Management of schizophrenia

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Management of schizophrenia

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 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]


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]

Studies have found that antipsychotic treatment following NMS and neutropenia may sometimes be successfully rechallenged (restarted) with clozapine.[20][21]

Tobacco smoking increases the metabolism of some antipsychotics, by strongly activitating CYP1A2, the enzyme that breaks them down, and a significant difference is found in these levels between smokers and non-smokers.[22][23][24] It is recommended that the dosage for those smokers on clozapine be increased by 50%, and for those on olanzapine by 30%.[23] The result of stopping smoking can lead to an increased concentration of the antipsychotic that may result in toxicity, so that monitoring of effects would need to take place with a view to decreasing the dosage; many symptoms may be noticeably worsened, and extreme fatigue, and seizures are also possible with a risk of relapse. Likewise those who resume smoking may need their dosages adjusted accordingly.[22][25] The altering effects are due to compounds in tobacco smoke and not to nicotine; the use of nicotine replacement therapy therefore has the equivalent effect of stopping smoking and monitoring would still be needed.[22]

Research findings suggested that other neurotransmission systems, including serotonin, glutamate, GABA, and acetylcholine, were implicated in the development of schizophrenia, and that a more inclusive medication was needed.[24] A new first-in-class antipsychotic that targets multiple neurotransmitter systems called lumateperone (ITI-007), was trialed and approved by the FDA in December 2019 for the treatment of schizophrenia in adults.[24][26][27] Lumateperone is a small molecule agent that shows improved safety, and tolerance. It interacts with dopamine, serotonin, and glutamate in a complex, uniquely selective manner, and is seen to improve negative and positive symptoms, and social functioning.[28] Lumateperone was also found to reduce potential metabolic dysfunction, have lower rates of movement disorders, and have lower cardiovascular side effects such as a fast heart rate.[24]

Add-on agents[edit]

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.[29] 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[30][31] Symptoms against which efficacy is known Notable adverse effects seen in clinical trials Highest quality of clinical data available N Notes
Adjuncts to clozapine[32][33]
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[34] 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[32] 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.
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
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[32] 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[35][36]
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.
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[37][38]
Aspirin[39][40] 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[41][42][43][44] Global Well tolerated 4 DB-RPCTs 164 Increased risk of blood dyscarsias.
Omega-3 fatty acids Global Well tolerated 6 DB-RPCTs (1 negative)[45] 362 May have protective effects against depression.
Pregnenolone[46][47][48][49] Global Well tolerated 3 DB-RPCTs 100 Levels of this neurosteroid in the body are elevated by clozapine treatment.
D-alanine[51][52] 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,[53] Heresco-Levy 2005,[54] Lane 2005,[55] Lane 2010,[56] Tsai 1999,[57] Weiser 2012[58]
Glycine Global (predominantly positive symptoms) Well tolerated 5 DB-RPCTs 219 Endogenous NMDA receptor ligand.
N-acetylcysteine[59] Global (especially negative symptoms) Well tolerated 3 DB-RPCTs 140 Cystine and glutathione prodrug.[60][61] Cystine increases intracellular glutamate levels via the glutamate-cystine anti porter.

Berk 2008,[62] Berk 2011,[63] Carmeli 2012,[64] Lavoie 2008[65]

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,[55] Lane 2006,[66] Lane 2008,[67] Lane 2010,[56] Tsai 2004[68]
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[71][72][73][74] Cognitive and negative symptoms Well tolerated 3 DB-RPCTs 120 Agonist at α7 nAChRs; antagonist at 5-HT3. Expensive (>$20 AUD/tablet).
Escitalopram[76] 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.[77] Risk of QT interval prolongation is lower than with escitalopram (but still exists).
Mianserin[78] 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.[79][80]
Mirtazapine[78] Cognition,[81][82] negative and positive symptoms†[83] 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.[84]
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.
Alpha-lipoic acid[85][86] 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.[87]
L-Theanine[88][89][90] 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.[91][92][93][94] 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.[95]
Famotidine[96] 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,[97] Doruk 2008,[98] Zhang 2001,[99] Zhang 2001,[100] Zhang 2006,[101] Zhang 2011,[102] Zhou 1999[103]
Ondansetron[104] Negative and cognitive symptoms Well tolerated 3 DB-RPCTs 151 5-HT3 antagonist. May prolong the QT interval. Expensive (>$4 AUD/tablet).
SAM-e[105] 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 [106]
Vitamin C[107][108][109][110] 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).


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.[111]

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[112] 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.[113][114] Nonetheless, more recent meta analyses have cast doubt upon the utility of CBT as a treatment for the symptoms of psychosis.[115][116][117]

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.[118]

Metacognitive training (MCT): In view of many empirical findings [119] suggesting deficits of metacognition (thinking about one's thinking, reflecting upon one's cognitive process) in patients with schizophrenia, metacognitive training (MCT) [119][120] 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),[121] 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.[119][120] Studies confirm the training's feasibility [122] and efficacy in ameliorating positive psychosis symptoms.[123][124] Studies of single training module show that this intervention target specific cognitive biases.[125] Recently, an individualized format has been developed which combines the metacognitive approach with methods derived from cognitive-behavioral therapy.[126]

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.[127][128][129] 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.[129] 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.[130][131] There is also some evidence for benefits from social skills training, although there have also been significant negative findings.[132][14] Some studies have explored the possible benefits of music therapy and other creative therapies.[133][134][135]

The Soteria model is alternative to inpatient hospitalization using full non professional care and a minimal medication approach.[136] 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.[137] Training in the detection of subtle facial expressions has been used to improve facial emotional recognition.[138]

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.[139]


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.[140]

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.[141] 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.[142] 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.[143]

Treatment resistant schizophrenia[edit]

About half of those with schizophrenia will respond favourably to antipsychotics, and have a good return of functioning.[144] However, positive symptoms persist in up to a third of people. Following two trials of different antipsychotics over six weeks, that also prove ineffective, they will be classed as having treatment resistant schizophrenia (TRS), and clozapine will be offered.[145][146] Clozapine is of benefit to around half of this group although it has the potentially serious side effect of agranulocytosis (lowered white blood cell count) in less than 4% of people.[147][148][149] Between 12 and 20 per cent will not respond to clozapine and this group is said to have ultra treatment resistant schizophrenia.[145][150] ECT may be offered to treat TRS as an add-on therapy, and is shown to sometimes be of benefit.[150] A review concluded that this use only has an effect on medium-term TRS and that there is not enough evidence to support its use other than for this group.[151]

