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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of a 44-year-old male with progressive subcortical gliosis was presented. The clinical manifestations included mental activity, difficulty in attention, euphoria and inability to work. The impairement of memory was not evident and his personality was fairly well preserved. Neurological examination showed no abnormality. The course was progressive without remission and the patient died with pneumonia approximately fifteen months after the onset of the disease. Laboratory tests revealed unremarkable except for slight degree of glucosuria and elevated F.B.S. Electroencephalography and carotid angiography were within normal. Neuropathological finding revealed that brain weighed 1200 g. and moderate degree of atrophy on frontal to parietotemporal lobes was evident. Occipital lobe was not involved. Microscopic examination revealed such changes as fibrillary gliosis in the cerebral white matter and grey matter in the spinal cord. The lesion in the cerebral white matter was predominent in the frontal lobe. Striatum and brain stem also showed mild degree of fibrillary gliosis. No senility related change such as senile plaque, granulovacuolar degeneration and Alzheimer's neurofibrillary tangle was found. The clinicopathologic findings in this case supported a diagnosis of progressive subcortical gliosis which was first described by Neumann in 1949.
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PMID:[Autopsy case of progressive subcortical gliosis]. 103 71

Using reverse genetic techniques, the gene responsible for familial Alzheimer's disease (FAD) is one of the clues to identify the pathogenesis of Alzheimer's disease (AD). Recently a missense mutation in the APP (amyloid precursor protein) gene (generally this mutation was called APP717) was detected in 2 Caucasian AD families and the same mutation was found in 3 Japanese AD families. We experienced brother's cases who were diagnosed as AD. Both of them and one normal person of the next generation had APP717. The first symptom of the elder brother (case 1) was forgetfulness at 52 years old, then dementia was advanced. In his clinical course there were characteristic findings such as the mirror sign, pseudodialog and jargon which has been rarely described in the Japanese literature. Finally he died of pneumonia at 57 years old. He was diagnosed as AD pathologically and physical findings of brain CT, SPECT (single photon emission computed tomography) and EEG supported this diagnosis clinically. The first symptom of the younger brother (case 2) was also forgetfulness at 45 years old, then severe dementia was advanced, at last he died of pneumonia at age 53 old. On the other hand the mother of the brothers died of severe dementia, so it was suspected that brothers died of severe dementia, so it was suspected that she had had AD. The clinical courses and pathological findings were thought to be typical of AD, namely there were no significant differences in comparison with other cases of FAD and sporadic AD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Affected siblings with Alzheimer's disease had missense mutation of codon 717 in amyloid precursor protein gene]. 134 30

We describe an elderly patient with probable Alzheimer's disease whose EEG and clinical status improved rapidly coincident with normalization of temperature. This finding suggests that her transient illness, of fever, pneumonia and confusional state, triggered the production of this periodic EEG pattern. With the increased prevalence of dementia in our aging population, we predict that the appearance of a multifocal periodic triphasic sharp wave pattern in the EEG of chronically demented patients (with superimposed infection) will become more common. Only when this pattern persists over time and the patient is not systemically ill, is this pattern a reliable discriminator for CJD. Serial EEGs in this setting (after treatment of the systemic illness) might reveal the transient nature of the periodic EEG change, thus avoiding the erroneous conclusion that the patient's dementia is a manifestation of CJD.
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PMID:Transient appearance of periodic EEG discharges in senile dementia. 203 43

A case of juvenile Alzheimer's disease with various neurological features such as myoclonus, also showing grumose degeneration in the dentate nucleus was reported. In a 35 year old woman, at first myoclonus, and 5 years later, progressive dementia were found. She, then, fell into apallic syndrome 9 years later, and died of pneumonia at the age of 53. She had no particular family history. Neurological examination disclosed cerebellar ataxia, left hemiparesis, convulsion in addition to myoclonus. Neuropathologically, there were a lot of senile plaques and neurofibrillary tangles in the cerebral cortex. A marked myelin loss in the white matter and a neuronal loss in the basal ganglia were also found. And grumose degeneration in the cerebellar dentate nucleus distinctively characterize the present case. The myoclonus and cerebellar ataxia could be attributed to the grumose degeneration. Two similar cases had been previously reported. Juvenile Alzheimer's disease with grumose degeneration like the present case was considered to be one of the subgroups of Alzheimer's disease.
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PMID:[A case of juvenile Alzheimer's disease with various neurological features such as myoclonus, showing grumose degeneration in the dentate nucleus]. 222 61

