Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 72-year-old man developed a sudden weakness in his left hand on October 5, 1991. He was admitted two weeks thereafter. Physical examination revealed minimal weakness, and clumsiness of the fingers on his left hand. Exaggerated tendon reflexes and spasticity were also noted only on his left upper limb. He had neither dementia nor psychiatric symptoms. Subsequently he developed weakness in his left leg on November 17. Within 12 days he developed left facial weakness, and myoclonic movements on the left side. By December 2, he developed spastic tetraparesis with bilateral facial palsy, and generalized myoclonic jerks. A few days after that he started to show decorticate posture. From December 16, his mental status deteriorated rapidly, and he became mute, and uncooperative within a week. His clinical course can be summarized as stepwise progression similar to a cerebrovascular accident. Electroencephalography was normal on admission, but periodic synchronous discharge developed in January 1992. Brain CT that showed only mild brain atrophy at first was considered to be compatible with his age, changed to have severe brain atrophy in March 1992. He died of pneumonia on May 24, 1992 after eight months of progressive clinical course. Autopsy was done. The brain weighed 930 grams. Macroscopically there was prominent cortical atrophy. Microscopic examination revealed severe spongy state throughout the cerebral cortex. Typical spongiform changes were confined to the hippocampus. The cerebral white matter appeared to be normal. In the cerebellar cortex, the granular cell layer disappeared and Purkinje's cells were reduced in number. Kuru plaques were not seen. The cerebellar white matter, dentate nucleus, and brainstem seemed to be normal. The spinal cord was not examined. There were no pathological changes to indicate cerebrovascular accident, except for a lacuna in the right basal ganglion and a small angionecrosis in the pons. Western blotting test using Anti-APC (amyloid plaque core) antibody was positive. Neuropathological changes of the present case were consistent with those of CJD. However, the sudden onset of monoparesis without dementia or ataxia is rare as the initial symptom of this disease. The subsequent clinical course with stepwise progression of hemiplegia, which was mimicking a progressive stroke, was also rare for CJD. In comparison to typical case of CJD, this case had a different clinical onset as acute monoparesis. We can find such cases of CJD presenting as stroke in 5.6% in the previous English literatures.
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PMID:[A case of Creutzfeldt-Jakob disease (CJD) started with monoparesis of the left arm]. 904 57

We report a 85-year-old woman who had an onset of gait disturbance at 80 years of the age. She had a dizzy spell when she was 80-year-old. She was evaluated at another hospital where paroxysmal tachycardia and sinus arrest lasting as long as 5.8 seconds were found. She was diagnosed as having sick sinus syndrome and a pace maker was inserted. She had a gradual onset of disturbance of gait shortly after the above dizzy spell. She became unable to walk fast and her steps became small. Neurologic examination at age 83 revealed small step gait with freezing episodes. Retropulsion was present. No motor weakness or origidity was noted. She had no tremor. Mentally she was alert and sound. Cranial nerves were essentially normal. Cranial CT scan revealed slight diffuse low density change in the bilateral cerebral white matter. She was treated with amantadine HCI and levodopa with carbidopa. Her gait and balance showed some improvement. She developed pneumonia and worsening of her gait when she was 85 years of the age, and she was admitted again to our hospital. She was mentally alert and sound but she showed marked freezing of gait with loss of postural reflex; she would have fallen down unless supported upon standing. Cranial nerves were again essentially normal. Her hospital course was complicated by pneumonia, DIC, and renal failure. She expired suddenly on the 10th day of her last admission. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had vascular parkinsonism due to lacunar state. However, paucity of vascular changes in her CT scan remained as a question. Other participants thought that she had nigral cell loss secondary to her aging and circulatory disturbance which would have been caused by her sick sinus syndrome. Post-mortem examination revealed marked loss of nigral pigmented cells; the cell loss was diffusely seen in the substantia nigra. Neurofibrillary tangles were seen in the remaining neurons. In addition, gliosis was noted in the globus pallidus and the subthalamic nucleus, however, neuronal loss was very mild in those nuclei. In the superior colliculus, neuronal loss was mild, however, gliosis was seen. No clear neuronal loss was observed in the locus coeruleus, however, Lewy bodies were seen in the remaining neurons. Furthermore, Lewy bodies were also found in the substantia sigra. It was thought that she had progressive supranuclear play (PSP). Question was whether or not she was complicated by Parkinson's disease. Clinically, she had no rigidity or tremor. Pathologically, locus coeruleus did not show neuronal loss. Therefore, incidental Lewy body disease was raised as a possibility. Finally, it should be pointed out that she had no oculomotor disturbance or dementia, yet she had PSP. Her clinical features were those of pure akinesia. Pathologic changes were also relatively mild except for those in the substantia nigra. Possibility of post-encephalitic parkinsonism without encephalitis was also discussed, however, over all distribution of her pathologic changes was more consistent with PSP.
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PMID:[A 85-year-old woman with the onset of progressive gait disturbance at 80 years of the age]. 912 48