TRS is often accompanied by a low quality of life, and greater social dysfunction.[152] TRS may be the result of inadequate rather than inefficient treatment; it also may be a false label due to medication not being taken regularly, or at all.[153] About 16 per cent of people who had initially been responsive to treatment later develop resistance. This could relate to the length of time on APs, with treatment becoming less responsive.[154] This finding also supports the involvement of dopamine in the development of schizophrenia.[153] Studies suggest that TRS may be a more heritable form.[155]

TRS may be evident from first episode psychosis, or from a relapse. It can vary in its intensity and response to other therapies.[152] This variation is seen to possibly indicate an underlying neurobiology such as dopamine supersensitivity (DSS), glutamate or serotonin dysfunction, inflammation and oxidative stress.[145] Studies have found that dopamine supersensitivity is found in up to 70% of those with TRS.[156] The variation has led to the suggestion that treatment responsive and treatment resistant schizophrenia be considered as two different subtypes.[145][155] It is further suggested that if the subtypes could be distinguished at an early stage significant implications could follow for treatment considerations, and for research.[150] Neuroimaging studies have found a significant decrease in the volume of grey matter in those with TRS with no such change seen in those who are treatment responsive.[150] In those with ultra treatment resistance the decrease in grey matter volume was larger.[145][150]

Rehabilitative interventions[edit]

Individual Placement and Support (IPS), where the rehabilitated person is directly placed and supported in the workplace with the support of a professional, promotes the employment of people with schizophrenia and their survival in the open labour market better than the model of gradual work practice before placement.[157]

Research evidence on the relative superiority of different types of housing units for people with psychosis in terms of symptomatic or functional development is scarce. The support and independence provided in a residential unit should be flexible, individualised and, as far as possible, at the choice of the person being rehabilitated. The living environment should be as normal as possible and the rehabilitated person should not be isolated from the rest of the community.[158][159]

Traditional Chinese medicine[edit]

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.[160] 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.[161]

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.[162][163]


Various brain stimulation techniques have been used to treat the positive symptoms of schizophrenia, in particular auditory verbal hallucinations (AVHs), and investigations are ongoing.[164] Most studies focus on transcranial direct-current stimulation (tDCM), and repetitive transcranial magnetic stimulation (rTMS).[165] Transcranial magnetic stimulation is low-cost, noninvasive, and almost free of side-effects making it a good therapeutic choice with promising outcomes.[164] Low-frequency TMS of the left temporoparietal cortex (the region containing Broca's area) can reduce auditory hallucinations.[164] rTMS seems to be the most effective treatment for those with persistent AVHs, as an add-on therapy.[165] AVHs are not resolved in up to 30 per cent of those on antipsychotics and a further percentage still experience only a partial response.[165] Techniques based on focused ultrasound for deep brain stimulation could provide insight for the treatment of AVHs.[165]

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,[166] 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.[167] Psychosurgery has now become a rare procedure and is not a recommended treatment for schizophrenia.[168]

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.[169]

There may be some benefit in trying several treatment modalities at the same time, especially those that could be classed as lifestyle interventions.[170] Nidotherapy is suggested to be a cost-effective social prescribing intervention using efforts to change the environment to improve functional ability.[171]

Numerous people diagnosed with schizophrenia have found it necessary to organize confidential groups with each other where they can discuss their experiences without clinicians present.[172][173] 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.[174]


