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)

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

In the course of a 74-year-old woman with corticobasal degeneration (CBD), bilateral putaminal signal hypointensity appeared on T2 weighted MR image. This right-handed woman noticed progressive difficulty in writing and using chopsticks during two years. Neurological examination in February 1998 showed apraxia, rigidity, akinesia and myoclonus, which were more marked in the right hand side. MRI revealed atrophy of the left frontotemporal lobes. These findings were compatible to CBD. Her symptoms progressed slowly. On re-admission due to aspiration pneumonia in December 1998, she showed difficulty in swallowing and walking in addition to the signs and symptoms described above. MRI revealed bilateral putaminal signal hypointensity on T2 weighted image. In the literature, totally 9 cases in 2 reports showed similar putaminal signal hypointensity. Although this finding is unusual in CBD, advanced degenerative process in the putamen might have induced this change due possibly to the accumulation of iron secondary to the nerve cell loss.
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PMID:[Putaminal signal hypointensity on T2 weighted MR image in a patient with corticobasal degeneration]. 1082 4

We report a 64-year-old man with parkinsonism as an initial symptom, which was followed by dementia and abnormal behaviours. He was well until 1985, when he was 49 years old, when he noted rest tremor in his right hand. Soon tremor appeared in his left hand as well. He was seen in our clinic and levodopa was prescribed. He was doing well with this medication, however, in 1993, he started to suffer from on-off phenomenon. He also noted visual hallucination. In 1994, he stole a watermelon and ate it in the shop. He repeated such abnormal behaviours. In 1995, he was admitted to the neurology service of Hatsuishi Hospital. On admission, he was alert and oriented. He did not seem to be demented; however, he admitted stealing and hypersexual behaviours. No aphasia, apraxia, or agnosia was noted. In the cranial nerves, downward gaze was markedly restricted. He showed masked and seborrhoic face, and small voice. No motor palsy was noted, but he walked in small steps with freezing and start hesitation. Marked neck and axial rigidity was noted. Tremor was absent except for in the tongue. No cerebellar ataxia was noted. Deep tendon reflexes were diminished. Plantar response was extensor bilaterally. Forced grasp was noted also bilaterally. He was treated with levodopa and pergolide, but he continued to show on-off phenomenon. His balance problem and akinesia became progressively worse; still he showed hypersexual behaviour problems. He also showed progressive decline in cognitive functions. In 1997, he started to show dysphagia. He developed aspiration pneumonia in July of 1998. In 1999, he developed emotional incontinence and became unable to walk. He also developed repeated aspiration pneumonia. He died on March 1, 2000. He was discussed in a neurological CPC and the chief discussant arrived at a conclusion that the patient had corticobasal degeneration. Other diagnoses entertained included dementia with Lewy bodies, diffuse Lewy body disease, and frontotemporal dementia. Majority of the participants thought that diffuse Lewy body disease was most likely. Post-mortem examination revealed marked nigral neuronal loss, gliosis and Lewy bodies in the remaining neurons. Abundant Lewy bodies of cortical type were seen wide spread in the cortical areas, but particularly many in the amygdaloid nucleus. Lewy bodies were also seen in the subcortical structures such as the dorsal motor nucleus, oculomotor nucleus, Meynert nucleus, putamen, and thalamus. What was interesting was marked neuronal loss of the pontine nuclei, demyelination of the pontocerebellar fiber, and moderate neuronal loss of the cerebellar Purkinje neurons, a reminiscent of pontocerebellar atrophy. However, the inferior olivary nucleus was intact.
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PMID:[A 64-year-old man with parkinsonism as an initial symptom followed by dementia associated with marked abnormal behaviours]. 1176 20

Corticobasal degeneration (CBD) is a neurodegenerative disorder characterized clinically by a combination of cortical and basal ganglia signs. Pathologically, it is classified as a tauopathy. The most distinctive clinical feature is its unilateral or markedly asymmetric presentation; among parkinsonian syndromes, with rare exceptions, only Parkinson's disease presents with such asymmetry. The most common presenting cortical features include apraxia (patients often complain of a "useless" limb), aphasia (usually nonfluent), parietal lobe sensory signs (agraphesthesia, extinction, astereognosis), frontal dementia, or myoclonus. Basal ganglia signs include rigidity, akinesia, limb dystonia, and postural instability. The diagnosis is often challenging for three reasons: 1) The full complement of findings are rarely seen at presentation; 2) If CBD is not suspected, subtle but relevant findings (eg, extinction, language impairment, myoclonus, or apraxia) may not be searched for or appreciated; 3) The clinical picture of CBD has substantial overlap with a variety of other parkinsonian and dementing illnesses. The differential diagnosis includes Parkinson's disease, progressive supranuclear palsy, frontotemporal dementia, primary progressive aphasia, and Alzheimer's disease. The clinical diagnosis is not confirmed pathologically in up to half of cases, so the term corticobasal syndrome is often preferred during life, reserving the term corticobasal degeneration for pathologically verified cases. Treatment of CBD is primarily supportive, and most patients die within 10 years of onset. Parkinsonian signs may improve to a modest degree with levodopa, clonazepam can suppress myoclonus, and botulinum toxin can relieve dystonia. Early speech therapy, physical therapy, and occupational therapy, as well as assist devices such as a rolling walker may improve functioning and reduce complications such as aspiration pneumonia and falls. With time, however, most patients lose their independence and mobility. Throughout the course of the illness (particularly when it is advanced), caring for the caregiver is as important as caring for the patient.
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PMID:Corticobasal degeneration. 1936 52

Progressive supranuclear palsy (PSP) is one of the rare diseases. PSP is characterized by oculomotor dysfunction, postural instability, akinesia, dysarthria, and dysphagia. The major cause of death in patients with PSP is aspiration pneumonia. Considering these complications, spinal anesthesia is useful in patients with PSP. However, the potential harmful effects of spinal anesthesia including neurotoxicity of local anesthetics and neurologic complications for patients with PSP are unclear, because there has been no report. Here, we present spinal anesthesia for a patient with PSP. An 80-year-old man with progressive oculomotor dysfunction, dysphagia, and history of repeated aspiration pneumonia was scheduled for inguinal hernia surgery. Acutely concerning about perioperative pulmonary complications, we performed spinal anesthesia. Fortunately, there was no complication associated with respiration or neural system during perioperative period. We hope our experience and case report will be helpful in specific perioperative anesthetic care for patients with PSP.
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PMID:A case of spinal anesthesia in a patient with progressive supranuclear palsy. 2945 22