Objective: To understand whether Acute Akinesia (AA) is a separate clinical entity in Parkinson’s Disease (PD), or it can be classified among the other known motor fluctuations. Methods: 26, out of 675, PD patients, regularly followed in our out-patient clinic for 5.2±2.1 years, who had been evaluated at least 4 months (1.6±0.9) before the onset of a critical condition characterized by acute akinesia, were regularly rated with UPDRS motor scale until recovery of symptoms or eventual complications appeared. Oral dopaminergic treatments were administered in all, 50-200mg/day continuous s.c. apomorphine infusion was added in 18 patients in order to understand whether akinesia was responsive to dopaminomimetic manipulation. L-Dopa kinetics were studied during and after AA. Results: 17 patients had AA concomitant with infectious diseases, or surgery and 9 patients had AA during gastro-intestinal tract disease or drug manipulation. Sudden worsening of motor symptoms by 31.4±12.8 UPDRS motor subscale score was observed for 11.2.±6.2 days despite treatment with drug dose increments or continuous s.c. apomorphine infusion. The recovery began 4-26 days after AA onset and was incomplete in 10 patients. 4 patients died despite treatments. L-Dopa kinetics were normal in all patients without gastro-intestinal tract disease, and in one patient with gastric stasis. Conclusions: Transient refractoriness to apomorphine, duration of motor worsening and partial recovery suggest that AA might be considered a separate clinical condition not akin to motor fluctuations or to drug withdrawal symptoms.

Acute akinesia in Parkinson disease.

ONOFRJ, Marco;THOMAS, Astrid Maria
2005-01-01

Abstract

Objective: To understand whether Acute Akinesia (AA) is a separate clinical entity in Parkinson’s Disease (PD), or it can be classified among the other known motor fluctuations. Methods: 26, out of 675, PD patients, regularly followed in our out-patient clinic for 5.2±2.1 years, who had been evaluated at least 4 months (1.6±0.9) before the onset of a critical condition characterized by acute akinesia, were regularly rated with UPDRS motor scale until recovery of symptoms or eventual complications appeared. Oral dopaminergic treatments were administered in all, 50-200mg/day continuous s.c. apomorphine infusion was added in 18 patients in order to understand whether akinesia was responsive to dopaminomimetic manipulation. L-Dopa kinetics were studied during and after AA. Results: 17 patients had AA concomitant with infectious diseases, or surgery and 9 patients had AA during gastro-intestinal tract disease or drug manipulation. Sudden worsening of motor symptoms by 31.4±12.8 UPDRS motor subscale score was observed for 11.2.±6.2 days despite treatment with drug dose increments or continuous s.c. apomorphine infusion. The recovery began 4-26 days after AA onset and was incomplete in 10 patients. 4 patients died despite treatments. L-Dopa kinetics were normal in all patients without gastro-intestinal tract disease, and in one patient with gastric stasis. Conclusions: Transient refractoriness to apomorphine, duration of motor worsening and partial recovery suggest that AA might be considered a separate clinical condition not akin to motor fluctuations or to drug withdrawal symptoms.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11564/119253
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