RESUMEN
We report a consensus statement of the collaborative research group on the prevention and treatment of malignant syndrome (MS) in Parkinson's disease. The syndrome is quite similar to neuroleptic MS. Although sudden withdrawal of levodopa was the most frequent cause, many other precipitating events were found such as intercurrent infections, dehydration, hot weather, discontinuation of other anti-parkinsonian drugs, and "wearing off" phenomenon. Awareness of this syndrome is most important for its early detection and the prompt commencement of treatment. MS should be suspected whenever the body temperature rises above 38 degrees C without an apparent cause. Treatment consists of ample intravenous fluid, cooling the body, anti-parkinsonian drugs (particularly levodopa and bromocriptine), dantrolene sodium, and antibiotics if infection is present. Rhabdomyolysis, disseminated intravascular coagulation, and acute renal failure constitute serious complications.
Asunto(s)
Antiparkinsonianos/efectos adversos , Síndrome Neuroléptico Maligno/prevención & control , Síndrome Neuroléptico Maligno/terapia , Enfermedad de Parkinson/tratamiento farmacológico , Humanos , Síndrome Neuroléptico Maligno/etiología , Síndrome de Abstinencia a SustanciasRESUMEN
A miniaturized planar-membrane-based gas collector of 800 nL internal liquid volume was integrated with a microfabricated conductivity detector to measure atmospheric SO2. This device is operated with a dilute H2SO4/ H202/2-propanol absorber for a finite integration period (typically, 1.5 min) without liquid flow. During this period, sulfuric acid is formed from SO2 that diffuses into the liquid and accumulates therein. The increase in conductivity with ongoing sampling is measured. The absorber is then replaced with fresh solution, and the process starts anew. The most important factors that govern sensitivity and the detection limit are the choice of the membrane, the nature of the internal collector solution, and the thickness of the solution layer. A porous polypropylene membrane with some 2-propanol (IPA) incorporated in the internal solution was found to be the best combination. The sensitivity was inversely proportional to the solution layer thickness, and a layer thickness of 100 microm resulted in a practical device with good performance characteristics. Greater applied pressure on the gas phase relative to the liquid side also can improve device performance. The system is operated with 12 V DC and does not require a liquid pump. Under optimized conditions, the LOD is 0.7-1.0 ppbv for a sampling period of 1.5 min. The device was field-tested around Mt. Aso in Japan. Changes in ambient SO2 concentrations could be followed with good time resolution. The results are compared with data obtained by a collocated macroscale instrument.
Asunto(s)
Contaminantes Atmosféricos/análisis , Dióxido de Azufre/análisis , Absorción , Membranas Artificiales , Nanotecnología , Presión , Reproducibilidad de los Resultados , SolucionesRESUMEN
We report a 52-year-old Japanese woman who developed dyskinesia, epilepsy, and gait disturbance. She was well until 35 years of age, when she noted the onset of gait disturbance. She also noted abnormal involuntary movements in her limbs. She also noted dysarthria at age 38. A neurologist examined her at age 41. The neurologist found cerebellar ataxia and dyskinesia. The atrophy of the brain stem and the cerebellum was on CT. She started to have generalized convulsion with loss of consciousness. Dementia became apparent at age 40. In October, 1993, she became psychotic in which she behaved violently taking off her clothes shouting as "Fire". She was treated with major tranquilizers and became quiet. However, choreic movements became prominent. Her subsequent course was complicated with dysphagia, dementia, convulsion, and frequent bouts of pneumonia. She expired on January 24, 2000 after developing pneumonia. Her father and one sibling had similar motor disturbances. She was discussed in a neurological CPC. The chief discussant arrived at conclusion that the patient had dentatorubral-pallidoluysian atrophy. Most of the participants agreed with this diagnosis. Postmortem examination revealed that entire brain looked smaller than normal including the brain stem and the cerebellum. The cerebellar dentate nucleus showed loss of neurons and gliosis; glumose degenerations were also seen. The external segment of the pallidum showed neuronal loss and gliosis. The subthalamic nucleus showed gliosis without neuronal loss. A demyelinated focus was found in the pons; the lesion looked similar to central pontine myelinolysis. The cerebral white matters were unremarkable. Other areas were unremarkable. The pathological diagnosis was dentatorubral-pallidoluysian atrophy. The pathologic lesion which might explain her dementia was not apparent.
Asunto(s)
Discinesias/etiología , Epilepsia/etiología , Trastornos Neurológicos de la Marcha/etiología , Epilepsias Mioclónicas Progresivas/patología , Ataxia Cerebelosa/etiología , Femenino , Humanos , Persona de Mediana Edad , Epilepsias Mioclónicas Progresivas/complicaciones , Epilepsias Mioclónicas Progresivas/genéticaRESUMEN
We report a 68-year-old woman who developed progressive dementia and parkinsonism. She was well until 1990 when she was 58 years of age. She started to show memory loss. Four years later, she developed difficulty in dressing and behavioral problems such as eating rice with her hands, going out of her house without purposes, and difficulty in finding the rest room in her house. She was admitted to the neurology service of Hatsuishi Hospital on January 19, 1996, when she was 64 years of the age. On admission, she was alert but markedly demented. The score of Hansegawa Dementia Scale was 0/30. She was unable to make any coherent conversation. She appeared to have dressing apraxia but did not appear to have aphasia. Cranial nerves were intact. She walked in small steps with stooped posture. She did not have motor weakness but she showed plastic rigidity in all four limbs. No tremor or ataxia was noted. Deep tendon reflexes were within normal limits but the plantar response was extensor bilaterally. She continued to deteriorate after admission. In May of 1998, she started to fall. In June of 1998, she had a generalized convulsion. In January of 1999, she became unable to take foods orally and a gastrostomy was placed. She expired on May 29, 1990. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had Alzheimer's disease. The question was whether her parkinsonism was a part of her Alzheimer's disease or she had an additional disease to explain her parkinsonism. Post-mortem examination revealed moderate to marked atrophy of the frontal and the temporal lobes as well as in the limbic areas with dilatation of the lateral ventricles. Marked neuronal loss was noted in the CA 1 to the subiculum region with gliosis. Neurofibrillary tangles were seen in the remaining neurons. Neuropil threads were seen by Gallyas-Braak staining. Similar changes were seen in the parahippocampal gyrus and in the entorhinal cortex. Senile plaques were seen in the insular cortex and in other cortical areas. Cortical type Lewy bodies were seen in the cingulate cortex. The Meynert nucleus showed marked neuronal loss and gliosis. The substantia nigra and the locus coeruleus showed moderate loss of pigmented neurons. Lewy bodies were seen in these regions. The dorsal motor nucleus of the vagal nerve was retained, however, one Lewy body was observed. Pathologic diagnosis was Alzheimer's disease plus Parkinson's disease. It is an interesting question whether or not her parkinsonism was due to nigral lesion or frontal lesions. It is known that parkinsonism may complicate in advanced Alzheimer's disease not necessarily due to nigral lesion. On the other hand, in incidental Lewy body disease, the substantia nigra shows mild Parkinson's disease-like change without clinical parkinsonism. This patient appeared to have been a true complication of Alzheimer's disease and Parkinson's disease.