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 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

We report the results of a collaborative study on malignant syndrome (MS) that developed in patients being treated with levodopa and other anti-parkinsonian drugs. We analyzed clinical features, laboratory findings, precipitating events, and risk factors for poor outcome. The study was conducted in five centers in Japan. Patients who developed MS between January 1991 and December 1997 were included. The enrollment criteria used were the same as those for neuroleptic MS proposed by Levenson et al. (1985).A total of 99 episodes were encountered in 93 patients (72 with Parkinson's disease and 21 with secondary parkinsonism); one patient had four recurrences of MS and three patients had two recurrences. High fever was the most frequent clinical manifestation of MS followed by worsening of parkinsonism, and then altered levels of consciousness. Serum creatine kinase was abnormally elevated in all the patients studied. Life-threatening complications were rhabdomyolysis, disseminated intravascular coagulation, and acute renal failure. The most frequent precipitating event was discontinuation or dose reduction of anti-parkinsonian drugs, particularly levodopa. No drug was the exception in the precipitation of MS. Intercurrent infection was the next most common precipitating event. MS developed without drug withdrawal or infection in some patients. In five patients, severe "wearing off" phenomenon was the only event preceding the onset of MS. Hot weather and dehydration appeared to be the cause in three patients. Among the total of 99 episodes, patients recovered to the pre-MS state following 68 episodes (68.7%); in the remaining 31.3%, patients failed to recover to their previous state. Older age, higher Hoehn and Yahr stage during the symptomatic phase of MS, higher akinesia score, and the absence of wearing off phenomenon prior to developing MS were associated with poor outcome. The most frequently used treatments of MS were intravenous fluid, levodopa, dantrolene sodium, and intragastric bromocriptine. Early introduction of treatment is important. Any elevation of body temperature during the course of anti-parkinsonian drug treatment should be considered as MS until proved otherwise.
 ...
PMID:A collaborative study on the malignant syndrome in Parkinson's disease and related disorders. 1273 13

Akinetic crisis (AC) is a life-threatening complication of parkinsonism characterized by an acute severe akinetic-hypertonic state, consciousness disturbance, hyperthermia, and muscle enzymes elevation. Injectable dopaminomimetic drugs, high-dose methylprednisolone, and dantrolene are advocated as putative specific treatments. The course of the illness is frequently complicated by infections, pulmonary embolism, renal failure, disseminated intravascular coagulation, and cardiac arrhythmias. Critical illness neuromyopathy (CINM) is an acquired neuromuscular disorder characterized by flaccid quadriparesis and muscle enzyme elevation, often occurring in intensive care units and primarily associated with inactivity, sepsis, multiorgan failure, neuromuscular blocking agents, and steroid treatment. In 3 parkinsonian patients, during the course of AC we observed disappearance of rigidity but persistent hypoactivity. In all, neurological examination showed quadriparesis with loss of tendon reflexes and laboratory investigation disclosed a second peak of muscle enzymes elevation, following the first increment due to AC. Electrophysiological studies showed absent or reduced sensory nerve action potentials and compound muscular action potentials, myopathic changes, and fibrillation potentials at electromyography recordings, and reduced excitability or inexcitability of tibialis anterior at direct muscle stimulation, leading to a diagnosis of CINM in all 3 patients. In 1 patient, the diagnosis was also confirmed by muscle biopsy. Outcome was fatal in 2 of the 3 patients. Although AC is associated with most of the known risk factors for CINM, the cooccurrence of the 2 disorders may be difficult to recognize and has never been reported. We found that CINM can occur as a severe complication of AC, and should be suspected when hypertonia-rigidity subsides despite persistent akinesia. Strict monitoring of muscle enzyme levels may help diagnosis. This finding addresses possible caveats in the use of putative treatments for AC.
 ...
PMID:Critical Illness Neuromyopathy Complicating Akinetic Crisis in Parkinsonism: Report of 3 Cases. 2618 47