C provision improves mood in acutely hospitalized patients". Nutrition 27 (5): 530–533. doi:10.1016/j.nut.2010.05.016. PMID 20688474.
  99. ↑ Kennedy, D. O.; Veasey, R.; Watson, A.; Dodd, F.; Jones, E.; Maggini, S.; Haskell, C. F. (2010). "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. doi:10.1007/s00213-010-1870-3. PMC 2885294. PMID 20454891.
  100. ↑ Smoking and schizophrenia
  101. ↑ Moran M (18 November 2005). "Psychosocial Treatment Often Missing From Schizophrenia Regimens". Psychiatr News 40 (22): 24–37. doi:10.1176/pn.40.22.0024b. Retrieved 2007-05-17.
  102. ↑ Cormac I, Jones C, Campbell C (2002). "Cognitive behaviour therapy for schizophrenia". Cochrane Database of systematic reviews (1): CD000524. doi:10.1002/14651858.CD000524. PMID 11869579.
  103. ↑ Wykes T, Steel C, Everitt B, Tarrier N (May 2008). "Cognitive behavior therapy for schizophrenia: effect sizes, clinical models, and methodological rigor". Schizophr Bull 34 (3): 523–37. doi:10.1093/schbul/sbm114. PMC 2632426. PMID 17962231.
  104. ↑ Zimmermann G, Favrod J, Trieu VH, Pomini V (September 2005). "The effect of cognitive behavioral treatment on the positive symptoms of schizophrenia spectrum disorders: a meta-analysis". Schizophrenia Research 77 (1): 1–9. doi:10.1016/j.schres.2005.02.018. PMID 16005380. Retrieved 2008-07-03.
  105. ↑ Lynch D., Laws K. R., McKenna P. J. (2010). "Cognitive behavioural therapy for major psychiatric disorder: does it really work? A meta-analytical review of well-controlled trials". Psychological Medicine 40 (01): 9–24. doi:10.1017/s003329170900590x.
  106. ↑ 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).
  107. ↑ Jones Christopher; et al. (2011). "Cognitive behaviour therapy versus other psychosocial treatments for schizophrenia". The Cochrane Library.
  108. ↑ Wykes T, Brammer M, Mellers J, et al. (2002). "Effects on the brain of a psychological treatment: cognitive remediation therapy: functional magnetic resonance imaging in schizophrenia". British Journal of Psychiatry 181: 144–52. doi:10.1192/bjp.181.2.144. PMID 12151286.
  109. 1 2 3 4 Moritz S, Woodward TS (2007). "Metacognitive training in schizophrenia: from basic research to knowledge translation and intervention". Current Opinion in Psychiatry 20: 619–625. doi:10.1097/YCO.0b013e3282f0b8ed.
  110. 1 2 Moritz S, Woodward TS, Burlon M (2005). "Metacognitive skill training for patients with schizophrenia (MCT)" (PDF). Hamburg: VanHam Campus. Retrieved 1 April 2011.
  111. ↑ Bell V, Halligan PW, Ellis HD (2006). "Explaining delusions: a cognitive perspective". Trends in Cognitive Sciences 10 (5): 219–226. doi:10.1016/j.tics.2006.03.004. PMID 16600666.
  112. ↑ Moritz S, Woodward TS (2007). "Metacognitive training for schizophrenia patients (MCT): A pilot study on feasibility, treatment adherence, and subjective efficacy" (PDF). German Journal of Psychiatry 10: 69–78.
  113. ↑ Aghotor J, Pfueller U, Moritz S, Weisbrod M, Roesch-Ely D (September 2010). "Metacognitive training for patients with schizophrenia (MCT): feasibility and preliminary evidence for its efficacy". J Behav Ther Exp Psychiatry 41 (3): 207–11. doi:10.1016/j.jbtep.2010.01.004. PMID 20167306.
  114. ↑ Ross K, Freeman D, Dunn G, Garety P (March 2011). "A randomized experimental investigation of reasoning training for people with delusions". Schizophr Bull 37 (2): 324–33. doi:10.1093/schbul/sbn165. PMC 3044626. PMID 19520745.
  115. ↑ Moritz S, Veckenstedt R, Randjbar S, Vitzthum F (in press). "Individualized metacognitive therapy for people with schizophrenia psychosis (MCT+)", Springer, Heidelberg.
  116. ↑ McFarlane WR, Dixon L, Lukens E, Lucksted A (April 2003). "Family psychoeducation and schizophrenia: a review of the literature.". Journal of marital and family therapy 29 (2): 223–45. doi:10.1111/j.1752-0606.2003.tb01202.x. PMID 12728780.