Aging is typically accompanied by gradual but progressive physiological changes and an increased prevalence of acute and chronic illness in any organs. Musculoskeltal system is one of the most involved organs in geriatric patients. Appropriate roles in geriatric rehabilitation for musculoskeltal disorders should be emphasized not only to treat the disorders, but also to prevent many complications cause by specific disease or injury. Representative management methods in geriatric rehabilitation are introduced in this section. Rest is often effective, especially in the acute phase of illness or injury. However, cautions should be paid in disuse syndrome which may be produced by prolonged bed rest. Major manifestations in this syndrome includes muscle weakness and atrophy, joint contracture, decubitus, osteoporosis, ectopic ossification, cardiovascular impairment, pneumonia, urological and mental problems. Physical agents such as heat, cold, light and pressure have been used as therapeutic agents. Electrical stimulation is often effective in the treatment of low-back pain syndrome. Traction is the act of drawing, or a pulling force. Its mechanism to relieve pain seems to immobilize the injured parts, to increase peripheral circulation by massage effect and to improve muscle spasm. Brace is very effective to control acute pain in musculoskeltal system. However, long-term wear of brace should be avoided to prevent the disuse syndrome. Exercise is one of the most important rehabilitation modalities. This includes stretching and muscle strengthening programs. Education of body mechanism in activity of daily living is essential in rehabilitation of geriatric patients.
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PMID:[Rehabilitation for musculoskeltal disorders in geriatric patients]. 926 51

The objective of this study was to assess the frequency, type, and severity of perioperative complications after a first surgery under general anesthesia in patients with myotonic dystrophy (DM) and to measure the association with suspected risk factors. Numerous cases of perioperative complications in DM patients have been reported. Hazards have been associated with the use of thiopentone, suxamethonium, neostigmine, and halothane. A retrospective study of perioperative complications was conducted for 219 DM patients who had their first surgery under general anesthesia at the Chicoutimi Hospital. The overall frequency of complications was 8.2% (18 of 219). Most complications (16 of 18) were pulmonary, including five patients with acute ventilatory failure necessitating ventilatory support, four patients with atelectasis, and three patients with pneumonia. Using multivariate analysis, we found that the risk of perioperative pulmonary complications (PPC) was significantly higher after an upper abdominal surgery (odds ratio (OR), 24.4; 95% CI, 4.0 to 149.3) and for patients with a severe muscular disability, as assessed by the presence of proximal limb weakness (OR, 14.1; 95% CI, 1.5 to 134.4). The likelihood of PPC was not related to any specific anesthetic drug. Because of the increased risk of PPC, careful monitoring during the early postoperative period, protection of upper airways, chest physiotherapy, and incentive spirometry are mandatory in all symptomatic DM patients, particularly those with a severe muscular disability or those who have undergone an upper abdominal surgery.
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PMID:Anesthetic and surgical complications in 219 cases of myotonic dystrophy. 940 61

A 48-year-old man, who had spastic tetraplegia and a marked atrophy of the medulla oblongata and upper cervical cord, was reported. He began to walk in spastic fashion at the age of 12 years, and was diagnosed as spastic paraplegia. His father, whose onset of the disorder was 35 years old and died of pneumonia at the age of 69 years, manifested symptoms and a course, both resembling those of the present patient. Generalized weakness progressed gradually, and the patient was confined to bed in his forties. On admission, he showed markedly increased tendon reflexes and pathological reflexes in all the extremities. Muscular weakness was severe in the neck, trunk and extremities, and mild in the facial muscles. There were neither bulbar sign, significant respiratory failure nor fasciculation of muscles. A needle EMG examination revealed no apparent neuropathic findings. MR imaging showed a marked atrophy of the medulla oblongata and upper cervical cord, which was not considered to be secondary to vascular or infectious diseases. Though sensory evoked potentials showed no response at the latencies of central nervous components, visual evoked potentials, brainstem auditory evoked response and blink reflex were normal. This case might represent an unknown hereditary degenerative disease with autosomal dominant inheritance.
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PMID:[A case of spastic tetraplegia with medullo-cervical atrophy]. 950 78

