Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of autoptically verified progressive subcortical gliosis (PSG) is reported. The 79 year old woman developed subacutely a right sided hemisyndrome and a cerebellar syndrome. Generalized action myoclonus of the left leg evolved into left sided Epilepsia partialis continua and dementia appeared. After a 6 month course the patient died of aspiration pneumonia. There was no indication of alcoholism or HIV-dementia neither clinically nor at autopsy. Morphologically the brain showed a diffuse proliferation of astrocytes in the subcortical white matter, thalamus, basal ganglia, brain stem and cerebellum. A severe neuronal dropout was found in medial thalamic neurons but Wernickes encephalopathy was ruled out. 21 cases of PSG confirmed by autopsy were found in the literature. Clinics, neuropathology and classification of PSG is discussed.
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PMID:[Progressive subcortical gliosis]. 193 41

Progressive supranuclear palsy is sufficiently rare and difficult to diagnose that it escaped clinical recognition until 1964, when Steele, Richardson, and Olszewski clarified it as a pathologic entity. From January 1981 to June 1989, 7 patients who fulfilled the Golbe's criteria of progressive supranuclear palsy were admitted to the neurological department of National Taiwan University Hospital. The mean age at onset was 60 years (range: 53-69 years), and the mean age at diagnosis was 63 years), and the mean age at diagnosis was 63 years (range: 55-71 years). The study failed to identify any specific risk factors associated with progressive supranuclear palsy. Unsteady gait, vertical gaze palsy, pseudobulbar palsy, parkinsonian features and dementia were noted in all cases. The brain computed tomography revealed mild cortical atrophy and ventricular dilatation in 5 patients. Additionally, electroencephalography revealed diffuse theta waves in 4 patients and temporal theta waves in 2 patients, but these findings were nonspecific. Nystagmograms were performed in 3 patients, and hypometric saccades were noted in all of these patients, and uninhibited neurogenic bladder was proven by cystometry in 2 of these patients. All patients were treated with levodopa, but none of the patients showed any beneficial effects. Two patients died of aspiration pneumonia; the average duration from onset to death was about 4 years.
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PMID:[Progressive supranuclear palsy: clinical report on 7 cases and review of literature]. 197 8

The terminal phase of dementia is initiated by the inability to swallow. New techniques of enteral alimentation permit more effective, longer intubation. To assess the application of these new techniques to late-stage demented aged patients, all current intubations in a teaching nursing home were reviewed. Of 52 feeding intubations, 26 had been in situ for more than 1 year. A randomly selected comparison group of nonintubated patients was also studied. Weight increased for 48% of the intubated group versus 17% of the nonintubated group (P less than .01). Aspiration pneumonia occurred more often in the intubated group (58%) than in the nonintubated group (17%) (P less than .01). Decubitus ulcers were also more common in the intubated group (21%) than in the nonintubated group (14%). Restraints were used more in the intubated group (71%) than in the nonintubated group (56%). These differences did not reach statistical significance. All of the intubated patients were severely demented, with MMSE scores of zero. Seventy-one percent of the nonintubated group were demented, with MMSE scores of less than 23. Prolongation of the terminal phase of dementia in the aged by tube feeding is now feasible. The implications of this change in the life-span of demented nursing home patients need attention by families, nursing homes, and those who make public health policy.
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PMID:Long-term enteral feeding of aged demented nursing home patients. 190 36

We report the clinical and neuropathological findings in an autopsy case of progressive dementia, Parkinsonism, pseudobulbar palsy and supranuclear ophthalmoplegia. Since 70 years old, this hypertensive patient developed forgetfulness, unsteady gait and festination. These symptoms rapidly worsened and he was admitted in October 1983, at age 71. He had severe dementia and showed stiff face. Voluntary vertical movement of the eyes was severely disturbed, but reflex vertical movement by the doll's head eye maneuver was not affected. Muscle tone in the limbs increased slightly, and deep tendon reflexes were hyperactive in jaw and the upper extremities. Babinski sign was negative bilaterally. Sensation and coordination remained normal. Although he was not paretic or ataxic, his movements were very slow. He could not stand by himself and easily fell backward. These clinical features resembled those of progressive supranuclear palsy except for severe dementia and rapid progression. Brain CT scan revealed marked dilatation of the lateral ventricles, prominent periventicular lucency and atrophy of brainstem and cerebral cortex. Treatment with levodopa slightly improved his movement, but difficulty in swallowing worsened increasingly. He died of hypoglycemic coma and aspiration pneumonia in September 1984, about two years after the initial symptoms. General autopsy showed severe pneumonia and atrophy of the liver. The brain weighed 1,210g. Atherosclerotic change in the cerebral arteries were mild. Coronal sections of the cerebral hemispheres revealed diffuse ischemic change and multiple small infarctions in the bilateral cerebral white matter. Cortical atrophy was observed in the cerebral hemispheres. The basal ganglia, thalamus, and pons showed status lacunaris. Atrophy of midbrain and depigmentation of the substantia nigra were observed macroscopically.
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PMID:[Progressive supranuclear palsy accompanied with progressive subcortical vascular encephalopathy of Binswanger type--a case report]. 275 47

