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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After reviewing the literature on nicotinic acid in the treatment of schizophrenia, the authors present the results of the Canadian collaborative study. The data indicate that nicotinic acid has no therapeutic effect of schizophrenia.
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PMID:Nicotinic acid in the treatment of schizophrenias. Practical and theoretical considerations. 0 43

The transmethylation hypothesis of schizophrenia was reviewed with considerations that large doses of methionine when combined with a monoamine oxidase inhibitor lead to exacerbation of psychotic symptoms in a significant percentage of chronic schizophrenic patients. It was noted that nicotinic acid in the dosage of 3,000 mg/day can neither prevent nor counteract the psychopathology thus induced.
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PMID:Transmethylation hypothesis of schizophrenia: methionine and nicotinic acid. 33 34

The hypothesis that endogenously formed, N-methylated metabolites of indoleamines may play a role in the pathogenesis of schizophrenia was reviewed. Although N-methylated indoleamines can be produced in vivo and have significant psychotomimetic effects, there is little evidence for a specific increase in the methylation of indoleamines in schizophrenic patients. It was noted that even if the relationship between schizophrenia and N-methylated indoleamines had existed, nicotinic acid would not be an appropriate therapeutic agent.
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PMID:A review of nicotinic acid, N-methylated indoleamines and schizophrenia. 34 36

Deficiencies of specific vitamins produce consistent symptoms of psychiatric disorder. Thiamine deficiency, which is common in alcoholism, can produce confusion and psychotic symptoms, in addition to neurological signs. Vitamin B12 and folate deficiency may contribute symptoms of disorientation, depression or psychosis; their measurement is a part of routine dementia work-ups. Pyridoxine deficiency results in seizures, although the effects of exogenously administered pyridoxine are not clearly understood in depression and anxiety - the disorders in which it is most frequently used clinically. The use of vitamins has been most prominent in psychiatry in the treatment of schizophrenia, where large doses of nicotinic acid were initially given alone and later combined with other vitamins and minerals. Several theoretical models were described to support the use of vitamins in schizophrenia. These included: the parallels of schizophrenia to the psychiatric symptoms of pellagra; hypotheses of a defect in adrenaline metabolism; and the accumulation of psychotoxic substances which produce psychotic symptoms. Initially, positive results were reported over 30 years ago, but have not been replicated by thorough investigations. An extensive series of comprehensive placebo-controlled trials failed to show efficacy for any of the vitamin therapies tested. Although clearly less effective than antipsychotic drug treatment, vitamin therapy is not without risks - adverse effects have been reported with nicotinic acid, pyridoxine and vitamin C.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Vitamins in psychiatry. Do they have a role? 389 44

A case is described of a young woman who first showed manifestations of schizophrenia in childhood. At the age of 13 years evidence was present of what was authoritatively diagnosed as a progressive degenerative cerebellar syndrome and her condition continued to deteriorate. Improvement commenced shortly after the institution of megavitamin therapy, notably nicotinic acid 3 grams daily. Her subsequent educational progress was satisfactory and her social rehabilitation is now complete. No medication other than nicotinic acid is required.
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PMID:A neurological form of schizophrenia. 468 27

Hepatic injury has been associated with nicotinic acid treatment of schizophrenia and hypercholesterolemia. This association was implicated when the liver and biliary tract were not visualized after 99mTc-HIDA in a patient taking 3 g daily of nicotinic acid. We studied hepatic transport of 99mTc-PIPIDA both in vitro in isolated hepatocytes and in vivo in rabbits pretreated with nicotinic acid to further examine this association. Nicotinic acid increased uptake of PIPIDA by isolated hepatocytes and 7 days of nicotinic acid treatment in rabbits produced no abnormalities in hepatic uptake, gallbladder visualization, or biliary excretion of PIPIDA. We conclude that nicotinic acid does not have an inhibitory effect on uptake of biliary imaging agents and actually may be useful in enhancing hepatic imaging in patients with reduced liver function.
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PMID:Acute effects of nicotinic acid on hepatic transport of 99mTc-PIPIDA. 683 82

There is evidence that schizophrenia may be related to excess biological activity of dopamine, deficient synthesis of a prostaglandin and to the presence of a normal opioid in excess or of an abnormal opioid. These three groups of observations seem to be interrelated since opioids are able to inhibit the formation of prostaglandin E1 and prostaglandin E1 and dopamine inhibit each other's effects. A low prostaglandin E1 level will therefore produce and apparent dopamine excess. Niacin causes flushing, apparently by stimulating production of prostaglandin E1. Much larger doses of oral niacin are required to produce flushing in schizophrenics than in normal individuals. Most schizophrenics do not flush when given 250 mg orally and this may be a simple biochemically-based test for a major group of schizophrenics.
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PMID:Schizophrenia: a biochemical disorder? 738 16

Participation of nicotinic acid and its derivates in the functioning of nervous system is considered basing on the data from literature. It is supposed that the favourable therapeutic effects of nicotinamide, nicotinic acid and their active biological form--NAD are realized due to the mechanisms of their functioning in the nervous system, for treating schizophrenia, epilepsy and other diseases of the nervous system.
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PMID:[Role of nicotinic acid and its derivatives in disorders of nervous system function]. 855 69

Several lines of evidence implicate altered phospholipid-dependent signal transduction (PDST) in the pathophysiology of schizophrenia. Niacin induces vasodilation through mechanisms requiring intact PDST. Thus, an altered response to a challenge dose of niacin may reflect disturbances in these signalling processes in this disorder. In the present study, niacin-induced vasodilation was estimated quantitatively in schizophrenic and comparison bipolar affective disorder and healthy subjects using thermocouple sensors to measure the change in skin temperature relative to core body and ambient room temperature. Twelve (42.9%) of 28 schizophrenic subjects did not vasodilate in response to a 200-mg niacin challenge dose, whereas only 1 of 18 (6%) bipolar disorder subjects and none of 28 controls showed impaired response (Fisher's Exact Test, p < .0001). These findings support the notion that the schizophrenic syndromes are biochemically heterogeneous and suggest the existence of a subgroup of schizophrenic subjects in whom phospholipid-dependent signalling responses may be impaired.
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PMID:The niacin challenge test: clinical manifestation of altered transmembrane signal transduction in schizophrenia? 904 82

The aim of this pilot study was to evaluate a potential skin test for schizophrenia based on the effect of aqueous methyl nicotinate (AMN) on the production of prostaglandin D2 (PGD2) from skin macrophages and the resultant cutaneous capillary vasodilatation. Four concentrations of AMN were applied topically to the forearm skin in patients and controls, and any resulting vasodilatation was rated as redness after 5 min. The test was carried out on 38 patients with schizophrenia diagnosed according to DSM-III-R criteria, and 22 normal control subjects. At all concentrations of AMN, the schizophrenics were highly significantly different from the controls. One concentration gave the greatest degree of differentiation: at this concentration at 5 min, 83% of schizophrenics but only 23% of controls had a zero or minimal response to AMN. The skin flushing seen after oral administration of nicotinic acid is due to the same reaction, and this has been normal in those with affective illness and neurosis; cyclo-oxygenase inhibitors, e.g., aspirin, give a false-positive result (failure of vasodilatation). This result is consistent with the concept of reduced membrane arachidonic acid levels in schizophrenia. This test may contribute to the reliable diagnosis of schizophrenia.
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PMID:Niacin skin flush in schizophrenia: a preliminary report. 951 68


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