Impact of anticholinergic drugs withdrawal on motor function in patients with Parkinson's disease.

OBJECTIVES: Physicians have prescribed anticholinergic agents as monotherapy or adjuvant therapy in patients with Parkinson's disease for decades. However, these medications can cause many adverse effects including gait freezing and falling. Herein we assessed the effects of anticholinergic medications on motor function, freezing of gait and falling in a group of patients with PD. PATIENTS AND METHODS: This prospective study evaluated the effect of gradual discontinuation of anticholinergics on motor function in 131 outpatients with Parkinson's disease. We assessed patients' motor function at baseline six and twelve months later using the UPDRS-III. We also evaluated freezing of gait and falling in patients using UPDRS-II part 14 and 13 respectively. The anticholinergics were tapered and gradually discontinued and additional levodopa doses were added as patients needed. RESULTS: 131patients successfully discontinued their anticholinergic medications. Stopping anticholinergics significantly improved the motor symptoms in PD patients as reflected in the change between the mean (±SD) UPDRS-III score of 36.85(±11.5) at the baseline to 32.51(±11.4) and 31.43 (±11.3) after six and twelve months (P < 0.001). The mean (±SD) scores of freezing of gait (FOG)significantly changed from 1.34(±1) to 1.17(±1) and 0.6(±0.7) and for falling down from 0.62(±0.8) to 0.5 (±0.8) and 0.29(±0.5) respectively (p-value of <0.001). CONCLUSION: Our finding demonstrated an improvement in motor function and FOG and falling incidences in PD patients, after discontinuation of anticholinergic drugs. As motor complications adversely affect the quality of life in PD patients, clinicians must be careful with the unnecessary use of anticholinergic drugs in their treatment strategies.

Tongue Protrusion Dystonia in Pantothenate Kinase-Associated Neurodegeneration.

BACKGROUND: Tongue protrusion dystonia is an uncommon focal dystonia involving the lingual muscles. Causes of tongue protrusion dystonia include tardive dystonia, posthypoxic dystonia, neuroacanthocytosis, pantothenate kinase-associated neurodegeneration, and Lesch-Nyhan syndrome. METHOD: We summarize three children with pantothenate kinase-associated neurodegeneration and tongue protrusion dystonia. All three patients underwent careful neurological examination, brain magnetic resonance imaging, and genetic testing. RESULTS: Tongue protrusion dystonia was a prominent and disabling symptom in all three patients. Brain magnetic resonance imaging revealed a typical eye of the tiger sign in all patients. Two patients had the same genetic mutation (c.1168 A>T mutation, p.I390F). CONCLUSIONS: Tongue protrusion dystonia may be a clue to the underlying etiology of dystonia, including hereditary forms of dystonia. Among them, pantothenate kinase-associated neurodegeneration is an important cause, especially in children.