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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The frequency of neurologic involvement in sarcoidosis is about 5%. When the clinical picture presents with only neurological manifestations, as it did in our patient, the diagnosis at presentation is often difficult. Involvement of other tissues must therefore be actively searched. We describe a case of neurosarcoidosis, presenting with hypothalamic hypopituitarism, progressive loss of visual fields, subacute dementia and hypothalamic hyperphagia. The disease very well responded to high dose corticosteroids. The pathology, diagnostic procedures, prognosis and treatment of neurosarcoidosis are discussed.
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PMID:[Hypothalamic hypopituitarism with hyperphagia and subacute dementia due to neurosarcoidosis: case report and literature review]. 133 20

In this paper the first case of Kluver-Bucy syndrome (KBS) in Huntington's chorea is reported. The patient, a 46-year-old man with advanced Huntington's disease, displayed prosopagnosia, oral tendencies, emotional changes, hypersexual behavior, and hyperphagia associated with severe dementia. Haloperidol in moderate doses controlled both the KBS and the chorea, suggesting a possible role for the dopaminergic system in the pathogenesis of KBS in Huntington's disease. The presence of profound dementia in our patient supports the previous assertion that human cases of KBS are invariably associated with severe cognitive dysfunction. Since KBS was established as an entity, a great deal of attention has been directed to its neuroanatomical basis. However, due to the multidetermined nature of human behavior, the role of physiological, psychological, and environmental factors should also be taken into consideration with regard to the pathogenesis of this syndrome.
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PMID:Kluver-Bucy syndrome in Huntington's chorea. 316 95

Aluminum exposure in man is unavoidable. The occurrence of dialysis dementia, vitamin D-resistant osteomalacia, and hypochromic microcytic anemia in dialysis patients underscores the potential for aluminum toxicity. Although exposure via dialysate and hyperalimentation leads to significant tissue aluminum accumulation, the ubiquitous occurrence of aluminum and the severe pathology associated with large aluminum burdens suggest that smaller exposures via the gastrointestinal tract and lungs could represent an important, though largely unrecognized, public health problem. It is clear that some aluminum absorption occurs with the ingestion of small amounts of aluminum in the diet and medicines, and even greater aluminum absorption is seen in individuals consuming large amounts of aluminum present in antacids. Aluminum absorption is enhanced in the presence of elevated circulating parathyroid hormone. In addition, elevated PTH leads to the preferential deposition of aluminum in brain and bone. Consequently, PTH is likely to be involved in the pathogenesis of toxicities in those organs. PTH excess also seems to lead to the deposition of aluminum in the parathyroid gland. The in vitro demonstration that aluminum inhibits parathyroid hormone release is consistent with the findings of a euparathyroid state in dialysis patients with aluminum related vitamin D-resistant osteomalacia. Nevertheless, it seems likely that hyperparathyroidism is at least initially involved in the pathogenesis of aluminum neurotoxicity and osteomalacia; the increases in tissue aluminum stores are followed by suppression of parathyroid hormone release, which is required for the evolution of osteomalacia. Impaired renal function is not a prerequisite for increased tissue aluminum burdens, nor for aluminum-related organ toxicity. Consequently, it is likely that these diseases will be observed in populations other than those with chronic renal disease.
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PMID:Aluminum, parathyroid hormone, and osteomalacia. 642 72

We studied the clinical features, pathology, and molecular genetics of a family (Mo) with an autosomal dominant disinhibition, frontal lobe dementia, parkinsonism, and amyotrophy. We examined seven affected members and gathered clinical information on another six. The mean onset was at age 45 years. Personality and behavioral changes (disinhibition, withdrawal, alcoholism, hyperphagia) were the first symptoms in twelve. There was early memory loss, anomia, and poor construction with preservation until late of orientation, speech, and calculations. All affected members examined had rigidity, bradykinesia, and postural instability. Mean duration to death was 13 years. We studied the neuropathology of six individuals, five of whom had been examined in life. There was atrophy and spongiform change in the frontotemporal cortex, and neuronal loss and gliosis in the substantia nigra and amygdala. Two individuals, including one with fasciculations and muscle wasting, had anterior horn cell loss. There were no Lewy bodies, neurofibrillary tangles, or amyloid plaques. We call this disorder the "disinhibition-dementia-parkinsonism-amyotrophy complex" (DDPAC), based on the clinical syndrome found in this family and linkage to chromosome 17.
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PMID:Clinical characteristics of a family with chromosome 17-linked disinhibition-dementia-parkinsonism-amyotrophy complex. 793 62