Progressive supranuclear palsy (PSP) is an uncommon, but debilitating, neurological disease. Characterized by paralysis of eye movements, difficulty talking and swallowing, body trunk rigidity, gait ataxia, and dementia, the disease progresses rapidly over a 6-8 year time span. Death usually occurs from aspiration pneumonia. To provide meaningful care for the PSP patient and his/her family, the neuroscience nurse must first understand the disease pathophysiology, then the appropriate care interventions.
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PMID:Progressive supranuclear palsy: nursing care implications. 297 88

To determine if there are any unique features of nursing home-acquired pneumonia we carried out a case-control study wherein each patient admitted with nursing home-acquired pneumonia was age- and sex-matched with a patient with community-acquired pneumonia. There were 36 men and 38 women in the nursing home group. The mean age of both groups was 74 years. The mortality rate for nursing home-acquired pneumonia it was 40.5%, whereas for community-acquired pneumonia it was 28% (P = NS). Patients with nursing home-acquired pneumonia had a significantly higher incidence of dementia and cerebrovascular accidents, and patients with community-acquired pneumonia were more likely to be smokers and to have chronic obstructive pulmonary disease. Aspiration pneumonia was more common among patients with nursing home-acquired pneumonia (P less than .001), and Hemophilus influenza pneumonia more common among the patients with community-acquired infection (P less than .01). Sputum for culture could be obtained in only 31 and 39% of the patients--contributory to the high rates of pneumonia of unknown etiology 63.5 and 56.1% for the nursing home group and the control subjects, respectively. Patients with nursing home-acquired pneumonia received cloxacillin and aminoglycosides more frequently than patients with community-acquired pneumonia (P less than .05), and patients with community-acquired pneumonia received erythromycin more frequently than patients with nursing home-acquired pneumonia (P less than .05). Complications were common during the hospital stay of these patients--the most frequent being congestive heart failure, urinary tract infection, renal failure, and respiratory failure.
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PMID:Nursing home-acquired pneumonia. A case-control study. 348 49

We report a 86-year-old woman who developed dementia, gait disturbance, speech disturbance, and right hemiparesis. The patient was well until March of 1979 when upon wakening up on one morning she noted slurring of her speech and weakness in her left upper and lower extremities. These symptoms cleared up during the next several months, however, she noted weakness in her left leg again in May 1985. In 1988, her posture became stooped and she walked in small steps. In 1990, she developed memory disturbance and difficulty in naming. In March 1993, she developed weakness in her right hand; she was treated with aspirin and amantadine HCl, however, she deteriorated during the next two week period, and was admitted to our hospital on March 27, 1993. On admission, she appeared alert, however, she could not answer verbally to questions; she could only utter unintelligible sounds. Apparently she was markedly demented. Her blood pressure was 170/98 mmHg, and general physical examination was unremarkable. Cranial nerves were grossly normal except for marked non-fluency in her word expression. She could not stand or walk, and apparently her right upper and lower extremities were paralyzed with some contracture. Deep reflexes were normally active without asymmetry. Chaddock sign was positive bilaterally. Sensory examination was difficult. Pertinent laboratory examination included WBC 13,000/microliters, BUN 152mg/dl, creatinine 3.75mg/dl, CRP 20.1mg/dl; a chest X-ray film revealed pneumonic shadow in the upper and the middle right lung fields. Cranial CT scan revealed multiple lacunar infarctions in both basal ganglia and cerebral white matters; periventricular lucency was also noted. She was treated with antibiotics and intravenous fluid. Acid-fast bacilli were recovered from sputum, and she was transferred to another hospital for the treatment of pulmonary tuberculosis. After its treatment she returned to our hospital on July 8, 1993, when her condition was complicated with aspiration pneumonia. On admission, she was semicomatose, and no intelligible words were heard. Right facial paresis of the central type was noted. She was unable to stand or walk, and her right upper and lower extremities were paretic. Deep reflexes were increased with extensor toe sign on the right. She was treated with chemotherapy and intravenous fluid, however, her clinical course was complicated with respiratory as well as urinary tract infections. She developed cardiac as well as renal failure and expired on September 25, 1993.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 86-year-old woman with dementia, gait and speech disturbance, and right hemiparesis]. 754 29

A 26-year-old housewife, born of consanguineous parentage, began to have gait and speech disturbance. Her brother had died from suffocation because of dysphagia. At thirty-two, she developed difficulty in swallowing, clumsiness and incontinence. When she was thirty-six she had pseudobulbar palsy, vertical gaze paresis, hyperreflexia and muscular atrophy of the upper half of the body. CT scan showed cerebral atrophy. Her mental function progressively deteriorated and amyotrophic lateral sclerosis associated with dementia was suspected. She died at the age of thirty-seven. Diagnosis was made only by autopsy. There was no particular general pathologic finding excepting aspiration pneumonia. Microscopical examination revealed numerous distended neurons with accumulation of light brown pigments by Luxol fast blue/H & E stains, especially in hypothalamus, substantia nigra and nuclei of oculomotor nerves. To a lesser extent such neurons were noted ubiquitously. The stored material was mainly composed of lipofuscin and ceroid. Ultrastructurally they presented the various structures which have previously been reported, except for finger print profiles. The pigmentary deposits were shown to be immunoreactive with polyclonal antibody directed against amyloid beta-protein.
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PMID:[Dementia and amyotrophy in Kufs disease. The adult type of neuronal ceroid lipofuscinosis]. 774 8

