Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A man aged 70, descendant of an apparently healthy family, showed disorientation, delusional ideas and rages at 66. Later there was slowly advancing deterioration with muteness, disorientation and dysphagia. He died of cardiac failure. There was the diffuse atrophy of the cerebrum, which was remarkably accentuated on both temporal lobes (poles, T2 and T3), where the loss of nerve cells and proliferation of astrocytes were found in the cortex and pallor and conspicuous fibrillary gliosis were noted in the white matter. These findings fundamentally suggest Pick's disease. On the one hand, numerous senile plaques and Alzheimer's neurofibrillary changes, suggestive of Alzheimer's disease (senile dementia), were observed throughout the cerebral cortex. On the other hand, a few inflated cells were also seen in the cingulate, superior frontal gyri and temporal lobes. Basilar artery was moderately atherosclerotic and cerebrovascular disorders were distributed throughout the cerebral cortex and basal ganglia, especially in the field of supply of middle cerebral artery. This case is similar to rare cases reported by Berlin (1949), Neumann (1949) and Oyanagi et al. (1975). The nosological situation as a disease entity remains to be determined.
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PMID:An autopsy case of atypical senile dementia with atrophy of the temporal lobes--a clinical and histopathological report. 66 3

Numerous Caucasian familial Alzheimer's disease (FAD) pedigrees have been described in the literature, while only 21 Japanese FAD families have been reported to date. Here we report the clinical findings and the result of molecular genetic analysis of 4 patients from two FAD kindreds, OS-2 and OS-3. The proband in OS-2 family has developed loss of recent memory and place disorientation age at 43. A brain CT showed severe diffuse cortical atrophy. Her younger brother had dementia at 42 years and her mother and other 3 siblings had also dementia symptoms suspected to be Alzheimer's disease. The proband in OS-3 family showed declining recent memory at 49 years and developed dysphagia, gait disturbance and emotional incontinent with cerebral atrophy at 52 years. His father and elder brother demonstrated dementia signs at 60 and 54 years old, respectively. Recently it was reported that affected members from 2 Caucasian kindreds with FAD had missense mutation in exon 17 of the gene for amyloid precursor protein (APP). Patients from three different Japanese kindreds with FAD also showed the same mutation on the APP gene. Amino acid substitution (Val-Ile) at codon 717 by this mutation is responsible for FAD in at least some kindreds. We used genomic DNA from 4 affected members of 2 families to determine whether the disease in these families is associated with a APP717 mutation and the mutated codons, 102, 117, 129, 178 and 200, on the gene for protease-resistance prion protein (PrP) which cause transmissible dementia, Creutzfelt-Jacob disease (CJD) and Gerstmann-Strausler syndrome (GSS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two kindreds with familial Alzheimer's disease--analysis of the APP717 mutation and the mutated genes for the prion protein]. 135 66

Atypical dementias confront the adequacy of current diagnostic concepts. The two patients with atypical dementia syndromes described here shared common postmortem features of numerous neocortical neuritic (senile) plaques and microvascular amyloid, sparing of hippocampus and substantia nigra, and the virtual absence of neurofibrillary tangles. Microscopically, the two differed only by the presence of a few subcortical Lewy bodies in case 1. These similar morphologic features were associated with dramatically different clinical presentations. In the first patient, visual hallucinations, Capgras' syndrome, cognitive slowing, myoclonus, parkinsonism, and primitive reflexes evolved over 3 years. Memory and language were relatively spared. In the second, dysphagia, nonfluent aphasia, hypophonia, motor perseveration, and a severe disorder of attention developed during this 18-month illness. At autopsy, an unrecognized colon malignancy was found. Despite high neuritic plaque counts in cortex, neither the clinical nor the pathologic criteria for Alzheimer's disease adequately describe either case. The cases will be examined first as clinical, then as neuropathologic, entities. From this approach, we conclude that a specific clinical dementia syndrome may be expressed by several neuropathologic "diseases" and that a variety of clinical syndromes may represent a single neuropathologic diagnosis. This strategy identifies a conceptual dichotomy between Alzheimer's syndrome and postmortem Alzheimer's disease. Meticulous clinical and neuropathologic observation is essential in advancing an understanding of the relationship between the two.
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PMID:Alzheimer's disease or plaque disease? Two cases at the frontier of a definition. 141 64

