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

Pre-natal infection with polioviruses could contribute to the subsequent development of schizophrenia. The hypothesis draws support from the declining incidence of schizophrenia, the excess of schizophrenic winter births, and the increased rates of schizophrenia among West Indian immigrants. There are parallels with other late sequelae of poliovirus infections. These postulations generate a testable hypothesis of a genetic link between schizophrenia and susceptibility to poliomyelitis.
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PMID:Are polioviruses a cause of schizophrenia? 131 38

In order to investigate a possible relationship between schizophrenic births and viral diseases, the birth month and year of all state hospital admissions for schizophrenia in Connecticut and Massachusetts from 1973-1974 were compared with the occurrence of reportable viral diseases for 1920-1955. Data was statistically examined by time series using spectral analysis. Statistically significant coherences were found between schizophrenic births and measles (both states), varicella-zoster (Connecticut) and polio (Connecticut). Influenza just missed statistical significance. No temporal relationship between schizophrenic births and rubella or mumps was found. The results are compared with similar studies in Minnesota and Finland. Definitive explanations for the observed relationships are precluded by the emerging complexity of virus-CNS interactions. A triggering of immune dysfunction by the infectious agents is proposed as the most reasonable explanation.
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PMID:Schizophrenic births and viral diseases in two states. 315 10

Rheumatic diseases have not proved to be more prevalent among neurologic or psychiatric patients than in the general population, except for osteoarthritis in some chronic disabling neurologic conditions (poliomyelitis, spinal cord injury). Some neurologic entities with relevant musculoskeletal manifestations are described here. The lower prevalence of rheumatoid arthritis in schizophrenia patients is mentioned, and a brief description is presented of somatoform disorders that may confound diagnosis with rheumatic diseases. Factitious disorders and malingering are frequently presented with rheumatic complaints such as low back pain and may have an important impact on the costs associated with the disease. Finally, some of the immune system abnormalities described in major depression and schizophrenia are mentioned with a clear reference to the growing field of psychoneuroimmunology. This paper will not address the issue of neurologic or psychiatric manifestations of rheumatic diseases.
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PMID:Rheumatic manifestations of neurologic and psychiatric diseases. 911 Jan 34

John M. Eagles suggested that polioviruses might cause schizophrenia because 1) several reports of a recent decline in the incidence of schizophrenia coinciding with the introduction of polio vaccination, 2) the observed winter excesses in schizophrenic births (in temperate climates) could be explained by fetal exposure to poliovirus during the second trimester of gestation which would occur during the summer when polio epidemics are most frequent, 3) there are increased rates of schizophrenia among immigrants to the UK from regions of the world with low frequencies if immunity to polioviruses, 4) there may be genetic variants in the poliovirus receptor gene that could increase susceptibility to poliovirus infection (1). The large discordance rates for schizophrenia in monozygotic twin pairs indicate the existence of both genetic and environmental factors. Numerous genetic studies indicate an interaction of several genes in the etiology of schizophrenia. These genes may encode a family of poliovirus receptor subunits, various active combinations of which are expressed on T-immunocytes, monocytes, endothelial cells, and limited populations of (glutamatergic?) neurons. The poliovirus receptor on the T-cell may require both a specific combination of V segments of the T-cell antigen receptor, as well as a specific major histocompatibility (MHC) antigen, acting in concert to infect monocytes, the primary transporter of poliovirus from blood into the brain. The very large discordance rates for schizophrenia that probably exist for dichorionic-monozygotic twins (about 90%), as well as the much smaller discordance rates for monochorionic-monozygotic twins (about 40%), may be due to several allelic exclusion events expressed both in T-cells and possibly in certain neurons. A child who has lost some glutamatergic neurons due to viral infection during the second trimester of gestation, may be able to compensate for this deficit to a large extent by the super-abundance of excitatory synapses that exists in the brain until sexual maturity, at which time a selective loss of excitatory (mainly glutamatergic) synapses occurs together with hormonally induced changes in behavior, leading to a much increased risk of a psychotic episode.
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PMID:How a poliovirus might cause schizophrenia: a commentary on Eagles' hypothesis. 913 45

Various factors have been implicated in the pathogenesis of schizophrenia. Evidence for an infectious cause includes the 5-8% increased risk among those born in the winter-spring months, when infectious diseases are more prevalent and at times when other infections (measles, varicella, poliomyelitis) show increased activity. Herpes simplex virus (HSV) has been implicated in schizophrenia as it has a tropism for the nervous system and is capable of replication in the brain. Although post-mortem studies of brain tissue of schizophrenic patients have failed to detect the virus, these studies have been hampered by the unknown cellular localization of HSV genomes and by attempting to detect the virus years after the symptom onset. A more recent, nested, case-control study evaluated pregnant women between 1959 and 1966 and identified 27 surviving offspring who were later diagnosed with schizophrenia. Analysis of stored blood samples showed an association between high levels of maternal antibody to HSV-2 and subsequent development of adult psychosis. No association was found between HSV-1 infection and psychosis. There is also evidence that human endogenous retroviruses (HERVs) may play a role in schizophrenia, as antibodies to these agents have been found at a greater frequency in the sera of affected individuals compared with controls. This is supported by the presence of reverse transcriptase, a retroviral marker, at levels four times higher in the cerebrospinal fluid (CSF) of people with recent onset schizophrenia compared with controls, and by its elevated presence in long-term schizophrenic patients. Further research to investigate the relationship between virus infection and schizophrenia is warranted.
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PMID:Viruses and schizophrenia: a focus on herpes simplex virus. 1531 94