We have studied 97 patients with dementia who have been discharged from our hospital and 106 inpatients with dementia who have been admitted during last two years in our hospital. The diagnosis of dementia was done according to the criteria of DSM-III. Based on their clinical course, neurological signs, Hachinski's ischemic score and neuroradiological findings, we divided patients into 4 groups, [senile dementia of the Alzheimer type (SDAT), vascular dementia (VD), unclassified dementia and other dementias which includes dementia with Parkinson's disease or motor neuron disease, etc.]. Concerning 70 demented patients who died during hospitalization, the average age of onset and the duration of illness of SDAT were 80.5 years old and 4.6 years respectively and those of VD were 77.6 years old and 2.7 years respectively. The common causes of death were pneumonia (50%) and cardiac failure (24%). Recurrence of cerebral vascular accident (CVA) was also another frequent cause of death in VD. The most common behavioral problems causing admission in patients of SDAT were aimless wandering, nocturnal delirium, illusion and hallucination. In VD, nocturnal delirium, aimless wandering, violence and abnormal monologue were most common causes of admission. The important causes degrading ADL of inpatients were fracture, especially fracture of the hip joint, pneumonia, intestinal bleeding and CVA. Concerning the increase of the population of over 75 years old, it will be suggested that the care and treatment of demented patients in this age group will become a major social problem.
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PMID:[Clinical and epidemiological studies on inpatients with dementia]. 238 92

A 60 year-old man was admitted to our hospital because of gait disturbance and dizziness. At 57 years of age, he noticed his walking unstable. After then, he had dizziness due to orthostatic hypotension, urinary difficulty, loss of livid, and forgetfulness. Neurological examination revealed he had severe orthostatic hypotension, cerebellar ataxia, dysarthria, hyperreflexia of four limbs, myoclonus of right leg, and atonic bladder. His brain CT showed cerebellar atrophy. Thereafter he had recurrent syncopic attacks. His gait disturbance progressed steadily, so he became bedridden. In his terminal stage, his limbs showed rigidity. About 3 years later he died of pneumonia and sepsis. At autopsy brain weighted 1,230 g. Glossly the putamens was bilaterally shrunken, the color of the substantia nigra and locus ceruleus became pale. Base of the pons and the cerebellum were atrophic. Microscopical examination confirmed the degeneration of striato-nigral and olivo-ponto-cerebellar systems without Lewy body. In the spinal cord there was depletion of neuronal cells in the intermediolateral nuclei and Onufrowitz nuclei. In addition to the conventional neuropathological staining methods, we performed the immunohistochemical studies using monoclonal antibody against synthetic peptide of beta protein which detected senile plaque of every stages with formic acid pretreatment, and compared to the modified Bielschowsky method and Congo red method. Our case showed many very primitive and primitive senile plaque in neocortices and hippocampal region. A few neurofibrally tangle were seen in hippocampus. We supposed our case might combine multiple system atrophy and Alzheimer' pathology.
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PMID:[An autopsy case of multiple system atrophy with many senile plaques]. 262 28

The histochemical demonstration of iron and the iron content was examined in the brain of a case of the special type of hepatocerebral encephalopathy (HCE). The patient had suffered from a liver disease since 36 years old. At 44 years old, she experienced the first attack of twilight state with flapping tremor. She had predilection for eating beans. Her personality gradually became euphoric with the recurrent episodes of unconsciousness. At 54 years old, she died of the complication of melena, renal insufficiency and pneumonia. The liver showed cirrhotic changes and iron content of liver was 0 or 1 after MacDonald's criterion scale. The histopathological findings of the brain showed the characteristic changes of HCE, which were incomplete softening and spongy state pseudolaminarilly extending in the deep layer of the cerebral cortex, the proliferation of the severely changed Alzheimer 2 type glia with or without intranuclear carmine positive substance. The deparaffinized sections, 20 mu in thickness, which were not fastened on slides were used for the histochemical study of iron, because iron deposits displaced inside of the brain tissues when the paraffin sections were fastened on slide glasses in the constant-temperature bath. The iron deposition was found in the central gyrus, superior temporal gyrus, medial and lateral occipito-temporal gyrus and middle temporal gyrus of occipital lobe. The iron accumulated in the ground substance, glia cell bodies, glia nuclei and unknown bodies in the 3-6 layers of cerebral cortex of these gyri. The iron accumulation demonstrated histochemically in other parts of the brain were group 1, 2 by Spatz, mammillary body, glia cell bodies in cerebellar white matter and pons.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Iron deposition in the brain of a case of the special type of hepatocerebral encephalopathy]. 280 22