  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). 12 February 2014.
  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. Supplementum. 113 (429): 9–16. doi:10.1111/j.1600-0447.2005.00711.x. PMID 16445476. S2CID 34615961.
  3. ^ McGurk SR, Mueser KT, Feldman K, Wolfe R, Pascaris A (March 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. ^ Frank D, Perry JC, Kean D, Sigman M, Geagea K (July 2005). "Effects of compulsory treatment orders on time to hospital readmission". Psychiatric Services. 56 (7). Washington, D.C.: 867–9. doi:10.1176/ 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. Archived from the original on 2007-09-27.
  6. ^ Eiring Ø, Landmark BF, Aas E, Salkeld G, Nylenna M, Nytrøen K (April 2015). "What matters to patients? A systematic review of preferences for medication-associated outcomes in mental disorders". BMJ Open. 5 (4): e007848. doi:10.1136/bmjopen-2015-007848. PMC 4390680. PMID 25854979.
  7. ^ Smith T, Weston C, Lieberman J (August 2010). "Schizophrenia (maintenance treatment)". American Family 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". Schizophrenia Research. 100 (1–3): 4–19. doi:10.1016/j.schres.2008.01.022. PMID 18291627. S2CID 14598183.
  9. ^ a b c Barry SJ, Gaughan TM, Hunter R (June 2012). "Schizophrenia". BMJ Clinical Evidence. 2012. PMC 3385413. PMID 23870705. Archived from the original on 2014-09-11.
  10. ^ Leucht S, Tardy M, Komossa K, Heres S, Kissling W, Salanti G, Davis JM (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. S2CID 2018124.
  11. ^ a b Harrow M, Jobe TH (September 2013). "Does long-term treatment of schizophrenia with antipsychotic medications facilitate recovery?". Schizophrenia Bulletin. 39 (5): 962–5. doi:10.1093/schbul/sbt034. PMC 3756791. PMID 23512950.
  12. ^ Turner T (January 2007). "Chlorpromazine: unlocking psychosis". BMJ. 334 (Suppl 1): s7. doi:10.1136/bmj.39034.609074.94. PMID 17204765. S2CID 33739419.
  13. ^ Ananth J, Parameswaran S, Gunatilake S, Burgoyne K, Sidhom T (April 2004). "Neuroleptic malignant syndrome and atypical antipsychotic drugs". The Journal of Clinical Psychiatry. 65 (4): 464–70. doi:10.4088/JCP.v65n0403. PMID 15119907. S2CID 32752143.
  14. ^ a b Lehman AF, Lieberman JA, Dixon LB, McGlashan TH, Miller AL, Perkins DO, et al. (February 2004). "Practice Guideline for the Treatment of Patients With Schizophrenia". American Journal of Psychiatry. 161 (2 supplement) (2nd ed.). American Psychological Association (APA). Archived from the original on 2014-03-06.
  15. ^ Semple D, Smyth R (July 2019). Oxford Handbook of Psychiatry. Oxford University Press. p. 207. ISBN 978-0-19-251496-7.
  16. ^ a b c Essali A, Al-Haj Haasan N, Li C, Rathbone J (January 2009). "Clozapine versus typical neuroleptic medication for schizophrenia". The Cochrane Database of Systematic Reviews. 2009 (1): CD000059. doi:10.1002/14651858.cd000059.pub2. PMC 7065592. PMID 19160174.
  17. ^ Haas SJ, Hill R, Krum H, Liew D, Tonkin A, Demos L, et al. (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. S2CID 1153693.
  18. ^ Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck RA, Perkins DO, et al. (Clinical Antipsychotic Trials of Intervention Effectiveness (CATIE) Investigators) (September 2005). "Effectiveness of antipsychotic drugs in patients with chronic schizophrenia". The New England Journal of Medicine. 353 (12): 1209–23. doi:10.1056/NEJMoa051688. PMID 16172203. S2CID 22499842.
  19. ^ Kozier B, Erb G, Olivieri R, Snyder S, Lake R, Harvey S (2008). "Chapter 10: Mental health". Fundamentals of Nursing: Concepts, Process and Practice (1st adaptation ed.). Harlow, England: Pearson Education. p. 189. ISBN 978-0-13-197653-5.
  20. ^ Manu P, Lapitskaya Y, Shaikh A, Nielsen J (2018). "Clozapine Rechallenge After Major Adverse Effects: Clinical Guidelines Based on 259 Cases". American Journal of Therapeutics. 25 (2): e218–e223. doi:10.1097/MJT.0000000000000715. PMID 29505490. S2CID 3689529.
  21. ^ Lally J, McCaffrey C, O Murchu C, et al. (July 2019). "Clozapine Rechallenge Following Neuroleptic Malignant Syndrome: A Systematic Review". Journal of Clinical Psychopharmacology. 39 (4): 372–379. doi:10.1097/JCP.0000000000001048. PMID 31205196. S2CID 189945135.
  22. ^ a b c Cather C, Pachas GN, Cieslak KM, Evins AE (June 2017). "Achieving Smoking Cessation in Individuals with Schizophrenia: Special Considerations". CNS Drugs. 31 (6): 471–481. doi:10.1007/s40263-017-0438-8. PMC 5646360. PMID 28550660.
  23. ^ a b Tsuda Y, Saruwatari J, Yasui-Furukori N (4 March 2014). "Meta-analysis: the effects of smoking on the disposition of two commonly used antipsychotic agents, olanzapine and clozapine". BMJ Open. 4 (3): e004216. doi:10.1136/bmjopen-2013-004216. PMC 3948577. PMID 24595134.
  24. ^ a b c d Li P, Snyder GL, Vanover KE (2016). "Dopamine Targeting Drugs for the Treatment of Schizophrenia: Past, Present and Future". Current Topics in Medicinal Chemistry. 16 (29): 3385–3403. doi:10.2174/1568026616666160608084834. PMC 5112764. PMID 27291902.
  25. ^ Lowe EJ, Ackman ML (April 2010). "Impact of tobacco smoking cessation on stable clozapine or olanzapine treatment". The Annals of Pharmacotherapy. 44 (4): 727–32. doi:10.1345/aph.1M398. PMID 20233914. S2CID 11456024.
  26. ^ "FDA Approves Caplyta (lumateperone) for the Treatment of Schizophrenia in Adults". 23 December 2019.
  27. ^ Blair HA (14 February 2020). "Lumateperone: First Approval". Drugs. 80 (4): 417–423. doi:10.1007/s40265-020-01271-6. PMID 32060882. S2CID 211110160.
  28. ^ Edinoff A, Wu N, deBoisblanc C, et al. (September 2020). "Lumateperone for the Treatment of Schizophrenia". Psychopharmacol Bull. 50 (4): 32–59. PMC 7511146. PMID 33012872.
  29. ^ Ortiz-Orendain J, Castiello-de Obeso S, Colunga-Lozano LE, Hu Y, Maayan N, Adams CE (June 2017). "Antipsychotic combinations for schizophrenia". The Cochrane Database of Systematic Reviews (Review). 6 (10): CD009005. doi:10.1002/14651858.CD009005.pub2. PMC 6481822. PMID 28658515.
  30. ^ Ritsner MS (2013). Ritsner MS (ed.). Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. doi:10.1007/978-94-007-5805-6. ISBN 9789400758056. S2CID 7705779.