(-)-Galanthamine is a selective, reversible competitive acetylcholinesterase inhibitor that has been recently approved for the symptomatic treatment of Alzheimer's disease. Galanthamine is a natural product belonging to the Amaryllidaceae family of alkaloids. The pharmacological history of galanthamine shows that the bioactive compound was discovered accidentally in the early 1950s, and the plant extracts were initially used to treat nerve pain and poliomyelitis. In addition, galanthamine had since been tested for use in anesthesiology, from facial nerve paralysis to schizophrenia. Galanthamine is a long-acting, selective, reversible and competitive AChE inhibitor that has recently been tested in AD patients and found to be readily absorbed, to be a performance enhancer on memory tests in some patients, and to be well tolerated, although some cholinergic side effects were observed. A number of total synthetic approaches have been reported, and a method for the industrial scale-up preparation of galanthamine is now being developed and patented. A variety of galanthamine derivatives have also been synthesized aiming to develop an agent free from cholinergic adverse effects. Galanthamine is a natural product that complements other synthetic drugs for the management of AD. In this account we will review the recent patent literature showing the most important advance on the chemistry of galanthamine.
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PMID:Galanthamine, a natural product for the treatment of Alzheimer's disease. 1822 Nov 96

Modafinil is a wake-promoting agent that is pharmacologically different from other stimulants. It has been investigated in healthy volunteers, and in individuals with clinical disorders associated with excessive sleepiness, fatigue, impaired cognition and other symptoms. This review examines the use of modafinil in clinical practice based on the results of randomized, double-blind, placebo-controlled clinical trials available in the English language in the MEDLINE database. In sleep-deprived individuals, modafinil improves mood, fatigue, sleepiness and cognition to a similar extent as caffeine but has a longer duration of action. Evidence for improved cognition in non-sleep-deprived healthy volunteers is controversial.Modafinil improves excessive sleepiness and illness severity in all three disorders for which it has been approved by the US FDA, i.e. narcolepsy, shift-work sleep disorder and obstructive sleep apnoea with residual excessive sleepiness despite optimal use of continuous positive airway pressure (CPAP). However, its effects on safety on the job and on morbidities associated with these disorders have not been ascertained. Continued use of CPAP in obstructive sleep apnoea is essential. Modafinil does not benefit cataplexy.In very small, short-term trials, modafinil improved excessive sleepiness in patients with myotonic dystrophy. It was efficacious in fairly large studies of attention deficit hyperactivity disorder (ADHD) in children and adolescents, and was as efficacious as methylphenidate in a small trial, but has not been approved by the FDA, in part because of its serious dermatological toxicity. In a trial of 21 non-concurrent subjects, with 2-week treatment periods, modafinil was as effective as dexamfetamine in adult ADHD. Modafinil was helpful for depressive symptoms in bipolar disorder in a trial that excluded patients with stimulant-induced mania. A single dose of modafinil may hasten recovery from general anaesthesia after day surgery. A single dose of modafinil improved the ability of emergency room physicians to attend didactic lectures after a night shift, but did not improve their ability to drive home and caused sleep disturbances subsequently.Modafinil had a substantial placebo effect on outcomes such as fatigue, excessive sleepiness and depression in patients with traumatic brain injury, major depressive disorder, schizophrenia, post-polio fatigue and multiple sclerosis; however, it did not provide any benefit greater than placebo.Trials of modafinil for excessive sleepiness in Parkinson's disease, cocaine addiction and cognition in chronic fatigue syndrome provided inconsistent results; all studies had extremely small sample sizes. Modafinil cannot be recommended for these conditions until definitive data become available.Modafinil induces and inhibits several cytochrome P450 isoenzymes and has the potential for interacting with drugs from all classes. The modafinil dose should be reduced in the elderly and in patients with hepatic disease. Caution is needed in patients with severe renal insufficiency because of substantial increases in levels of modafinil acid. Common adverse events with modafinil include insomnia, headache, nausea, nervousness and hypertension. Decreased appetite, weight loss and serious dermatological have been reported with greater frequency in children and adolescents, probably due to the higher doses (based on bodyweight) used. Modafinil may have some abuse/addictive potential although no cases have been reported to date.
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PMID:Approved and investigational uses of modafinil : an evidence-based review. 1872 34