Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a 36-year-old woman with right hemiplegia, anosognosia, and rapidly deteriorating course. She was well until the end of January, 1995 when she had an onset of fever, sputum, and cough. A 5 x 5 tumor was found in her left lower lobe. She was admitted to the Pulmonary Medicine on May 24, 1995 when she was 36-year-old. General physical examination was unremarkable. Bone scintigraphy revealed increased uptake in the skull, sternum, right scapula, vertebrae, right femur, and in ribs. Cranial CT scan revealed a large mass lesion in the right frontal subcortical region with central low density and peripheral high density areas, and small low density lesions in the right thalamic area and in the right posterior frontal region; ring enhancement was observed in the latter two lesions. On the second day of admission, she noted left-sided weakness which improved by corticosteroid treatment. On June 17, there was a sudden onset of left hemiparesis and a neurologic consultation was asked. Upon neurologic examination, she appeared somnolent but could understand verbal commands. She showed constructional apraxia, neglect of the left hemisphere, and anosognosia. Cranial nerves were unremarkable. Motor-wise, she showed flaccid left hemiplegia. Deep tendon reflexes were exaggerated on the left and the plantar response was extensor bilaterally. Nuchal stiffness was noted. Her cranial CT scan on June 17 revealed enlargement of the right frontal mass lesion. The subsequent course was complicated by DIC and progressive worsening of her consciousness. On June 18, she was comatose and pupillary light reflex was lost. She developed Cheyne-Stokes respiration and expired on that evening. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that the patient had a primary adenocarcinoma in the lung with multiple metastases including the brain. The fulminant terminal course was ascribed to hemorrhage within the tumor and subsequent central type of transtentorial herniation. Opinions were divided regarding the cause of hemorrhage; some participants thought hemorrhage was caused by DIC. Post-mortem examination revealed an adenocarcinoma arising at the S6 segment of the left lung with multiple organ metastases. In the brain, a huge hemorrhagic metastasis was found in the right frontal lobe and a non-hemorrhagic metastasis in the right thalamic region. Probably, the size of the metastases influenced the occurrence of hemorrhage. The direct cause of the death was transtentorial herniation.
 ...
PMID:[A 36-year-old woman with acute onset left hemiplegia and anosognosia]. 912 37

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.
 ...
PMID:[A 85-year-old woman with the onset of progressive gait disturbance at 80 years of the age]. 912 48