Beta-blocker supplementation of standard drug treatment for schizophrenia

Shek, Elena; Bardhan, Sabyasachi; Cheine, Maxim V; Ahonen, Juha; Wahlbeck, Kristian

doi:10.1002/14651858.cd000234

Cited by 9 publications

(5 citation statements)

References 98 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Treatments such as lithium (Leucht 2007b, indicated for bipolar a ective disorder), carbamazepine (Leucht 2007c), valproate (Casey 2003), benzodiazepine (Dold 2012), beta-blockers (Cheine 2003) and electroconvulsive therapy (Tharyan 2005) have all been used for people whose psychosis did not respond to traditional therapy. The situation has improved somewhat in recent years, with the re-introduction of clozapine, which has proven e icacy for those that have not responded to traditional antipsychotic medications (Essali 2010).…”

Section: B a C K G R O U N Dmentioning

confidence: 99%

Valproate for schizophrenia

Wang

Xia

Helfer

et al. 2016

Cochrane Database of Systematic Reviews

View full text Add to dashboard Cite

There is limited evidence, based on a number of trials, that the augmentation of antipsychotics with valproate may be effective for overall clinical response, and also for specific symptoms, especially in terms of excitement and aggression. However, this evidence was entirely based on open RCTs. Moreover, valproate was associated with a number of adverse events among which sedation and dizziness appeared significantly more frequently than in the control groups. Further randomised studies which are blinded are necessary before any clear recommendation can be made. Ideally these would focus on people with schizophrenia and aggression, on those with treatment-resistant forms of the illness and on those with schizoaffective disorders.

show abstract

Section: B a C K G R O U N Dmentioning

confidence: 99%

Valproate for schizophrenia

Wang

Xia

Helfer

et al. 2016

Cochrane Database of Systematic Reviews

View full text Add to dashboard Cite

show abstract

“…For total and positive symptoms, augmentation strategies have included the addition of a second antipsychotic, 7,8 valproic acid, 9 carbamazepine, 10 lithium, 11 lamotrigine, 12,13 benzodiazepines, 14 and beta blockers. 15 Augmentation treatments for negative and/or cognitive symptoms have included the addition of antidepressants, [16][17][18] acetylcholinesterase inhibitors, 19 omega-3 fatty acids, 20,21 modafinil, 22 and N-methyl D-aspartate receptor modulators. 23 Other potentially promising strategies studied in very few and small studies have included electroconvulsive therapy, 24 alpha2-antagonists, 25 testosterone, 26 estrogen, 27 and nonsteroidal anti-inflammatory drugs (NSAIDs).…”

Section: Introductionmentioning

confidence: 99%

Adjunctive Use of Nonsteroidal Anti-inflammatory Drugs for Schizophrenia: A Meta-analytic Investigation of Randomized Controlled Trials

Nitta

Kishimoto

Müller

et al. 2013

Schizophrenia Bulletin

175

106

View full text Add to dashboard Cite

show abstract

“…delusions, hallucinations, thought disorder) in schizophrenia (Zhou et al ., ). A recent review suggested that whereas it is unclear from existing studies that adjunctive beta‐blocker treatment is therapeutic in schizophrenia, it may nonetheless be justified to carry out well conducted and reported trials on this topic (Shek et al ., ). In persons with schizophrenia who were clinically stable on their antipsychotic regimen, a single low dose of clonidine normalized the sensorimotor gating deficits that characterize this disorder (Oranje & Glenthøj, ).…”

Section: Introductionmentioning

confidence: 99%

Noradrenaline transmission reducing drugs may protect against a broad range of diseases.

Fitzgerald

2014

Auton Autocoid Pharmacol

View full text Add to dashboard Cite

1 A growing body of evidence suggests that the signalling molecule, noradrenaline (NA), plays a pathophysiological role in a broad range of psychiatric, neurological and peripheral disorders. Both preclinical and clinical data suggest that elevated NA signalling may be involved in the aetiology of major diseases such as depression, Alzheimer's disease and diabetes mellitus. 2 The molecular pathways by which NA may cause the manifestation of disease remain poorly understood, although they may include G protein-coupled receptor modulation of the Ras/MAP kinase, Stat3 and PI3K pathways, among others. In both individual animals and humans, NA tone may be elevated largely due to genetics, but also because of the exposure to marked psychological stress or trauma, or other environmental factors. 3 As NA is involved in the 'fight or flight' response by the sympathetic nervous system, this transmitter may be elevated in a large number of organisms due to evolutionary selection of enhancing responses to immediate environmental dangers. Likewise, acetylcholine signalling by the parasympathetic ('rest and digest') nervous system may be relatively diminished. This putative autonomic imbalance may result in diminished engagement in homeostatic processes, resulting in the emergence and progression of a number of diseases throughout the body. 4 In this scenario, a large number of individuals may benefit from chronic use of pharmacological agents - such as clonidine, guanfacine, propranolol or prazosin - that diminish NA signalling throughout the body. If so, NA transmission lowering drugs may protect against a wide range of diseases.

show abstract

Beta-blocker supplementation of standard drug treatment for schizophrenia

Cited by 9 publications

References 98 publications

Valproate for schizophrenia

Valproate for schizophrenia

Adjunctive Use of Nonsteroidal Anti-inflammatory Drugs for Schizophrenia: A Meta-analytic Investigation of Randomized Controlled Trials

Noradrenaline transmission reducing drugs may protect against a broad range of diseases.

Contact Info

Product

Resources

About