  31. ^ Ritsner MS (2013). Ritsner MS (ed.). Polypharmacy in Psychiatry Practice, Volume II. Springer Science+Business Media Dordrecht. doi:10.1007/978-94-007-5799-8. ISBN 9789400757998. S2CID 2077519.
  32. ^ a b c Porcelli S, Balzarro B, Serretti A (March 2012). "Clozapine resistance: augmentation strategies". European Neuropsychopharmacology. 22 (3): 165–82. doi:10.1016/j.euroneuro.2011.08.005. PMID 21906915. S2CID 39716777.
  33. ^ 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". Schizophrenia Bulletin. 38 (5): 1003–11. doi:10.1093/schbul/sbr004. PMC 3446238. PMID 21422107.
  34. ^ 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): 329–34. doi:10.1111/j.1463-1326.2011.01529.x. PMID 22059694. S2CID 28553141.
  35. ^ a b Singh SP, Singh V (October 2011). "Meta-analysis of the efficacy of adjunctive NMDA receptor modulators in chronic schizophrenia". CNS Drugs. 25 (10): 859–85. doi:10.2165/11586650-000000000-00000. PMID 21936588. S2CID 207299820.
  36. ^ a b 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): 172–8. doi:10.1192/bjp.bp.111.107359. PMC 3759029. PMID 23999481.
  37. ^ 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): 337–42. doi:10.1177/0269881112467089. PMC 3641824. PMID 23151612.
  38. ^ Sommer IE, van Westrhenen R, Begemann MJ, de Witte LD, Leucht S, Kahn RS (January 2014). "Efficacy of anti-inflammatory agents to improve symptoms in patients with schizophrenia: an update". Schizophrenia Bulletin. 40 (1): 181–91. doi:10.1093/schbul/sbt139. PMC 3885306. PMID 24106335.
  39. ^ Laan W, Grobbee DE, Selten JP, Heijnen CJ, Kahn RS, Burger H (May 2010). "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. doi:10.4088/JCP.09m05117yel. hdl:11370/5644f8cd-b8ea-4ecc-9755-0f7c9ed86d02. PMID 20492850.
  40. ^ Schmidt L, Phelps E, Friedel J, Shokraneh F (August 2019). "Acetylsalicylic acid (aspirin) for schizophrenia". The Cochrane Database of Systematic Reviews. 2019 (8): CD012116. doi:10.1002/14651858.CD012116.pub2. PMC 6699651. PMID 31425623.
  41. ^ Liu F, Guo X, Wu R, Ou J, Zheng Y, Zhang B, et al. (March 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. S2CID 5908680.
  42. ^ Khodaie-Ardakani MR, Mirshafiee O, Farokhnia M, Tajdini M, Hosseini SM, Modabbernia A, et al. (March 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. S2CID 5442977.
  43. ^ Chaudhry IB, Hallak J, Husain N, Minhas F, Stirling J, Richardson P, et al. (September 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): 1185–93. doi:10.1177/0269881112444941. PMID 22526685. S2CID 19246435.
  44. ^ Levkovitz Y, Mendlovich S, Riwkes S, Braw Y, Levkovitch-Verbin H, Gal G, et al. (February 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): 138–49. doi:10.4088/JCP.08m04666yel. PMID 19895780. S2CID 10554795.
  45. ^ Joy CB, Mumby-Croft R, Joy LA (July 2006). "Polyunsaturated fatty acid supplementation for schizophrenia". The Cochrane Database of Systematic Reviews. 2006 (3): CD001257. doi:10.1002/14651858.CD001257.pub2. PMC 7032618. PMID 16855961.
  46. ^ Ritsner MS, Gibel A, Shleifer T, Boguslavsky I, Zayed A, Maayan R, et al. (October 2010). "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. doi:10.4088/JCP.09m05031yel. PMID 20584515. S2CID 25628072.
  47. ^ Marx CE, Keefe RS, Buchanan RW, Hamer RM, Kilts JD, Bradford DW, et al. (July 2009). "Proof-of-concept trial with the neurosteroid pregnenolone targeting cognitive and negative symptoms in schizophrenia". Neuropsychopharmacology. 34 (8): 1885–903. doi:10.1038/npp.2009.26. PMC 3427920. PMID 19339966.
  48. ^ Wong P, Chang CC, Marx CE, Caron MG, Wetsel WC, Zhang X (2012). Hashimoto K (ed.). "Pregnenolone rescues schizophrenia-like behavior in dopamine transporter knockout mice". PLOS ONE. 7 (12): e51455. Bibcode:2012PLoSO...751455W. doi:10.1371/journal.pone.0051455. PMC 3519851. PMID 23240026.
  49. ^ Marx CE, Stevens RD, Shampine LJ, Uzunova V, Trost WT, Butterfield MI, et al. (June 2006). "Neuroactive steroids are altered in schizophrenia and bipolar disorder: relevance to pathophysiology and therapeutics". Neuropsychopharmacology. 31 (6): 1249–63. doi:10.1038/sj.npp.1300952. PMID 16319920. S2CID 2499760.
  50. ^ Javitt DC, Zukin SR, Heresco-Levy U, Umbricht D (September 2012). "Has an angel shown the way? Etiological and therapeutic implications of the PCP/NMDA model of schizophrenia". Schizophrenia Bulletin. 38 (5): 958–66. doi:10.1093/schbul/sbs069. PMC 3446214. PMID 22987851.
  51. ^ Hatano T, Ohnuma T, Sakai Y, Shibata N, Maeshima H, Hanzawa R, et al. (May 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. S2CID 10174006.
  52. ^ Tsai GE, Yang P, Chang YC, Chong MY (February 2006). "D-alanine added to antipsychotics for the treatment of schizophrenia". Biological Psychiatry. 59 (3): 230–4. doi:10.1016/j.biopsych.2005.06.032. PMID 16154544. S2CID 19372446.
  53. ^ D'Souza DC, Radhakrishnan R, Perry E, Bhakta S, Singh NM, Yadav R, et al. (February 2013). "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.
  54. ^ Heresco-Levy U, Javitt DC, Ebstein R, Vass A, Lichtenberg P, Bar G, et al. (March 2005). "D-serine efficacy as add-on pharmacotherapy to risperidone and olanzapine for treatment-refractory schizophrenia". Biological Psychiatry. 57 (6): 577–85. doi:10.1016/j.biopsych.2004.12.037. PMID 15780844. S2CID 46348188.
  55. ^ a b Lane HY, Chang YC, Liu YC, Chiu CC, Tsai GE (November 2005). "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. doi:10.1001/archpsyc.62.11.1196. PMID 16275807.
  56. ^ a b Lane HY, Lin CH, Huang YJ, Liao CH, Chang YC, Tsai GE (May 2010). "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. doi:10.1017/S1461145709990939. PMID 19887019.
  57. ^ Tsai GE, Yang P, Chung LC, Tsai IC, Tsai CW, Coyle JT (November 1999). "D-serine added to clozapine for the treatment of schizophrenia". The American Journal of Psychiatry. 156 (11): 1822–5. doi:10.1176/ajp.156.11.1822. PMID 10553752. S2CID 29054148.
  58. ^ Weiser M, Heresco-Levy U, Davidson M, Javitt DC, Werbeloff N, Gershon AA, et al. (June 2012). "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. doi:10.4088/JCP.11m07031. PMID 22795211.