We report a 78-year-old man with progressive gait disturbance, dementia, and dysphagia. He was apparently well until 75 years of age in 1989 when he had an insidious onset of gait disturbance. In October of 1991, he was treated with levodopa and amantadine HCl in another hospital, but he developed visual hallucination right after these medications, and the drugs were discontinued. He also developed difficulty in swallowing with frequent aspiration pneumonia. He was admitted to our hospital on January 13, 1992. On admission, the patient was chronically ill Japanese man; his blood pressure was 118/70 mmHg, body temperature 35.4 degrees C, and heart rate 72 and regular. No anemia or jaundice was noted; lungs were clear and no heart murmur was audible. The abdomen was flat but rigid to palpation without tenderness; no organomegaly was noted. On neurologic examination, he was alert but disoriented to all spheres; he was apparently demented and the score of the mini-mental test was 11. He did not appear to have aphasia or apraxia. Cranial nerves appeared intact, but he had a mask-like face and a slight limitation in the upward gaze; his voice was small. He was unable to stand or walk; he showed marked akinesia and moderate rigidity in his neck and the trunk. Deep reflexes were generally elicited normally or slightly weakly. Plantar response was extensor on the left and flexor on the right. No grasp reflex was present. Sensory examination showed questionable loss of touch in the glove- and -stocking distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 78-year-old man with progressive gait disturbance, dysphagia, and dementia]. 819 46

We report a right-handed 62-year-old man with early onset familial parkinsonism. The patient was well until 24 years of the age when he noted an onset of resting tremor in his right hand. During the next four years, he noted rigidity, bradykinesia, and difficulty in walking. He was seen in another hospital at 28 years of the age, where he received left pallidotomy. Rigidity on the left side showed marked improvement. He received right pallidotomy at age 30 years. He developed right hemiplegia after this surgery. He was admitted to our hospital in March, 1983 when he was 51 years of the age. He was treated with levodopa but improvement was rather of minor degree. He was transferred to another hospital, but his motor disturbance progressed slowly, and was admitted again to our hospital in November 1990. He had 6 siblings 4 of whom including himself suffered from parkinsonism. No consanguinity was noted in parents. On admission, he appeared chronically ill but the general physical examination was unremarkable. Neurologic examination revealed an alert and mentally sound man. Hasegawa dementia scale was 28.5/32.5. Upward gaze was slightly restricted (3/5). Cranial nerve examination revealed oculogyric crisis, apraxia of eyelid opening, masked face, and small voice. He was able to stand with support; his posture showed left-ward leaning. He had right hemiparesis with moderate weakness. He showed marked bradykinesia and moderate rigidity in his left upper extremity. Fine postural tremor was noted in the left hand. Deep tendon reflexes were diminished in the upper extremities. No Babinski sign was noted. Pain sensation was somewhat diminished on the right side. Results of routine laboratory examination were unremarkable. Cranial CT scan revealed atrophy in the frontal lobe, particularly in the prefrontal area. In addition, MRI revealed T1-and-T2-low signal intensity lesions in the right ventral pallidal region and in the left ventrolateral thalamic-hypothalamic areas. He was treated with 600 mg of levodopa with benserazide and 22.5 mg of bromocriptine with mild to moderate improvement in his bradykinesia and rigidity. He was discharged in January 1991. His clinical course was complicated by intestinal obstruction in October, 1994. He was admitted to another hospital where he was operated on the obstruction on November 5, 1994. The sigmoid colon was markedly dilated but no mass was found. Postoperative course was uneventful until November 18, 1994 when he was found dead in his hospital room shortly after 4 am. The patient was discussed in neurological CPC, and the chief discussant arrived at the conclusion that the patient had young-onset familial Lewy body-negative parkinsonism. Opinions were divided between Lewy body-positive familial Parkinson's disease and Lewy body negative young onset parkinsonism. Postmortem examination revealed aspiration pneumonia, which appeared to be the cause of his death, in the right lung. Neuropathologic examination revealed loss of malanized neurons in the substantia nigra and the locus coeruleus. In the substantia nigra, neuronal loss was particularly severe in the ventrolateral area. No Lewy bodies were seen. The dorsal motor nucleus of the vagal nerve was well preserved. Stereotaxic lesions involved bilateral thalamic areas. This patient appears to represent a case of autosomal recessive juvenile parkinsonism (AR-JP). Early onset, superb response to levodopa, sleep effect, and easy development of dyskinesias and motor fluctuations characterize AR-JP. The reason why this patient did not show these clinical features is probably bilateral sterotaxic surgeries. Particularly, the second surgery was complicated by right hemiparesis. His siblings who developed parkinsonism showed typical clinical features of AR-JP.
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PMID:[A 62-year-old man with familial parkinsonism with the onset at 24 years of the age]. 870 64


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