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Pharmacological tests of hypotheses for acquired pendular nystagmus
Journal article   Open access   Peer reviewed

Pharmacological tests of hypotheses for acquired pendular nystagmus

Aasef G Shaikh, Matthew J Thurtell, Lance M Optican and R John Leigh
Annals of the New York Academy of Sciences, Vol.1233(1), pp.320-326
09/2011
DOI: 10.1111/j.1749-6632.2011.06118.x
PMCID: PMC3187918
PMID: 21951011
url
https://www.ncbi.nlm.nih.gov/pmc/articles/3187918View
Open Access

Abstract

Acquired pendular nystagmus (APN) occurs with multiple sclerosis (MS) and oculopalatal tremor (OPT); distinct features of the nystagmus have led to the development of separate models for their pathogenesis. APN in MS has been attributed to instability in the neural integrator, which normally ensures steady gaze. APN in OPT may result from electrotonic coupling between neurons in the hypertrophied inferior olivary nucleus, which induces maladaptive learning in cerebellar cortex. We tested these two hypotheses by analyzing the effects of gabapentin, memantine, and baclofen on both forms of nystagmus. No drug changed the dominant frequency of either form of APN, but the variability of frequency was affected with gabapentin and memantine in patients with OPT. The amplitude of APN in both MS and OPT was reduced with gabapentin and memantine, but not baclofen. Analyzing the effects of drug therapies on ocular oscillations provides a novel approach to test models of nystagmus.
Baclofen - pharmacology Cerebellar Cortex - physiopathology Memantine - pharmacology Humans gamma-Aminobutyric Acid - pharmacology Eye Movements - drug effects Nystagmus, Pathologic - physiopathology Myoclonus - physiopathology Multiple Sclerosis - complications Multiple Sclerosis - physiopathology Myoclonus - complications Cyclohexanecarboxylic Acids - pharmacology Nystagmus, Pathologic - etiology Olivary Nucleus - physiopathology Models, Neurological Amines - pharmacology Nystagmus, Pathologic - drug therapy

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