The nutritional consequences of dementia and the role of diet in the etiology, treatment, and prevention of dementia are the subjects of this review. The major cause of dementia is Alzheimer's disease. Although it has been suggested that aluminum intake may cause this disease, the bulk of scientific evidence suggests that this is unlikely. Dietary supplements of choline and lecithin have been used to treat Alzheimer's disease but are ineffective. Alzheimer's disease patients are at risk of developing protein-energy malnutrition because of poor food intake and increased energy requirements. The second most common cause of dementia is multi-infarct dementia, caused by multiple strokes. Diet may play a role in the prevention of this form of dementia through effects on blood pressure and other risk factors. Control of risk factors may also prevent further progression of the dementia. Patients with multi-infarct dementia often have dysphagia. The third most common cause of dementia appears to be excessive alcohol intake, due both to the direct neurotoxic effects of alcohol and to the effects of alcohol on nutritional status. Alcoholic dementia may be at least partially reversible with abstinence and good nutrition. Other causes are vitamin B-12 and folate deficiencies; these are reversible dementias. In all types of dementia, adequate nutrition may improve physical well-being, help maximize the patient's functioning, and improve the quality of life.
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PMID:Nutrition and dementia. 224 59

17 parameters of vital activity (VA) were scanned in 35 female and 12 male dependent geriatric patients (mean age 81). These included mental testing, Barthel score, lung function, urinanalysis, creatinine clearance, Hb, albumin, globulin and electrolytes, skin-folds, locomotion, presence of IHD, hemodynamic state, continence, infections, WBC and lymphocyte count, pressure sores and dysphagia, 4 main templates of VA deterioration identified were: IHD, hemisyndrome (due to CVA), vegetative state (post-CVA) and senile dementia (SDAT). The IHD template was characterized by marked variations in VA, ending in death due to cardiac complications (pulmonary edema, ischemia, etc.). In the 3 other templates VA gradually deteriorated. Gradual declining VA allowed assessment of individual mortality prognosis. Assessment was by approximation of the computed exponent of the extrapolated VA curves; the longer the observation, the fewer the mistakes in assessment. Epidemiologic prognosis data of 48 dependent patients is described; mean age was about 81 years. Hospitalization mean was 853.5 +/- 601 days and for patients with dementia, 1158.6 +/- 622.7 days.
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PMID:[Assessment of vital activity in geriatric patients]. 781 43

We reported a 67-year-old male, who suffered from apraxia and amnesia for 2 years and for muscle rigidity of right extremities for a year. Neurological examination revealed dysarthria, dysphagia, marked dystonia of right arm, hyperreflexia of all limbs and ataxic gait. He also had dementia and many other higher cortical dysfunction mostly due to left hemisphere damage. No impairment of eye movement was disclosed. Brain MRI as well as CT showed the significant brain atrophy in the left parieto-occipital region. A degenerative atrophy was suspected by 123I-IMP-SPECT and 18F-FDG-PET. By FDG-PET, the decrease of cerebral blood flow and glucose metabolism was detected not only affected unilateral cerebral cortex including primary motor area but ipsilateral basal ganglia and thalamus. Although, it is difficult to distinguish clinically CBD from atypical case of Alzheimer's disease, we speculated that in early stage of dementia, significant unilateral hypoperfusion and hypometabolism of basal ganglia and thalamus is characteristic of CBD.
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PMID:[Clinically diagnosed corticobasal degeneration (CBD)]. 833 74