  59. ^ Dean O, Giorlando F, Berk M (March 2011). "N-acetylcysteine in psychiatry: current therapeutic evidence and potential mechanisms of action". Journal of Psychiatry & Neuroscience. 36 (2): 78–86. doi:10.1503/jpn.100057. PMC 3044191. PMID 21118657.
  60. ^ Aoyama K, Watabe M, Nakaki T (November 2008). "Regulation of neuronal glutathione synthesis". Journal of Pharmacological Sciences. 108 (3): 227–38. doi:10.1254/jphs.08R01CR. PMID 19008644.
  61. ^ Jain A, Mårtensson J, Stole E, Auld PA, Meister A (March 1991). "Glutathione deficiency leads to mitochondrial damage in brain". Proceedings of the National Academy of Sciences of the United States of America. 88 (5): 1913–7. Bibcode:1991PNAS...88.1913J. doi:10.1073/pnas.88.5.1913. PMC 51136. PMID 2000395.
  62. ^ Berk M, Copolov D, Dean O, Lu K, Jeavons S, Schapkaitz I, et al. (September 2008). "N-acetyl cysteine as a glutathione precursor for schizophrenia—a double-blind, randomized, placebo-controlled trial". Biological Psychiatry. 64 (5): 361–8. doi:10.1016/j.biopsych.2008.03.004. PMID 18436195. S2CID 10321144.
  63. ^ Berk M, Munib A, Dean O, Malhi GS, Kohlmann K, Schapkaitz I, et al. (July 2011). "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. doi:10.4088/JCP.09m05741yel. PMID 20868637.
  64. ^ Carmeli C, Knyazeva MG, Cuénod M, Do KQ (2012). Burne T (ed.). "Glutathione precursor N-acetyl-cysteine modulates EEG synchronization in schizophrenia patients: a double-blind, randomized, placebo-controlled trial". PLOS ONE. 7 (2): e29341. Bibcode:2012PLoSO...729341C. doi:10.1371/journal.pone.0029341. PMC 3285150. PMID 22383949.
  65. ^ Lavoie S, Murray MM, Deppen P, Knyazeva MG, Berk M, Boulat O, et al. (August 2008). "Glutathione precursor, N-acetyl-cysteine, improves mismatch negativity in schizophrenia patients". Neuropsychopharmacology. 33 (9): 2187–99. doi:10.1038/sj.npp.1301624. hdl:10536/DRO/DU:30071388. PMID 18004285. S2CID 237232.
  66. ^ Lane HY, Huang CL, Wu PL, Liu YC, Chang YC, Lin PY, et al. (September 2006). "Glycine transporter I inhibitor, N-methylglycine (sarcosine), added to clozapine for the treatment of schizophrenia". Biological Psychiatry. 60 (6): 645–9. doi:10.1016/j.biopsych.2006.04.005. PMID 16780811. S2CID 42741531.
  67. ^ Lane HY, Liu YC, Huang CL, Chang YC, Liau CH, Perng CH, Tsai GE (January 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. S2CID 26037874.
  68. ^ Tsai G, Lane HY, Yang P, Chong MY, Lange N (March 2004). "Glycine transporter I inhibitor, N-methylglycine (sarcosine), added to antipsychotics for the treatment of schizophrenia". Biological Psychiatry. 55 (5): 452–6. doi:10.1016/j.biopsych.2003.09.012. PMID 15023571. S2CID 35723786.
  69. ^ Singh J, Kour K, Jayaram MB (January 2012). "Acetylcholinesterase inhibitors for schizophrenia". The Cochrane Database of Systematic Reviews. 1 (1): CD007967. doi:10.1002/14651858.CD007967.pub2. PMC 6823258. PMID 22258978.
  70. ^ 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): 303–17. doi:10.2165/11530260-000000000-00000. PMID 20297855. S2CID 45807136.
  71. ^ Koike K, Hashimoto K, Takai N, Shimizu E, Komatsu N, Watanabe H, et al. (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. S2CID 25260365.
  72. ^ Shiina A, Shirayama Y, Niitsu T, Hashimoto T, Yoshida T, Hasegawa T, et al. (June 2010). "A randomised, double-blind, placebo-controlled trial of tropisetron in patients with schizophrenia". Annals of General Psychiatry. 9 (1): 27. doi:10.1186/1744-859X-9-27. PMC 2901366. PMID 20573264.
  73. ^ Zhang XY, Liu L, Liu S, Hong X, Chen DC, Xiu MH, et al. (September 2012). "Short-term tropisetron treatment and cognitive and P50 auditory gating deficits in schizophrenia". The American Journal of Psychiatry. 169 (9): 974–81. doi:10.1176/appi.ajp.2012.11081289. PMID 22952075.
  74. ^ Noroozian M, Ghasemi S, Hosseini SM, Modabbernia A, Khodaie-Ardakani MR, Mirshafiee O, et al. (August 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. S2CID 15652697.
  75. ^ 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): 174–9. doi:10.1192/bjp.bp.109.067710. PMID 20807960.
  76. ^ 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. S2CID 261170.
  77. ^ White N, Litovitz T, Clancy C (December 2008). "Suicidal antidepressant overdoses: a comparative analysis by antidepressant type". Journal of Medical Toxicology. 4 (4): 238–50. doi:10.1007/BF03161207. PMC 3550116. PMID 19031375.
  78. ^ a b 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): 202–6. doi:10.1016/j.schres.2011.11.030. PMID 22169246. S2CID 36119981.
  79. ^ Rossi, S, ed. (2013). Australian Medicines Handbook (2013 ed.). Adelaide: The Australian Medicines Handbook Unit Trust. ISBN 978-0-9805790-9-3.
  80. ^ Joint Formulary Committee (2013). British National Formulary (BNF) (65 ed.). London, UK: Pharmaceutical Press. p. 247. ISBN 978-0-85711-084-8.
  81. ^ Ritsner MS (2013). Ritsner MS (ed.). Polypharmacy in Psychiatry Practice, Volume I. Springer Science+Business Media Dordrecht. doi:10.1007/978-94-007-5805-6. ISBN 9789400758056. S2CID 7705779.
  82. ^ 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. 9 (2): 88–95. doi:10.3371/CSRP.VIRE.030813. PMID 23491969.
  83. ^ 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 & Biological Psychiatry. 35 (4): 1080–6. doi:10.1016/j.pnpbp.2011.03.004. PMID 21402120. S2CID 37328991.
  84. ^ Kumar R, Sachdev PS (May 2009). "Akathisia and second-generation antipsychotic drugs". Current Opinion in Psychiatry. 22 (3): 293–99. doi:10.1097/YCO.0b013e32832a16da. PMID 19378382. S2CID 31506138.
  85. ^ Koh EH, Lee WJ, Lee SA, Kim EH, Cho EH, Jeong E, et al. (January 2011). "Effects of alpha-lipoic Acid on body weight in obese subjects". The American Journal of Medicine. 124 (1): 85.e1–8. doi:10.1016/j.amjmed.2010.08.005. PMID 21187189.
  86. ^ Kim E, Park DW, Choi SH, Kim JJ, Cho HS (April 2008). "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. doi:10.1097/JCP.0b013e31816777f7. PMID 18344723. S2CID 7873991.