Research into dementia has tended to concentrate on memory loss and other cognitive impairment, but attention has recently turned to the associated psychiatric symptoms and behavioral abnormalities. Among them, increases in the amount eaten or hyperphagia are not uncommon in dementia. This problem is of clinical importance since it not only jeopardizes patient's health, but also is a cause of caregiver burden. The aim of this study was to assess the prevalence of hyperphagia in dementia. Additionally, possible mechanisms underlying this problem were reviewed and related to the demographic data, cognitive function test, radiological findings and other psychiatric symptoms. Out of a sample of 91 demented inpatients, hyperphagia was present in 30.8%. Hyperphagia was significantly associated with delusion, misidentification, aggressive behavior, hoarding behavior and pica phenomena. But these patients did not show difference in cognitive function, radiological abnormalities, repetitive behavior and depressed mood when compared with other demented patients. The possible etiologies were discussed, including physiological and psychological factors. Hyperphagia is a complex phenomenon, better understanding of the underlying pathogenesis may highlight specific pharmacological or behavioral methods for the management this troublesome behavior.
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PMID:[Characteristics of dementia patients with hyperphagia]. 870 88

The disease is named after George H. Whipple who, in 1907, was the first to describe an intestinal "lipodystrophy". Although Whipple's disease is generally recognized as a multisystem chronic granulomatous disease, primarily involving the digestive system, it can also appear as a primary neurological disorder in rare cases. Most often it is manifested with loss of weight, diarrhea, malabsorption, abdominal pain, lymphadenopathy, cardiopathy, hyperpigmentation and hypotension. The presence of periodic acid-Schiff (PAS)-positive macrophages in biopsy specimens (not only jejunal) and demonstration of "Whipple's bacilli" visible by electron microscopy, are diagnostic signs of active Whipple's disease. Whipple's disease confined to the CNS is rare. It is rarely found in the differential diagnosis of patients with progressive neurological deterioration. The most common neurological picture includes progressive dementia, external ophalmoplegia, myoclonus, seizures, ataxia, hypothalamic dysfunction (sleep disorders, hyperphagia, polydipsia) and meningitis. Oculofacial-skeletal myorhythmia as a movement disorder, associated with Whipple's disease, is reported. Fulminant course of cerebral Whipple's disease is unusual and unfavourable. The confusing and nonspecific clinical appearance is typical for primary CNS involvement. It has recently been suggested that CNS involvement occurs in all cases, although only 10-20% of patients may show it. The CNS is the most common site of disease relapse. The CT scans and MRI of the brain are often normal, but may show cortical/subcortical atrophy, hydrocephalus, focal or intracerebral mass lesions. The cerebrospinal fluid can sometimes contain PAS-positive macrophages. Brain biopsy is suggested as a diagnostic method in cases of high suspicion of CNS Whipple's disease. However, the lesions are frequently inaccessible and false negative. Without extended antibiotic therapy, the course of Whipple's disease is lethal. Now, the prognosis is good, although the optimal antimicrobial regimen is not clearly established. Initial parenteral therapy (tetracycline, penicilline, streptomycine, chloramphenicol, ampicilline) and peroral long-term treatment with trimetoprime-sulphametoxasole, are recommended. As CNS relapse of Whipple's disease may occur after several years, long-term treatment should include antibiotics that are able to cross the blood-brain barrier. The CNS relapse, in contrast to the systemic ones, is resistant to the treatment. Appropriate therapy instituted earlier in the course of the disease is associated with a better neurological outcome. Early recognition can be critical in Whipple's disease because of irreversible neurological sequelae seen later in the course of this potentially treatable condition. In cases with high clinical suspicion in which Whipple's disease cannot be diagnosed with procedures such as jejunal biopsy, antibiotic therapy is recommended. Recovery of an established neurological deficit may rarely occur. Longterm follow-up studies would help to identify the optimal antibiotic regimen and duration of treatment.
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PMID:[Neurologic disorders in Whipple's disease]. 910 28