The history of the spinal muscular atrophies (SMA) began in the 1890s with Guido Werdnig and Johann Hoffmann. Together, their papers present a rather complete picture of the clinical and pathologic aspects of infantile SMA: onset during the first year of life, occurrence in siblings with normal parents, progressive floppiness and weakness, hand tremor, and death from pneumonia in early childhood. Based on the work of an international collaboration, the following is current nomenclature: SMA type 1 (or I) for onset of symptoms before age 6 months, SMA type 2 (II) for onset between 6 and 18 months, and SMA type 3 (III) for onset after age 18 months. Linkage of autosomal recessive SMA to chromosome 5q11.2-13.3 was reported by Gilliam et al in 1990. A novel gene, whose function remains unknown, called the survival motor neuron gene (SMN) at 5q13, contains deletions in more than 98% of SMA patients. Some patients with atypical forms of SMA have been shown to have mutations in SMN. Because there is no effective therapy for SMA, management consists of preventing or treating the complications of severe weakness, such as restrictive lung disease, poor nutrition, orthopedic deformities, immobility, and psychosocial problems.
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PMID:Spinal muscular atrophy. 956 64

We report a case of Swyer-James syndrome with pneumothorax. A 20 year-old man was admitted to our hospital with dyspnea. Right pneumothorax was diagnosed by chest X-ray. He had a history of current pneumonia in childhood. After improvement of the pneumothorax, chest X-ray revealed hyperlucency of the right upper lung. Chest-CT revealed a low attenuation area and a cystic space in the right upper lobe. Xenon-133 clearance was delayed in ventilation scintigraphy. Bronchography showed cylindrical bronchiectasis in the proximal bronchi and poor filling of the peripheral bronchi in the right upper lobe. Pulmonary angiography showed a small right upper pulmonary artery. Swyer-James syndrome was diagnosed. The pneumothorax was probably caused by weakness of the cystic spaces.
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PMID:[Swyer-James syndrome with pneumothorax]. 961 45

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

A 72-year-old man was exposed to the sarin gas attack in a Tokyo subway on March 20 th, 1995. After exposure, he noticed eye discomfort, chest tightness, headache and weakness of the lower limbs and oropharyngeal muscles. Despite these symptoms, he visited a hot spring on the same day with his family. On March 25 th, his muscle weakness progressed, and a low grade fever appeared. His muscle weakness disappeared 8 days after exposure to sarin, but respiratory failure rapidly developed, necessitating artificial ventilation within four day after hospitalization on March 28th. Chemotherapy with erythromycin, imipenem/cilastatin, and steroid pulse therapy was begu. PCR and culture of sputum collected by bronchofiberscopy were positive for Legionella pneumophila, serogroup I. His respiratory state improved, but subsequent infection with Pseudomonous aeruginosa. Enterobacter cloacae, and Candida tropicalis/glabrata caused his death 71 days after admission. Oropharyngeal muscle weakness caused by sarin-mediated cholinesterase inhibition was strongly suspected as the cause of hot spring water aspiration. Transbronchial lung biopsy revealed organizing pneumonia with fibrosis. Bronchoscopic findings included redness, edema and fragility of all visible areas of the airway, which was thought to be due to bronchitis caused by Legionellosis.
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PMID:[Legionella pneumonia caused by aspiration of hot spring water after sarin exposure]. 965 77

A 56-year-old man experienced dyspnea since August 1995 and the chest X-ray film showed abnormal shadow. The diagnosis of bronchiolitis obliterans organizing pneumonia (BOOP) was established based on the histological findings of transbronchial lung biopsy. The patient was treated with prednisolone and symptoms improved. Myalgia and muscle weakness developed associated with relapse of BOOP after withdrawal of prednisolone. Patient was admitted to our department on December 1995 for further examination. An increased level of serum CPK, histological findings of muscle biopsy consistent with myositis, and positive anti-Jo-1 antibody were identified. Those findings supported a diagnosis of polymyositis (PM), and BOOP was considered as a pulmonary complication of PM. Myositis and pulmonary lesion improved after second course of steroid therapy and patient was discharged on May 1996. Both chronic pulmonary fibrosis and acute progressive interstital pneumonia are well known as pulmonary lesion associated with PM. The former is frequently recognized in cases of PM with anti-Jo-1 antibody and the latter is often observed in cases without autoantibodies. The association of PM and BOOP, however, has rarely been reported. The findings that BOOP frequently preceded PM and anti-Jo-1 antibody was positive in half of the cases were observed in the literature.
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PMID:[A case of polymyositis with anti-Jo-1 antibody preceded by BOOP]. 966 82


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