  87. ^ Jariwalla RJ, Lalezari J, Cenko D, Mansour SE, Kumar A, Gangapurkar B, Nakamura D (March 2008). "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. doi:10.1089/acm.2006.6397. PMID 18315507.
  88. ^ Ritsner MS, Miodownik C, Ratner Y, Shleifer T, Mar M, Pintov L, Lerner V (January 2011). "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. doi:10.4088/JCP.09m05324gre. PMID 21208586. S2CID 4937207.
  89. ^ Miodownik C, Maayan R, Ratner Y, Lerner V, Pintov L, Mar M, et al. (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): 155–60. doi:10.1097/WNF.0b013e318220d8c6. PMID 21617527. S2CID 9786949.
  90. ^ Lardner AL (July 2014). "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. doi:10.1179/1476830513Y.0000000079. PMID 23883567. S2CID 206849271.
  91. ^ Kelly SP, Gomez-Ramirez M, Montesi JL, Foxe JJ (August 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. doi:10.1093/jn/138.8.1572S. PMID 18641209.
  92. ^ Park SK, Jung IC, Lee WK, Lee YS, Park HK, Go HJ, et al. (April 2011). "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. doi:10.1089/jmf.2009.1374. PMID 21303262. S2CID 19296401.
  93. ^ Foxe JJ, Morie KP, Laud PJ, Rowson MJ, de Bruin EA, Kelly SP (June 2012). "Assessing the effects of caffeine and theanine on the maintenance of vigilance during a sustained attention task". Neuropharmacology. 62 (7): 2320–7. doi:10.1016/j.neuropharm.2012.01.020. PMID 22326943. S2CID 13232338.
  94. ^ Nobre AC, Rao A, Owen GN (2008). "L-theanine, a natural constituent in tea, and its effect on mental state". Asia Pacific Journal of Clinical Nutrition. 17 (Suppl 1): 167–8. PMID 18296328.
  95. ^ Di X, Yan J, Zhao Y, Chang Y, Zhao B (December 2012). "L-theanine inhibits nicotine-induced dependence via regulation of the nicotine acetylcholine receptor-dopamine reward pathway". Science China Life Sciences. 55 (12): 1064–74. doi:10.1007/s11427-012-4401-0. PMID 23233221. S2CID 17803427.
  96. ^ Meskanen K, Ekelund H, Laitinen 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): 472–8. doi:10.1097/JCP.0b013e3182970490. PMID 23764683. S2CID 13048121.
  97. ^ Atmaca M, Tezcan E, Kuloglu M, Ustundag B, Kirtas O (December 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): 652–6. doi:10.1111/j.1440-1819.2005.01432.x. PMID 16401239. S2CID 1892988.
  98. ^ Doruk A, Uzun O, Ozşahin A (July 2008). "A placebo-controlled study of extract of ginkgo biloba added to clozapine in patients with treatment-resistant schizophrenia". International Clinical Psychopharmacology. 23 (4): 223–7. doi:10.1097/YIC.0b013e3282fcff2f. PMID 18545061. S2CID 42478246.
  99. ^ Zhang XY, Zhou DF, Su JM, Zhang PY (February 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): 85–8. doi:10.1097/00004714-200102000-00015. PMID 11199954. S2CID 7836683.
  100. ^ Zhang XY, Zhou DF, Zhang PY, Wu GY, Su JM, Cao LY (November 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): 878–83. doi:10.4088/JCP.v62n1107. PMID 11775047.
  101. ^ Zhang XY, Zhou DF, Cao LY, Wu GY (September 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): 12–7. doi:10.1007/s00213-006-0476-2. PMID 16906395. S2CID 12411168.
  102. ^ Zhang WF, Tan YL, Zhang XY, Chan RC, Wu HR, Zhou DF (May 2011). "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. doi:10.4088/JCP.09m05125yel. PMID 20868638. S2CID 37085462.
  103. ^ Zhou D, Zhang X, Su J, Nan Z, Cui Y, Liu J, et al. (December 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): 1093–6. PMID 11721446.
  104. ^ Bennett AC, Vila TM (July–August 2010). "The role of ondansetron in the treatment of schizophrenia". The Annals of Pharmacotherapy. 44 (7–8): 1301–6. doi:10.1345/aph.1P008. PMID 20516364. S2CID 21574153.
  105. ^ Strous RD, Ritsner MS, Adler S, Ratner Y, Maayan R, Kotler M, et al. (January 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. S2CID 207712279.
  106. ^ Guidotti A, Ruzicka W, Grayson DR, Veldic M, Pinna G, Davis JM, Costa E (January 2007). "S-adenosyl methionine and DNA methyltransferase-1 mRNA overexpression in psychosis". NeuroReport. 18 (1): 57–60. doi:10.1097/WNR.0b013e32800fefd7. PMID 17259861. S2CID 25378736.
  107. ^ Dakhale GN, Khanzode SD, Khanzode SS, Saoji A (November 2005). "Supplementation of vitamin C with atypical antipsychotics reduces oxidative stress and improves the outcome of schizophrenia". Psychopharmacology. 182 (4): 494–8. doi:10.1007/s00213-005-0117-1. PMID 16133138. S2CID 24917071.
  108. ^ Wang Y, Liu XJ, Robitaille L, Eintracht S, MacNamara E, Hoffer LJ (September 2013). "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. doi:10.3945/ajcn.112.056366. PMID 23885048.
  109. ^ Zhang M, Robitaille L, Eintracht S, Hoffer LJ (May 2011). "Vitamin C provision improves mood in acutely hospitalized patients". Nutrition. 27 (5): 530–3. doi:10.1016/j.nut.2010.05.016. PMID 20688474.
  110. ^ Kennedy DO, Veasey R, Watson A, Dodd F, Jones E, Maggini S, Haskell CF (July 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.
  111. ^ Moran M (18 November 2005). "Psychosocial Treatment Often Missing From Schizophrenia Regimens". Psychiatric News. 40 (22): 24–37. doi:10.1176/pn.40.22.0024b.
  112. ^ Jones C, Cormac I, Silveira da Mota Neto JI, Campbell C (October 2004). Jones C (ed.). "Cognitive behaviour therapy for schizophrenia". The Cochrane Database of Systematic Reviews (4): CD000524. doi:10.1002/14651858.CD000524.pub2. PMID 15495000. (Retracted)
  113. ^ Wykes T, Steel C, Everitt B, Tarrier N (May 2008). "Cognitive behavior therapy for schizophrenia: effect sizes, clinical models, and methodological rigor". Schizophrenia Bulletin. 34 (3): 523–37. doi:10.1093/schbul/sbm114. PMC 2632426. PMID 17962231.
  114. ^ 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. S2CID 31560136.
  115. ^ Lynch D, Laws KR, McKenna PJ (January 2010). "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. doi:10.1017/s003329170900590x. hdl:2299/5741. PMID 19476688. S2CID 1001891.
  116. ^ 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).
  117. ^ Jones C, Hacker D, Meaden A, Cormac I, Irving CB (April 2011). "WITHDRAWN: Cognitive behaviour therapy versus other psychosocial treatments for schizophrenia". The Cochrane Database of Systematic Reviews (4): CD000524. doi:10.1002/14651858.cd000524.pub3. PMID 21491377.
