Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0917816 (mental retardation)
 15,867 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intellectual deterioration, changing in behavior and affect are often seen in association with long continued and heavy alcohol ingestion and such deteriorated states of patients are called alcoholic dementia. A large number of investigators have attempted to designate clinical concept of alcoholic dementia throughout the centuries and many kinds of term like as alcoholic pseudo-paralysis, alcoholic mental deficiency and alcoholic deterioration, etc, have been submitted since the beginning of 19th century. Numerous psychometric studies have indicated cognitive impairment and memory disturbance in chronic alcohol abusers and moreover brain PEG and CT-scan studies have shown sulcal widening and enlarged ventricles to be common in alcoholics. However, alcoholic dementia is hard to classify as a distinct disorder caused by alcoholic ingestion. The reason is lack of specific findings, both clinical and histopathological, like as Wernicke-Korsakoff syndrome and other nutritional disorders in alcoholics. Victor, M. describes in his work the majority of patients who have come to autopsy with the clinical diagnosis of primary alcoholic dementia have shown the lesions of the Wernicke-Korsakoff syndrome and he postulates alcoholic dementia is heavily contaminated with burned-out Wernicke-Korsakoff disease. The clinical and pathological observations presented by this time represent alcoholic dementia is a residual category for cases in which there are severe impairment of intelligence with marked deterioration of personality following prolonged and heavy drinking.
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PMID:[Clinical concept of alcoholic dementia]. 189 48

The Berlin Deinstitutionalization Study investigates effects of the planned reduction of psychiatric hospital beds in Berlin prospectively. In the beginning cross-sectional survey all adult psychiatric patients from two and a half districts, who had been hospitalized for more than 6 months, were examined. The total sample was 422 patients. Treatment situation and needs for nursing care are reported. The primary diagnosis according to ICD-10 was organic disorder (incl. Korsakov's syndrome) in 70 patients and mental retardation in 61. Psychopathology and social disabilities were examined in 237 of the remaining 291 patients. On average, psychopathology and disabilities were moderate. A cluster analysis classified three groups. When patients should be discharged, special protective measures might be necessary only for the two smaller groups (together 31%).
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PMID:[Clinical characteristics of long-term hospitalized patients. Part I of the Berlin Deinstitutionalization Study]. 885 Dec 26

Heavy alcohol exposure produces profound damage to the developing central nervous system (CNS) as well as the adult brain. Children with fetal alcohol spectrum disorders (FASD) have a variety of cognitive, behavioral, and neurological impairments. FASD currently represents the leading cause of mental retardation. Excessive alcohol consumption is associated with Wernicke-Korsakoff syndrome (WKS) and neurodegeneration in the adult brain. Although the cellular/molecular mechanism underlying ethanol's neurotoxicity has not been fully understood, it is generally believed that oxidative stress plays an important role. Identification of neuroprotective agents that can ameliorate ethanol neurotoxicity is an important step for developing preventive/therapeutic strategies. Targeting ethanol-induced oxidative stress using natural antioxidants is an attractive approach. Anthocyanins, a large subgroup of flavonoids present in many vegetables and fruits, are safe and potent antioxidants. They exhibit diverse potential health benefits including cardioprotection, anti-atherosclerotic activity, anti-cancer, anti-diabetic, and anti-inflammation properties. Anthocyanins can cross the blood-brain barrier and distribute in the CNS. Recent studies indicate that anthocyanins represent novel neuroprotective agents and may be beneficial in ameliorating ethanol neurotoxicity. In this review, we discuss the evidence and potential of anthocyanins in alleviating ethanol-induced damage to the CNS. Furthermore, we discuss possible underlying mechanisms as well as future research approaches necessary to establish the therapeutic role of anthocyanins.
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PMID:Anthocyanins: are they beneficial in treating ethanol neurotoxicity? 1959 Sep 29

Lithium has long been used as a mood stabilizer in the treatment of manic-depressive (bipolar) disorder. Recent studies suggest that lithium has neuroprotective properties and may be useful in the treatment of acute brain injuries such as ischemia and chronic neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease and amyotrophic lateral sclerosis. One of the most important neuroprotective properties of lithium is its anti-apoptotic action. Ethanol is a neuroteratogen and fetal alcohol spectrum disorders (FASD) are caused by maternal ethanol exposure during pregnancy. FASD is the leading cause of mental retardation. Ethanol exposure causes neuroapoptosis in the developing brain. Ethanol-induced loss of neurons in the central nervous system underlies many of the behavioral deficits observed in FASD. Excessive alcohol consumption is also associated with Wernicke-Korsakoff syndrome and neurodegeneration in the adult brain. Recent in vivo and in vitro studies indicate that lithium is able to ameliorate ethanol-induced neuroapoptosis. Lithium is an inhibitor of glycogen synthase kinase 3 (GSK3) which has recently been identified as a mediator of ethanol neurotoxicity. Lithium's neuroprotection may be mediated by its inhibition of GSK3. In addition, lithium also affects many other signaling proteins and pathways that regulate neuronal survival and differentiation. This review discusses the recent evidence of lithium-mediated protection against ethanol neurotoxicity and potential underlying mechanisms.
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PMID:Lithium-mediated protection against ethanol neurotoxicity. 2066 53

There are few systems in place for patients with psychiatric disorders who need treatments for physical complications. In Tokyo, "The Tokyo metropolitan psychiatric emergency system" was established in 1981, and Ome Municipal General Hospital participated in it. Under this system, fifteen patients with psychiatric disorders were treated for otorhinolaryngological diseases in our department from April 2005 to March 2011. We reviewed the fifteen patients. The coexisting psychiatric disorders were schizophrenia in twelve patients, and mental retardation, Korsakoff's syndrome, and Alzheimer's dementia in one patient each, respectively. All the patients had been receiving psychiatric treatment. The otorhinolaryngological diseases were head and neck cancer in nine patients, chronic sinusitis in three patients, and benign salivary gland tumor, cholesteatoma, and epistaxis in one patient each, respectively. Among the fifteen patients, thirteen could complete their treatment, but two dropped out due to exacerbation of their psychiatric symptoms. The therapeutic course is uncertain in otorhinolaryngological diseases occurring concomitantly with psychiatric disorders, especially in head and neck cancer, because it may be difficult to prioritize the problem when determining the treatment options and delivering the treatment. Thus, we should treat patients with psychiatric disorders carefully on a case-by-case basis depending on their psychiatric symptoms. It is also important to cooperate with psychiatrists and patients' families.
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PMID:[Treatments for otorhinolaryngological patients with psychiatric disorders]. 2353 58