ABSTRACT
OBJECTIVE: To determine whether brain white matter hyperintensities (WMH) influence l-dopa response in Parkinson's disease (PD) patients. METHODS: We prospectively evaluated 60 PD patients with an acute l-dopa challenge test, and assessed motor performance with the Movement Disorders Society revised Unified Parkinson's Disease Rating Scale (MDS-UPDRS) during "ON" and "OFF" medication states. Magnetic resonance images were examined using a visual semi-quantitative rating scale for quantification and distribution analysis of WMH. l-dopa challenge test response was correlated to extent and location of WMH, to determine a potential association between them. RESULTS: Subjects with greater deep WMH burden, showed less response to l-dopa on axial motor symptoms (R = -0.35; p < 0.027), when tested with Part III of the MDS-UPDRS before and after acute levodopa challenge. CONCLUSIONS: Results suggest WMH may affect response to l-dopa on axial function of PD patients, which could be due to either non-dopaminergic (cortico-basal ganglia) motor pathway disruption, or postsynaptic nigrostriatal pathway involvement.
Subject(s)
Antiparkinson Agents/therapeutic use , Levodopa/therapeutic use , Magnetic Resonance Imaging , Parkinson Disease/drug therapy , White Matter/drug effects , White Matter/diagnostic imaging , Aged , Female , Gait Disorders, Neurologic/diagnostic imaging , Gait Disorders, Neurologic/etiology , Humans , Male , Middle Aged , Parkinson Disease/complications , Retrospective Studies , Statistics, Nonparametric , Treatment OutcomeABSTRACT
We tested the vehicles of six different commercially available depot corticosteroids (Celestone Soluspan, Depo-Medrol, Decadron, Decadron L. A., Aristocort, and Kenalog) for possible toxicity when injected intravitreally. When tested on rabbit eyes, the Celestone Soluspan and the Depo-Medrol vehicles caused remarkable retinal degeneration with preretinal membrane formation or cataracts in their standard concentrations. Three other vehicles (Decadron and Decadron L. A.) caused localized retinal degeneration in twice the standard concentration. Thus, toxic effects can be caused by preservatives or inadequate osmolarity of the vehicles alone. The development of proliferative vitreoretinopathy in some cases of injections of intraocular depot corticosteroid can be explained by retinal necrosis and repair processes caused by these vehicles.