  117. ↑ Glynn SM, Cohen AN, Niv N (January 2007). "New challenges in family interventions for schizophrenia". Expert Review of Neurotherapeutics 7 (1): 33–43. doi:10.1586/14737175.7.1.33. PMID 17187495.
  118. ↑ Pharoah FM, Rathbone J, Mari JJ, Streiner D (2003). Pharoah, Fiona, ed. "Family intervention for schizophrenia". Cochrane Database of Systematic Reviews (4): CD000088. doi:10.1002/14651858.CD000088. PMID 14583908.
  119. ↑ Jones, S., Hayward, P. (2004). Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. Oxford, England: Oneworld Pub. ISBN 1-85168-344-5.
  120. ↑ Torrey, EF (2006). Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th Edition). HarperCollins. ISBN 0-06-084259-8.
  121. ↑ Kopelowicz A, Liberman RP, Zarate R (Oct 2006). "Recent advances in social skills training for schizophrenia". Schizophrenia Bulletin 32 (Suppl 1): S12–23. doi:10.1093/schbul/sbl023. PMC 2632540. PMID 16885207.
  122. ↑ American Psychiatric Association (2004) Practice Guideline for the Treatment of Patients With Schizophrenia. Second Edition.
  123. ↑ Talwar N, Crawford MJ, Maratos A, Nur U, McDermott O, Procter S (November 2006). "Music therapy for in-patients with schizophrenia: Exploratory randomised controlled trial". The British Journal of Psychiatry 189 (5): 405–9. doi:10.1192/bjp.bp.105.015073. PMID 17077429.
  124. ↑ Ruddy R, Milnes D (2005). Ruddy, Rachel, ed. "Art therapy for schizophrenia or schizophrenia-like illnesses". Cochrane Database of Systematic Reviews (4): CD003728. doi:10.1002/14651858.CD003728.pub2. PMID 16235338.
  125. ↑ Ruddy RA, Dent-Brown K (2007). Ruddy, Rachel, ed. "Drama therapy for schizophrenia or schizophrenia-like illnesses". Cochrane Database of Systematic Reviews (1): CD005378. doi:10.1002/14651858.CD005378.pub2. PMID 17253555.
  126. ↑ Mosher LR. Soteria and other alternatives to acute psychiatric hospitalization: a personal and professional review. Journal of Nervous and Mental Disease. 1999 [Retrieved 2008-07-03];187(3):142–9. doi:10.1097/00005053-199903000-00003. PMID 10086470.
  127. ↑ Calton T, Ferriter M, Huband N, Spandler H. A systematic review of the Soteria paradigm for the treatment of people diagnosed with schizophrenia. Schizophrenia Bulletin. 2008 [Retrieved 2008-07-03];34(1):181–92. doi:10.1093/schbul/sbm047. PMID 17573357. PMC 2632384.
  128. ↑ Bartholomeusz, Call (2011). Handbook of Schizophrenia Spectrum Disorders, Volume III: Therapeutic Approaches, Comorbidity, and Outcomes. Springer. p. 189. ISBN 9789400708341.
  129. ↑ Peet M, Stokes C (2005). "Omega-3 fatty acids in the treatment of psychiatric disorders". Drugs 65 (8): 1051–9. doi:10.2165/00003495-200565080-00002. PMID 15907142.
  130. ↑ Emsley R, Oosthuizen P, van Rensburg SJ (2003). "Clinical potential of omega-3 fatty acids in the treatment of schizophrenia". CNS Drugs 17 (15): 1081–91. doi:10.2165/00023210-200317150-00003. PMID 14661986.
  131. ↑ Freeman MP, Hibbeln JR, Wisner KL, Davis JM, Mischoulon D, Peet M, Keck PE, Marangell LB, Richardson AJ, Lake J, Stoll AL (2006). "Omega-3 fatty acids: evidence basis for treatment and future research in psychiatry". Journal of Clinical Psychiatry 67 (12): 1954–67. doi:10.4088/JCP.v67n1217. PMID 17194275.
  132. ↑ Ross BM, Seguin J, Sieswerda LE (2007). "Omega-3 fatty acids as treatments for mental illness: which disorder and which fatty acid?". Lipids Health Dis 6: 21. doi:10.1186/1476-511X-6-21. PMC 2071911. PMID 17877810.
  133. ↑ Arroll MA, Wilder L, Neil J (Sep 16, 2014). "Nutritional interventions for the adjunctive treatment of schizophrenia: a brief review". Nutr J (Review) 13: 91. doi:10.1186/1475-2891-13-91. PMC 4171568. PMID 25228271.