Up to one third of dementia sufferers eat an increased quantity of food, compared with their premorbid intake, at some stage during the dementia. A proportion of these eat extraordinarily large quantities if food intake is not restricted. In order to investigate this phenomenon in detail, a reliable and standardized method of quantifying the degree of hyperphagia is required. We report the development of such a method. Twenty-six people with dementia, who were reported by their carers to be hyperphagic, were compared with 14 matched non-hyperphagic controls with dementia and 14 matched normal elderly. Subjects were offered two standardized meals, under specified conditions, ad libitum. One meal consisted of a single food, the other of a mixture of foods. The total energy intake provided a reliable measure of the degree of hyperphagia. The single food meal was more reliable but the mixed meal was a more sensitive measure of the hyperphagia.
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PMID:Hyperphagia in dementia: 1. The use of an objective and reliable method for measuring hyperphagia in people with dementia. 915 49

This report studied behavioural disturbances in psychiatric inpatients with dementia of the Alzheimer's type (DAT) in Taiwan. The sample consisted of 75 inpatients with DAT who were consecutively admitted to the geropsychiatric ward. Their behavioural disturbances were obtained from semistructured interviews with families and ward observation. There were eight main behavioural disturbances: getting lost, repetitive phenomena, sleep disturbance, aggression, wandering, hyperphagia, hoarding behaviour, and inappropriate sexual behaviour. Number of behavioural disturbances, wandering, hyperphagia and sleep disturbance were significantly associated with the severity of cognitive impairment.
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PMID:Behavioural disturbances in psychiatric inpatients with dementia of the Alzheimer's type in Taiwan. 930 67

The patient was an 86-year-old man with mild dementia, and a urinary bladder catheter already inserted for benign prostata hypertrophy. At this time he had jaundice due to duodenal papillary cancer and was inserted with a percutaneous transhepatic bile drainage tube (PTBD). Additionally, due to an obstruction of his duodenum, he received a percutaneous endoscopic gastrostomy tube (PEG) for suction of gastric juice and intravenous hyperalimentation catheter (IVH) for nutrition. He always wished to return home. The medical staff and his family discussed this many times to realize his hope. We his daughter-in-law how to handle the 4 tubes. When she learned how, he went home and was on the visiting care system. But only one week after, despite his stability, his son, who was living apart got drunk and sent him back to the hospital. We tried to persuade them, including all family members living apart. At last he could return home again, and one week after died quietly at home. We learn from this case that it is important and very difficult for a family to accept a terminal cancer patient at home. It is necessary to advice them from two stand-points, the medical techniques and the mental aspects.
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PMID:[For terminal cancer patient inserted with four tubes to live at home--from discussion with family]. 942 58

This study examined patterns and associates of excessive eating (hyperphagia) in a community-based registry of patients with dementia. From patients enrolled in the Mayo Clinic Alzheimer's Disease Patient Registry (n = 439), 39 were identified with excessive eating reported on the Behavior Symptom Checklist at some time during their illness. They were matched for age, gender, duration of disease, and Global Deterioration Scale (GDS) score to "normal eaters." Annualized weight change was determined based on weight from the 6 months before the evaluation to weight 6 months after the evaluation. Annualized weight change scores were not significantly different between excessive eaters and normal eaters nor between wanderers and nonwanderers. In cross-sectional analysis, univariate modeling suggested age at onset, GDS, and Mini-Mental State Examination score to be significant predictors of excessive eating. Using multivariate logistic model with backward elimination, only age of onset and GDS were retained as associates of excess eating. Rater type also emerged as a significant predictor for excessive eating with family raters reporting this behavior in 16% of patients compared to 5% for other raters. In chi-square analyses excessive eating was associated with greater frequency of wandering, unpredictable behavior, inappropriate dressing, inappropriate bodily concerns, and threatening self-harm. Associates of excess eating were subsequently examined separately in wandering and nonwandering excessive eaters. Logistic modeling suggested that among nonwanderers, patients who were younger but more severely demented were likely to have reported excessive eating. These results suggest hyperphagia to be present in approximately 10% of a community-based cohort of patients with dementia and associated with increasing functional decline. Excessive eating does not appear to arise from memory dysfunction, but for wanderers may result from needing increased caloric intake because of increased activity levels. Thus, for wandering excessive eaters, it may be appropriate to endure the eating to ensure appropriate caloric intake. Nonwandering excessive eaters were younger, had greater dementia severity, and had more unpredictable behavior. They may have dementia with prominent frontal lobe involvement and may respond to any food stimulus respective of hunger. Restricting food exposure may be an effective management intervention for them.
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PMID:Patterns and associates of hyperphagia in patients with dementia. 965 90


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