Ultrastructural studies of spongiform encephalopathy (SE) reveal no very early pathological changes in kuru where membrane lamellation has been reported. This observation is challenged. In the later stages of SE, two main theories are examined--the spiroplasma theory and the prion (6 nm filament) theory. Neither are sufficiently convincing at present. In my own ultrastudies of Creutzfeldt-Jakob disease brain, extensive dismantling of the dendritic microtubule cytoskeleton has been observed. Loss of dendritic cytoskeleton implies loss of dendritic cytotransport with abolition of postsynaptic events. This would explain neurological symptoms and death where other causes, pneumonia etc. are not involved. My experimental model, involving depletion or loss of dendritic microtubules, indicates that spongy vacuoles may be fixation artifacts. In a brief consideration of Alzheimer's disease, loss of dendritic microtubules has also been observed, with the implications mentioned above. Finally, the neuritic plaque will be considered.
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PMID:Spongiform encephalopathy: a neurocytologist's viewpoint with a note on Alzheimer's disease. 352 Mar 70

The mortality experience of 5,406 men (cohort I) employed at one aluminum smelter on Jan. 1, 1950, and 485 men employed at a second plant (cohort II) on Jan. 1, 1951, is reported. For each man, the total number of years of exposure to tars, the number of years since first exposure to tars, and an index of exposure to tars expressed in tar-years were calculated. More than 99% of the men in the first cohort and 98% of the men in the second cohort were traced. Of the 1,539 men in cohort I who were deceased as of December 31, 1977, death certificates were obtained for 1,432 (93%). Of the 92 men in cohort II who were deceased as of December 31, 1977, death certificates were obtained for 80 (87%). The results showed that men in cohort I died of the following causes at approximately the same rate as or less frequently than men of similar age in the Province of Quebec: tuberculosis; circulatory disease; hypertensive heart disease; trauma; leukemia and aleukemia; and malignant neoplasms of the pancreas, genital organs, brain, intestine, and rectum and other abdominal areas. There were no deaths from pneumoconiosis or Alzheimer's disease. Although the observed and expected numbers of deaths in some of the cause-of-death categories were small, men in cohort I died of the following causes more frequently than did men of similar age in the Province of Quebec: respiratory disease; pneumonia and bronchitis; malignant neoplasms (all sites); malignant neoplasms of the stomach and esophagus, bladder, and lung; other malignant neoplasms; Hodgkin's disease; and other hypertensive disease. Mortality from malignant neoplasms of the bladder and lung was meaningfully related to numbers of tar-years and of years of exposure. Exposure-response relationships were less clear for malignant neoplasms of the esophagus and stomach and for other malignancies. Mortality from respiratory disease for men with 21 or more tar-years of exposure was approximately twice that of persons never exposed to tars. The apparent excess of other hypertensive disease was restricted to men never exposed to tars. Malignant neoplasm of the lung was the only cause of death in cohort II that was in excess of that expected at Quebec provincial rates.
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PMID:Mortality of aluminum reduction plant workers, 1950 through 1977. 406 80

Postmortem evaluation of ten individuals with a diagnosis of Alzheimer's disease (AD) confirmed the clinical diagnostic accuracy at our institution and showed significant ventricular dilatation with reduced brain mass, increased neuritic plaques, neurofibrillary tangles, vascular amyloid, and Lewy bodies in these individuals. A matched control group had no or fewer cortical neuritic plaques and neurofibrillary tangles, and two of the four control patients with rare neuritic plaques had terminal dementia. Cancer and cardiovascular disease occurred more often in the control group, but pneumonia and respiratory failure were more prevalent in the patients with AD. Thorough clinical assessment can accurately indicate Alzheimer's disease, as shown in this study.
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PMID:Postmortem evaluation of Alzheimer's disease. 407 Nov 64


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