  134. ↑ Rabany, L.; Deutsch, L.; Levkovitz, Y. (2014). "Double-blind, randomized sham controlled study of deep-TMS add-on treatment for negative symptoms and cognitive deficits in schizophrenia". Journal of Psychopharmacology 28: 686–690. doi:10.1177/0269881114533600.
  135. ↑ Prikryl, R.; Ustohal, L.; Prikrylova Kucerova, H.; Kasparek, T.; Venclikova, S.; Vrzalova, M.; Ceskova, E. (2013). "A detailed analysis of the effect of repetitive transcranial magnetic stimulation on negative symptoms of schizophrenia: A double-blind trial". Schizophrenia Research 149 (1–3): 167–73. doi:10.1016/j.schres.2013.06.015. PMID 23810122.
  136. ↑ Barr, M. S.; Farzan, F.; Rajji, T. K.; Voineskos, A. N.; Blumberger, D. M.; Arenovich, T.; Fitzgerald, P. B.; Daskalakis, Z. J. (2013). "Can Repetitive Magnetic Stimulation Improve Cognition in Schizophrenia? Pilot Data from a Randomized Controlled Trial". Biological Psychiatry 73 (6): 510–7. doi:10.1016/j.biopsych.2012.08.020. PMID 23039931.
  137. ↑ Guse, B.; Falkai, P.; Gruber, O.; Whalley, H.; Gibson, L.; Hasan, A.; Obst, K.; Dechent, P.; McIntosh, A.; Suchan, B.; Wobrock, T. (2013). "The effect of long-term high frequency repetitive transcranial magnetic stimulation on working memory in schizophrenia and healthy controls—A randomized placebo-controlled, double-blind fMRI study". Behavioural Brain Research 237: 300–307. doi:10.1016/j.bbr.2012.09.034.
  138. ↑ Schneider, A. L.; Schneider, T. L.; Stark, H. (2008). "Repetitive transcranial magnetic stimulation (rTMS) as an augmentation treatment for the negative symptoms of schizophrenia: A 4-week randomized placebo controlled study". Brain Stimulation 1 (2): 106–11. doi:10.1016/j.brs.2008.01.001. PMID 20633377.
  139. ↑ Jin, Y.; Kemp, A. S.; Huang, Y.; Thai, T. M.; Liu, Z.; Xu, W.; He, H.; Potkin, S. G. (2012). "Alpha EEG guided TMS in schizophrenia". Brain Stimulation 5 (4): 560–8. doi:10.1016/j.brs.2011.09.005. PMID 22019083.
  140. ↑ Prikryl, R.; Kasparek, T.; Skotakova, S.; Ustohal, L.; Kucerova, H.; Ceskova, E. (2007). "Treatment of negative symptoms of schizophrenia using repetitive transcranial magnetic stimulation in a double-blind, randomized controlled study". Schizophrenia Research 95 (1–3): 151–7. doi:10.1016/j.schres.2007.06.019. PMID 17689931.
  141. ↑ Goyal, N; Nizamie, S. H.; Desarkar, P (2007). "Efficacy of adjuvant high frequency repetitive transcranial magnetic stimulation on negative and positive symptoms of schizophrenia: Preliminary results of a double-blind sham-controlled study". Journal of Neuropsychiatry 19 (4): 464–7. doi:10.1176/appi.neuropsych.19.4.464. PMID 18070852.
  142. ↑ Lee, S. H.; Kim, W.; Chung, Y. C.; Jung, K. H.; Bahk, W. M.; Jun, T. Y.; Kim, K. S.; George, M. S.; Chae, J. H. (2005). "A double blind study showing that two weeks of daily repetitive TMS over the left or right temporoparietal cortex reduces symptoms in patients with schizophrenia who are having treatment-refractory auditory hallucinations". Neuroscience Letters 376 (3): 177–81. doi:10.1016/j.neulet.2004.11.048. PMID 15721217.
  143. ↑ Greenhalgh J, Knight C, Hind D, Beverley C, Walters S (March 2005). "Clinical and cost-effectiveness of electroconvulsive therapy for depressive illness, schizophrenia, catatonia and mania: systematic reviews and economic modeling studies.". Health Technol Assess. 9 (9): 1–156. doi:10.3310/hta9090. PMID 15774232.
  144. ↑ 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. Retrieved 2007-06-17.
  145. ↑ Mashour GA, Walker EE, Martuza RL (2005). "Psychosurgery: past, present, and future". Brain Research: Brain Research Reviews 48 (3): 409–19. doi:10.1016/j.brainresrev.2004.09.002. PMID 15914249.
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