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Transcranial sonographic findings may predict prognosis of gastroprokinetic drug-induced parkinsonism.
Parkinsonism & related Disorders 2018 January
BACKGROUND: Drug-induced parkinsonism (DIP) is one important cause of parkinsonism and a major cause of misleading diagnosis of Parkinson's disease (PD). DIP is caused by dopamine receptor blocking agents. Its symptoms will improve after withdrawal of offending drugs. However, parkinsonism does not regress in several individuals. It may persist or exacerbate despite drug withdrawal. Transcranial sonography (TCS) of the substantia nigra (SN) has been widely used to diagnose PD and differentiate parkinsonism types. The objective of this study was to investigate the value of early TCS findings for predicting clinical outcome of patients with newly diagnosed gastroprokinetic drug-induced parkinsonism after withdrawal of dopamine receptor blocking agents.
METHODS: Fifty PD, 69 DIP, and 74 healthy controls were enrolled in this study. Patients with DIP were categorized into two subgroups: clinically improved after drug withdrawal (pure DIP) and clinically persistent or aggravated parkinsonism after drug withdrawal (unmasked PD). TCS was performed for all individuals to detect echogenicity in the SN.
RESULTS: Transcranial sonographic SN echogenicity was significantly increased in PD while DIP and controls had similar SN echogenicity. In subgroup analysis of DIP, transcranial sonographic SN echogenicity was significantly increased in unmasked PD compared to that in pure DIP or healthy controls.
CONCLUSIONS: SN echogenicity on TCS could be a useful tool to differentiate PD from DIP in clinical situations. Pure DIP and unmasked PD exhibited different SN echogenicity patterns. Early SN echogenicity findings on TCS could be used a biomarker to predict clinical prognosis of DIP.
METHODS: Fifty PD, 69 DIP, and 74 healthy controls were enrolled in this study. Patients with DIP were categorized into two subgroups: clinically improved after drug withdrawal (pure DIP) and clinically persistent or aggravated parkinsonism after drug withdrawal (unmasked PD). TCS was performed for all individuals to detect echogenicity in the SN.
RESULTS: Transcranial sonographic SN echogenicity was significantly increased in PD while DIP and controls had similar SN echogenicity. In subgroup analysis of DIP, transcranial sonographic SN echogenicity was significantly increased in unmasked PD compared to that in pure DIP or healthy controls.
CONCLUSIONS: SN echogenicity on TCS could be a useful tool to differentiate PD from DIP in clinical situations. Pure DIP and unmasked PD exhibited different SN echogenicity patterns. Early SN echogenicity findings on TCS could be used a biomarker to predict clinical prognosis of DIP.
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