  118. ^ Wykes T, Brammer M, Mellers J, Bray P, Reeder C, Williams C, Corner J (August 2002). "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. doi:10.1192/bjp.181.2.144. PMID 12151286. S2CID 221295938.
  119. ^ a b c Moritz S, Woodward TS (November 2007). "Metacognitive training in schizophrenia: from basic research to knowledge translation and intervention". Current Opinion in Psychiatry. 20 (6): 619–25. doi:10.1097/YCO.0b013e3282f0b8ed. PMID 17921766. S2CID 3193086.
  120. ^ a b Moritz S, Woodward TS, Burlon M (2005). "Metacognitive skill training for patients with schizophrenia (MCT)" (PDF). Hamburg: VanHam Campus. Retrieved 1 April 2011. {{cite journal}}: Cite journal requires |journal= (help)
  121. ^ Bell V, Halligan PW, Ellis HD (May 2006). "Explaining delusions: a cognitive perspective". Trends in Cognitive Sciences. 10 (5): 219–26. doi:10.1016/j.tics.2006.03.004. PMID 16600666. S2CID 24541273.
  122. ^ 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. Archived from the original (PDF) on 2016-03-05. Retrieved 2011-04-01.
  123. ^ Pankowski D, Kowalski J, Gawęda Ł (2016). "The effectiveness of metacognitive training for patients with schizophrenia: a narrative systematic review of studies published between 2009 and 2015". Psychiatria Polska (in Polish). 50 (4): 787–803. doi:10.12740/pp/59113. PMID 27847929.
  124. ^ Eichner C, Berna F (July 2016). "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. doi:10.1093/schbul/sbv225. PMC 4903058. PMID 26748396.
  125. ^ Kowalski J, Pankowski D, Lew-Starowicz M, Gawęda Ł (2017-07-03). "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. doi:10.1080/17522439.2017.1300186. ISSN 1752-2439. S2CID 151353395.
  126. ^ Moritz S, Veckenstedt R, Randjbar S, Vitzthum F (in press). "Individualized metacognitive therapy for people with schizophrenia psychosis (MCT+)", Springer, Heidelberg. [clarification needed]
  127. ^ 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.
  128. ^ 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. S2CID 25863992.
  129. ^ a b Pharoah F, Mari J, Rathbone J, Wong W (December 2010). Pharoah F (ed.). "Family intervention for schizophrenia". The Cochrane Database of Systematic Reviews (12): CD000088. doi:10.1002/14651858.CD000088.pub2. PMC 4204509. PMID 21154340.
  130. ^ Jones S, Hayward P (2004). Coping with Schizophrenia: A Guide for Patients, Families and Caregivers. Oxford, England: Oneworld Pub. ISBN 978-1-85168-344-4.
  131. ^ Torrey EF (2006). Surviving Schizophrenia: A Manual for Families, Consumers, and Providers (5th ed.). HarperCollins. ISBN 978-0-06-084259-8.
  132. ^ Kopelowicz A, Liberman RP, Zarate R (October 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.
  133. ^ 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.
  134. ^ Ruddy R, Milnes D (October 2005). Ruddy R (ed.). "Art therapy for schizophrenia or schizophrenia-like illnesses". The Cochrane Database of Systematic Reviews (4): CD003728. doi:10.1002/14651858.CD003728.pub2. PMID 16235338.
  135. ^ Ruddy RA, Dent-Brown K (January 2007). Ruddy R (ed.). "Drama therapy for schizophrenia or schizophrenia-like illnesses". The Cochrane Database of Systematic Reviews (1): CD005378. doi:10.1002/14651858.CD005378.pub2. PMID 17253555.
  136. ^ Mosher LR (March 1999). "Soteria and other alternatives to acute psychiatric hospitalization: a personal and professional review". The Journal of Nervous and Mental Disease. 187 (3): 142–9. doi:10.1097/00005053-199903000-00003. PMID 10086470.
  137. ^ Calton T, Ferriter M, Huband N, Spandler H (January 2008). "A systematic review of the Soteria paradigm for the treatment of people diagnosed with schizophrenia". Schizophrenia Bulletin. 34 (1): 181–92. doi:10.1093/schbul/sbm047. PMC 2632384. PMID 17573357.
  138. ^ Bartholomeusz C (2011). Handbook of Schizophrenia Spectrum Disorders, Volume III: Therapeutic Approaches, Comorbidity, and Outcomes. Springer. p. 189. ISBN 9789400708341.
  139. ^ Aali G, Kariotis T, Shokraneh F (May 2020). "Avatar Therapy for people with schizophrenia or related disorders". The Cochrane Database of Systematic Reviews. 2020 (5): CD011898. doi:10.1002/14651858.CD011898.pub2. PMC 7387758. PMID 32413166.
  140. ^ Ng QX, Soh AY, Venkatanarayanan N, Ho CY, Lim DY, Yeo WS (2019). "A Systematic Review of the Effect of Probiotic Supplementation on Schizophrenia Symptoms". Neuropsychobiology. 78 (1): 1–6. doi:10.1159/000498862. PMID 30947230.
  141. ^ Patrick RP, Ames BN (June 2015). "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. doi:10.1096/fj.14-268342. PMID 25713056. S2CID 2368912.
  142. ^ Lim SY, Kim EJ, Kim A, Lee HJ, Choi HJ, Yang SJ (July 2016). "Nutritional Factors Affecting Mental Health". Clinical Nutrition Research. 5 (3): 143–52. doi:10.7762/cnr.2016.5.3.143. PMC 4967717. PMID 27482518.
  143. ^ Bosnjak Kuharic D, Kekin I, Hew J, Rojnic Kuzman M, Puljak L (November 2019). "Interventions for prodromal stage of psychosis". The Cochrane Database of Systematic Reviews. 2019 (11). doi:10.1002/14651858.CD012236.pub2. PMC 6823626. PMID 31689359.
  144. ^ Elkis H, Buckley PF (June 2016). "Treatment-Resistant Schizophrenia". The Psychiatric Clinics of North America. 39 (2): 239–65. doi:10.1016/j.psc.2016.01.006. PMID 27216902.
  145. ^ a b c d e Gillespie AL, Samanaite R, Mill J, Egerton A, MacCabe JH (13 January 2017). "Is treatment-resistant schizophrenia categorically distinct from treatment-responsive schizophrenia? a systematic review". BMC Psychiatry. 17 (1): 12. doi:10.1186/s12888-016-1177-y. PMC 5237235. PMID 28086761.
  146. ^ Siskind D, Siskind V, Kisely S (November 2017). "Clozapine Response Rates among People with Treatment-Resistant Schizophrenia: Data from a Systematic Review and Meta-Analysis". Canadian Journal of Psychiatry. 62 (11): 772–777. doi:10.1177/0706743717718167. PMC 5697625. PMID 28655284.
