Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 36-year-old man with prolonged confusion developed after psychomotor status was reported. He had no past history of epileptic seizures or psychotic disorders. The status continued for 20 hours, and twilight state and a slight fever lasted for about 10 days. Thereafter gross impairment of memory and disorientation became remarkable, and, in addition, strong psychic and autonomic disturbances developed, such as visual and auditory hallucinations, excessive excitement, disturbance of sleep, polyphagia, polydypsia, polyuria and hyperhidrosis. The CT scan, carotide angiography, CSF examination, and complement fixation tests for viruses were all within normal limits. The EEGs showed a slowing of the background activity, 0.6--0.8 Hz periodic high voltage wave discharges and random spikes in each temporal area. The clinical symptoms and EEG findings gradually improved without remarkable damage.
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PMID:A case of prolonged confusion after temporal lobe psychomotor status. 52 Sep 42

An overview of the literature is given and an attempt is made to describe the diagnostic problems associated with this etiologically unclear disorder. The only successful therapy to date is treatment with lithium. A case study is presented of a 14-year-old boy with typical symptoms. Within a period of 12 months the boy had 6 episodes characterized by hypersomnia and hyperphagia, each lasting between 8 and 14 days. The symptom-free intervals lasted from 10 days to 8 months. Extensive medical and neurological evaluation including single-photon emission-computed tomography (SPECT) showed no abnormalities, and no criteria for another psychiatric disorder were met. After the sixth episode we considered treating the patient with lithium, but this option was rejected by his family. The patient has remained asymptomatic (36-month follow-up). A possible relationship to endogenous psychotic disorders and the role of neurotransmitter metabolism are discussed. Computer-assisted analysis of electroencephalographic activity revealed high signal complexity, which we believe suggests a primary cortical regulatory defect.
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PMID:[Kleine-Levin syndrome--diagnostic and therapeutic problems]. 945 1

The psychopathology of Alzheimer's disease (AD) is varied and includes both behavioural and psychological symptoms. Behavioural and psychological symptoms are common and contribute to the difficulties experienced by carers. However, the mechanism whereby these symptoms occur in some individuals with AD is not understood. We hypothesized that common genetic polymorphisms in neurotransmitter systems are risk factors for these symptoms in the course of AD. A total of 211 subjects from a population-based prospective study of psychopathology within late-onset AD were genotyped for the 5-HT2A receptor polymorphism 102-T/C and the 5-HT2C receptor polymorphism Cys23Ser. Associations were found between the presence of the C102 allele and the presence of visual (Fisher's exact test, one-tailed, P = 0.003) and auditory hallucinations (Fisher's exact test, one-tailed, P = 0.004) and between the presence of the Ser23 allele and visual hallucinations (chi2 = 7.5, df = 1, P = 0.006) (P = 0.03, 0.04 and 0.06, respectively, after Bonferroni correction). In addition, there was an association between the Cys23Ser polymorphism and hyperphagia (chi2 = 6.7, df = 2, P = 0.03) (P = 0.3 after Bonferroni correction). We conclude that common 5-HT2A and 5-HT2C genetic polymorphisms previously showing only weak associations with psychotic illness are associated with psychotic symptoms in AD but are clinically silent until the onset of the neurodegenerative process.
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PMID:5-HT2A and 5-HT2C receptor polymorphisms and psychopathology in late onset Alzheimer's disease. 970 Feb 7

Dexfenfluramine (DF) is contraindicated in severe psychiatric disorders and in depression. We used DF in 3 patients with chronic psychosis and severe overeating without changes in psychiatric pharmacotherapy. Two patients had paranoid schizophrenic psychosis with hallucinations, one patient mixed psychosis, beginning with lactation psychosis, and several attacks of hallucinations and depression later. Overeating was removed in all 3 patients without any negative effect on the psychotic state. All patients were able to maintain their body weight. Two patients with poorly controlled diabetes improved markedly their metabolic status. Doses up to 75 mg per day of DF were necessary during binge eating episodes in one patient. We conclude that DF can be used with care under close psychiatric supervision in psychotic patients with severe overeating.
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PMID:Dexfenfluramine in psychotic patients. 974 Oct 46

Although people with intellectual disabilities are at increased risk for psychiatric disorders, the type and rate of these problems differ between those with different causes for their retardation. In this paper, we review behavioural and psychiatric problems in persons with Prader-Willi syndrome, a disorder caused by a paternally derived deletion at chromosome 15(q11-q13) in about 70% of affected patients, and by maternal uniparental disomy in the majority of the remaining patients. In addition to the syndrome's characteristic hyperphagia and food seeking, individuals with Prader-Willi syndrome also have increased risks of nonfood, compulsive behaviours. These include skin picking, which is highly prevalent, as well as more variable rates of hoarding, redoing and concerns with symmetry, exactness, cleanliness, ordering and arranging. Relative to others with mental retardation, persons with Prader-Willi syndrome are at a marked increased risk for developing full-blown, obsessive-compulsive disorder. In addition, many people with Prader-Willi syndrome show increased rates of tantrums, oppositionality and aggression. Recent findings suggest that they also have an increased risk of psychotic disorder or affective illness with a psychotic component, especially young adult patients and those with the maternal uniparental disomy as opposed to paternal deletion. Dietary approaches include a reduced-calorie diet and increased physical activity, as well as close supervision around food and keeping food locked away. To date, neither CNS stimulants nor anorectic agents have been effective in treating hyperphagia, in part because hyperphagia in Prader-Willi syndrome is attributed to decreased satiation as opposed to increased hunger. Treatment for compulsivity and maladaptive behaviours include: behavioural programming; a structured, predictable routine; extra help with transitions; family support; and pharmacotherapy. Although formal drug studies have yet to be conducted, SSRIs have been effective in reducing skin picking, compulsivity and aggressive episodes in some individuals with Prader-Willi syndrome. Atypical antipsychotics have also proven helpful in persons with psychotic features or extreme aggression and impulsivity. Largely on the basis of case studies, the risks and benefits of these and other drugs in Prader-Willi syndrome are reviewed. Drug trials that move beyond case studies and that assess the relative efficacy of behavioural treatments alone or in combination with pharmacotherapy are sorely needed.
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PMID:Psychiatric disorders in Prader-Willi syndrome: epidemiology and management. 1261 96

Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested as a natural animal model of human depression and mood disorders.
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PMID:Metabolic depression in hibernation and major depression: an explanatory theory and an animal model of depression. 1606 29

We report the first episode of Kleine-Levin (KLS) syndrome in a 17-year-old male. The illness onset, clinical features, neuropsychological evaluation and polysomnographic recording are described. Typical symptoms hypersomnia, hyperphagia and sexual disinhibition were observed besides behavioral disturbances, polysomnographic and neuropsychological alterations. Behavioral disturbances similar to a manic episode including psychotic symptoms were relevant. The pharmacologic treatment included lithium, methylphenidate and risperidone. The introduction of risperidone aimed the control of psychotic symptoms and the persistent manifestations of hypersexuality after sleepiness control and to the best of our knowledge there are no other reports regarding risperidone use for KLS in the literature.
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PMID:Kleine-Levin syndrome: interface between neurology and psychiatry. 1742 Aug 45

People with serious mental illnesses have higher rates of morbidity and premature mortality compared with the general population. This population loses from 13 to over 20 years of life compared with their nonpsychiatric cohorts. A multitude of factors contribute to this silent tragedy. A major problem is that multiple barriers exist, making it difficult for individuals with serious mental illness to access quality health care. Additionally, compared with the average American, people with serious mental illness are more likely to engage in unhealthy lifestyle practices, such as lack of regular physical activity, poor nutrition and overeating, smoking and other substance abuse, irregular and inadequate sleep, and failure to visit health care practitioners regularly. These unhealthy behaviors and the added burden of anti-psychotic medication side effects increase the risk for cardiac and metabolic diseases. However, best-practice models exist that provide the knowledge and tools to assist people with serious mental illness in making informed decisions about healthier lifestyle behaviors, including addressing tobacco use and excess weight. The challenge is how to integrate these practices effectively into routine behavioral health care. The growing problem of premature death calls for urgent public action to transform the current mental health care system into a more integrated system of care. Because of their holistic training and approach to care, nurses are well prepared to work collaboratively with both mental and physical health care providers and systems. In the new mental health care system, both psychiatric and physical health care providers will need to broaden their treatment paradigm to address the whole person. An integral part of behavioral health services will be to ensure that the health status of all individuals is assessed, that there are medical monitoring protocols in place for people taking antipsychotic medication, that each individual has a primary care provider, and that there is an effective mechanism in place for communication between behavioral health and primary care providers. A transformation of the existing mental health care system toward a system that utilizes a coordinated, multi-disciplinary, holistic approach not only may effectively bridge the existing gap between mental and physical health, but also may ultimately save lives.
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PMID:Bridging the gap between mental and physical health: a multidisciplinary approach. 1753 97

A 15-year-old Hispanic female was started on risperidone for new-onset psychosis. The patient responded well to the gradual dose increase but developed rapid weight gain secondary to polydipsia and polyphagia. She also began complaining of nipple discharge and griping abdominal pain on the left lower quadrant by the third week of treatment. Her prolactin level escalated to three times normal with a weight gain of 12 pounds in 16 days. Risperidone was switched to another antipsychotic. Her prolactin level then dropped to a normal level within 7 days and she lost 7 pounds in the next 2 weeks. Her abdominal pain, galactorrhea, polydipsia, and polyphagia subsided within the first few days of the cessation of risperdione.
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PMID:Risperidone-induced polydipsia and polyphagia associated with galactorrhea, abdominal pain, and rapid weight gain in an adolescent Hispanic female. 1798 54

Prader-Willi syndrome (PWS) is well-known for its genetic and phenotypic complexities. Caused by a lack of paternally derived imprinted material on chromosome 15q11-q13, individuals with PWS have mild to moderate intellectual disabilities, repetitive and compulsive behaviors, skin picking, tantrums, irritability, hyperphagia, and increased risks of obesity. Many individuals also have co-occurring autism spectrum disorders (ASDs), psychosis, and mood disorders. Although the PWS 15q11-q13 region confers risks for autism, relatively few studies have assessed autism symptoms in PWS or directly compared social, behavioral, and cognitive functioning across groups with autism or PWS. This article identifies areas of phenotypic overlap and difference between PWS and ASD in core autism symptoms and in such comorbidities as psychiatric disorders, and dysregulated sleep and eating. Though future studies are needed, PWS provides a promising alternative lens into specific symptoms and comorbidities of autism.
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PMID:Prader-Willi syndrome and autism spectrum disorders: an evolving story. 2185 56


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