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1.
Metab Brain Dis ; 29(3): 813-24, 2014 Sep.
Artículo en Inglés | MEDLINE | ID: mdl-24599759

RESUMEN

In 1949, asterixis was first described in patients with hepatic encephalopathy. It was quickly recognized that this phenomenon also occurs in other generalized encephalopathies and sometimes results from structural brain lesions. This paper is a study of asterixis in the general neurology clinic and on the inpatient neurology consultation service. The neurologists recorded the findings on inpatients and clinic patients for 12 consecutive months. Of the 1,109 inpatients with adequate examination, asterixis was documented in 97. Eighteen of the 97 cases were unilateral (18.6%) and 79 cases were bilateral (81.4%). Of the 614 outpatient visits with well documented examination, 6 (1%) individuals had asterixis. Since a small number of patients were examined more than once, the study yielded 103 individuals with adequate data for analysis. Asterixis resulted from varied causes: medications, renal disorder, hepatic dysfunction, pulmonary insufficiency, stroke and other brain lesions (including malignancy, subdural hematoma, and epidural abscess). Asterixis occurred in various patterns: in some cases it was easier to elicit in the upper extremities, in some it was easier to elicit in the lower limbs, and some it was solely or predominantly unilateral. The findings are discussed in light of the literature on asterixis with regard to its varied causes, patterns and presentations. Lastly, asterixis is examined from a historical perspective and the terminology is elucidated.


Asunto(s)
Encéfalo/patología , Discinesias/diagnóstico , Discinesias/patología , Humanos , Índice de Severidad de la Enfermedad , Evaluación de Síntomas
2.
J Mov Disord ; 12(1): 37-42, 2019 01.
Artículo en Inglés | MEDLINE | ID: mdl-30732431

RESUMEN

OBJECTIVE: To evaluate whether less pulsatile levodopa therapy (LPT) can reduce the development of levodopa-induced dyskinesia (LID). METHODS: This is a retrospective cohort study of patients with Parkinson's disease at the movement disorders clinic of Medstar Washington Hospital Center. The study was not blinded or randomized. Patients were seen between August 2002 and August 2018. During these years, we treated patients with less pulsatile (6 doses daily) levodopa treatment to reduce LID. Occurrence of LID was recorded. RESULTS: Ninety-five patients with Parkinson's disease taking levodopa were divided into two groups: 1) patients who were initially managed on LPT or who switched from traditional therapy (TT) (n = 61) (mean disease duration: 7.7 ± 4.8 years, mean levodopa duration: 5.6 ± 4.5 years and mean observation time: 4.3 ± 3.4 years), and 2) patients on TT throughout the observation period or until they developed dyskinesia (n = 34) (mean disease duration: 8.3 ± 3.8 years, mean levodopa duration: 6.2 ± 4.2 years and mean observation time: 4.1 ± 3.4 years). Three of the 61 LPT patients developed dyskinesia during the observation period. One of the patients developed dyskinesia after being switched to pulsatile doses by another doctor. In the other two, dyskinesia was minimal. In contrast to this 4.9% cumulative incidence, dyskinesia occurred in 50% (17/34) of TT patients, an incidence similar to that in published data (p < 0.001). CONCLUSION: Less pulsatile levodopa with 6 daily doses was associated with a low incidence of LID. Further study of this method of treatment is warranted.

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