  147. ^ van Os J, Kapur S (August 2009). "Schizophrenia" (PDF). Lancet. 374 (9690): 635–45. doi:10.1016/S0140-6736(09)60995-8. PMID 19700006. S2CID 208792724. Archived from the original (PDF) on 23 June 2013. Retrieved 23 December 2011.
  148. ^ Picchioni MM, Murray RM (July 2007). "Schizophrenia". BMJ. 335 (7610): 91–5. doi:10.1136/bmj.39227.616447.BE. PMC 1914490. PMID 17626963.
  149. ^ Essali A, Al-Haj Haasan N, Li C, Rathbone J (January 2009). "Clozapine versus typical neuroleptic medication for schizophrenia". The Cochrane Database of Systematic Reviews. 2009 (1): CD000059. doi:10.1002/14651858.CD000059.pub2. PMC 7065592. PMID 19160174.
  150. ^ a b c d e Potkin SG, Kane JM, Correll CU, et al. (7 January 2020). "The neurobiology of treatment-resistant schizophrenia: paths to antipsychotic resistance and a roadmap for future research". npj Schizophrenia. 6 (1): 1. doi:10.1038/s41537-019-0090-z. PMC 6946650. PMID 31911624.
  151. ^ Sinclair DJ, Zhao S, Qi F, et al. (19 March 2019). "Electroconvulsive therapy for treatment-resistant schizophrenia". The Cochrane Database of Systematic Reviews. 2019 (3): CD011847. doi:10.1002/14651858.CD011847.pub2. PMC 6424225. PMID 30888709.
  152. ^ a b Miyamoto S, Jarskog LF, Fleischhacker WW (November 2014). "New therapeutic approaches for treatment-resistant schizophrenia: a look to the future". Journal of Psychiatric Research. 58: 1–6. doi:10.1016/j.jpsychires.2014.07.001. PMID 25070124.
  153. ^ a b Sriretnakumar V, Huang E, Müller DJ (2015). "Pharmacogenetics of clozapine treatment response and side-effects in schizophrenia: an update". Expert Opinion on Drug Metabolism & Toxicology. 11 (11): 1709–31. doi:10.1517/17425255.2015.1075003. PMID 26364648. S2CID 207492339.
  154. ^ Agarwal P, Sarris CE, Herschman Y, Agarwal N, Mammis A (December 2016). "Schizophrenia and neurosurgery: A dark past with hope of a brighter future". Journal of Clinical Neuroscience. 34: 53–58. doi:10.1016/j.jocn.2016.08.009. PMID 27634495. S2CID 6929780.
  155. ^ a b Nucifora FC, Woznica E, Lee BJ, Cascella N, Sawa A (November 2019). "Treatment resistant schizophrenia: Clinical, biological, and therapeutic perspectives". Neurobiology of Disease. 131: 104257. doi:10.1016/j.nbd.2018.08.016. PMC 6395548. PMID 30170114.
  156. ^ Servonnet A, Samaha AN (February 2020). "Antipsychotic-evoked dopamine supersensitivity". Neuropharmacology. 163: 107630. doi:10.1016/j.neuropharm.2019.05.007. PMID 31077727. S2CID 147704473.
  157. ^ "Skitsofreniapotilaiden tuettu työllistyminen". Retrieved 2023-04-03.
  158. ^ Richter, D.; Hoffmann, H. (September 2017). "Independent housing and support for people with severe mental illness: systematic review". Acta Psychiatrica Scandinavica. 136 (3): 269–279. doi:10.1111/acps.12765. ISSN 1600-0447. PMID 28620944. S2CID 32054475.
  159. ^ McPherson, Peter; Krotofil, Joanna; Killaspy, Helen (2018-05-15). "Mental health supported accommodation services: a systematic review of mental health and psychosocial outcomes". BMC Psychiatry. 18 (1): 128. doi:10.1186/s12888-018-1725-8. ISSN 1471-244X. PMC 5952646. PMID 29764420.
  160. ^ Shen X, Xia J, Adams CE (October 2014). "Acupuncture for schizophrenia". The Cochrane Database of Systematic Reviews. 2014 (10): CD005475. doi:10.1002/14651858.CD005475.pub2. PMC 4193731. PMID 25330045.
  161. ^ van den Noort M, Yeo S, Lim S, Lee SH, Staudte H, Bosch P (March 2018). "Acupuncture as Add-On Treatment of the Positive, Negative, and Cognitive Symptoms of Patients with Schizophrenia: A Systematic Review". Medicines. 5 (2): 29. doi:10.3390/medicines5020029. PMC 6023351. PMID 29601477.
  162. ^ Deng H, Xu J (June 2017). "Wendan decoction (Traditional Chinese medicine) for schizophrenia". The Cochrane Database of Systematic Reviews. 2017 (6): CD012217. doi:10.1002/14651858.CD012217.pub2. PMC 6481906. PMID 28657646.
  163. ^ Wieland LS, Santesso N (October 2017). "Summary of a Cochrane review: Wendan decoction traditional Chinese medicine for schizophrenia". European Journal of Integrative Medicine. 15: 81–82. doi:10.1016/j.eujim.2017.09.009. PMC 5649251. PMID 29062436.
  164. ^ a b c Pinault D (March 2017). "A Neurophysiological Perspective on a Preventive Treatment against Schizophrenia Using Transcranial Electric Stimulation of the Corticothalamic Pathway". Brain Sciences. 7 (4): 34. doi:10.3390/brainsci7040034. PMC 5406691. PMID 28350371.
  165. ^ a b c d Nathou C, Etard O, Dollfus S (2019). "Auditory verbal hallucinations in schizophrenia: current perspectives in brain stimulation treatments". Neuropsychiatric Disease and Treatment. 15: 2105–2117. doi:10.2147/NDT.S168801. PMC 6662171. PMID 31413576.
  166. ^ 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 modelling studies". Health Technology Assessment. 9 (9): 1–156, iii–iv. doi:10.3310/hta9090. PMID 15774232.
  167. ^ 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.
  168. ^ Mashour GA, Walker EE, Martuza RL (June 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. S2CID 10303872.
  169. ^ 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.
  170. ^ Helman DS (2018). "Recovery from schizophrenia: An autoethnography". Deviant Behavior. 39 (3): 380–399. doi:10.1080/01639625.2017.1286174. S2CID 151705012.
  171. ^ Tyrer P (June 2019). "Nidotherapy: a cost-effective systematic environmental intervention". World Psychiatry. 18 (2): 144–145. doi:10.1002/wps.20622. PMC 6502418. PMID 31059613.
  172. ^ Ruddle A, Mason O, Wykes T (July 2011). "A review of hearing voices groups: evidence and mechanisms of change". Clin Psychol Rev. 31 (5): 757–66. doi:10.1016/j.cpr.2011.03.010. PMID 21510914.
  173. ^ Corstens D, Longden E, McCarthy-Jones S, Waddingham R, Thomas N (July 2014). "Emerging perspectives from the hearing voices movement: implications for research and practice". Schizophr Bull. 40 (Suppl 4): S285–94. doi:10.1093/schbul/sbu007. PMC 4141309. PMID 24936088.
  174. ^ Chien WT, Clifton AV, Zhao S, Lui S, et al. (Cochrane Schizophrenia Group) (April 2019). "Peer support for people with schizophrenia or other serious mental illness". The Cochrane Database of Systematic Reviews. 4 (6): CD010880. doi:10.1002/14651858.CD010880.pub2. PMC 6448529. PMID 30946482.