Placebo responses schizophrenia

Wilson WH. Addition of lithium to haloperidol in non-affective antipsychotic non-responsive schizophrenia a double blind, placebo controlled, parallel design clinical ttial. Psychopharmacology (Bed) (1993) 111, 359-66. 

Utman RE, Su TP, Potter WZ, et al Idazoxan and response to typical neuroleptics in treatment-resistant schizophrenia comparison with the atypical neuroleptic, clozapine. Br J Psychiatry 168 571-579, 1996 Uttle A, Levy R, Chuaqui-Kidd P, et al A double-blind placebo-controlled trial of high-dose lecithin in Alzheimer s disease. J Neurol Neurosurg Psychiatry 12 110-118, 1985... 

Breier A, Meehan K, Birkett M, et al A double-blind, placebo-controlled dose-response comparison of intramuscular olanzapine and haloperidol in the treatment of acute agitation in schizophrenia. Arch Gen Psychiatry 59 441 48, 2002... 

On each experimental day, the Repeatable Battery for Assessment of Neuropsychological Status (RBANS) was administered (Randolph, 1998). It assesses attention, immediate memory, visuospatial/ construction, language, and delayed memory (Gold et al., 1999). Schizophrenics score significantly lower than normal subjects the decrement is correlated with diminished psychosocial status. Compared to placebo, the DMXB-A significantly improved overall performance and specifically improved function on the Attention subscale. Inhibition of the P50 response to repeated stimulus, the sensory gating measure that led to identification of nicotinic receptor deficits in schizophrenia, also improved (Olincy et al., 2006). 

The cardiovascular response to an oral dose of d-amfe-tamine 0.5 mg/kg has been determined in 81 subjects with schizophrenia, 8 healthy controls who took amfetamine, and 7 subjects with schizophrenia who took a placebo (18). Blood pressure increased in both amphetamine groups, whereas placebo had no effect. However, pulse... 

In summary, existing drug treatments for schizophrenia are of limited efficacy and have substantial side effects. New treatment can arise only on the basis of a new hypothesis. The phospholipid hypothesis of schizophrenia provides the theoretical basis for treatment with PUPA supplementation. Pre vlous studies using n-6 supplementation have had mixed results. We now have evidence from a double-blind, placebo-controlled trial that EPA, but not DHA, is effective in reducing the symptoms of schizophrenia. It is possible that the response to EPA is impaired by concomitant treatment with antipsychotic drugs that damage membrane phospholipids. The best treatment effects of EPA have been seen in patients who are otherwise unmedicated or who are currently taking clozapine. This remains to be explored further. 

A recent study showed abnormal niacin sensitivity in schizophrenia patients as evidenced by attenuation of the flush response to niacin in schizophrenia. However, there is still an ongoing debate whether this response is due to altered pharmacological sensitivity to niacin or an inadequate cutaneous vasodilatory response to the stimulus (Messamore et al. 2003). Early studies even attempted to use niacin as an augmenting agent for the treatment of schizophrenia with mixed results (Ananth et al. 1973 Petrie et al. 1981). In a placebo-controlled comparative study by Ramsay et al. (1970), it was found that, while no significant differences were seen in total Brief Psychiatric Rating Scale (BPRS) scores prior to commencement of the clinical trial, statistically significant... 

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