Neuroleptic medications may result in extrapyramidal symptoms that can affect swallowing. Both oral and pharyngeal phases of swallowing may be affected. Unlike the more common causes of dysphagia, especially in the elderly, drug-induced dysphagia may be reversible. This report describes a case of neuroleptic-induced dysphagia in an elderly male with Alzheimer's disease. When the loxapine was discontinued, the dysphagia improved significantly.
Dysphagia 1997
PMID:Neuroleptic-induced dysphagia. 929 35

Eating impairment is well documented in the late stage of Alzheimer's disease (AD) but when these eating changes actually begin in the disease process is not known. Eating was defined as consisting of two components, self-feeding and swallowing. Self-feeding and swallowing of healthy elderly were compared with a group of individuals with mild AD. AD subjects received significantly more partner-initiated cues or direct assistance than controls. In addition, subject-initiated cued behaviors occurred more frequently in the AD group. AD subjects demonstrated significantly prolonged swallow durations for the oral transit duration (cookie), pharyngeal response duration (liquid), and total swallow duration (liquid). This pilot study suggests that self-feeding and swallowing changes may occur early in the course of AD.
Dysphagia 1997
PMID:Eating changes in mild-stage Alzheimer's disease: a pilot study. 929 42

Making palliative care decisions for a patient who lacks decision-making capacity presents several challenges. Other people, such as family and caregivers, must choose for the patient. The goals and values of these decision makers may conflict with those of each other and with those of the patient, who now lacks the capacity to participate in the decision. This paper presents a case study of a patient with severe Alzheimer disease who has two common clinical problems: neurogenic dysphagia and aspiration pneumonia. The case study describes a consensus-based decision-making strategy that keeps what is known about the patient's wishes and values in the foreground but also expects guidance from the physician and elicits input from family members and other people who care for and have knowledge about the patient. The steps of this process, including key clinical prompts and potential transition statements, are outlined and described. The overall goal of the case commentary is to demonstrate that physicians can guide a highly emotional and personal process in a structured manner that has meaning for the patient, family, physician, and other caregivers.
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PMID:A consensus-based approach to providing palliative care to patients who lack decision-making capacity. ACP-ASIM End-of-Life Care Consensus Panel. American College of Physicians-American Society of Internal Medicine. 1036 74

In Alzheimer's disease (AD), an association was found between autonomic dysfunction and frontal hypoperfusion in brain during orthostatic testing. To ascertain whether frontal hypoperfusion is dependent on longitudinal effects of hemodynamic disturbances, or contributes to them, we studied the relationship between the presence of orthostatic hypotension (OH) and resting cerebral blood flow (CBF) in late stages of AD. Twelve women with senile dementia of Alzheimer type (SDAT), and 15 non-demented women (mean age 82.6 years, SD 3.8 vs 81.8 years, SD 3.5) were examined with the orthostatic test. Four of 12 patients with SDAT, and 9 controls had OH (defined as systolic blood pressure fall > or = 20 mmHg). CBF was determined under resting conditions using 600 Mbq 99mTc HMPAO single photon emission computerized tomography (SPECT), and quantified in cortical areas in relation to cerebellum. In patients with SDAT and OH, CBF was lower in frontal and parieto-frontal cortical areas than in SDAT patients without OH. The former group was younger and had a shorter dementia duration. No significant differences in CBF were observed between controls with vs without OH. No differences in SDAT patients with or without OH were observed in the Berger dementia scale or Katz' ADL index. No difference in incidence of symptoms related to autonomic disturbances (diarrhea, obstipation, dysphagia, vertigo) was observed in either the SDAT or control group with regard to OH presence. We conclude that during the course of AD, OH can contribute to frontal brain changes and may exacerbate the disease. The further involvement of frontal dysfunction in aggravating blood pressure dysregulation in the elderly is discussed.
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PMID:Orthostatic hypotension in Alzheimer's disease: result or cause of brain dysfunction? 1047 10


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