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Cortical myoclonus during lithium exposure.
John N Caviness1, Virgilio G H Evidente
1Department of Neurology, Parkinson's Disease and Movement Disorders Center, Mayo Clinic Scottsdale, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA. jcaviness@mayo.edu
Archives of Neurology
|March 14, 2003
Summary
Lithium therapy can cause disabling myoclonus, characterized by cortical action myoclonus. Electrophysiologic studies reveal a focal EEG transient preceding myoclonus EMG discharge, distinct from other forms.
Area of Science:
- Neuroscience
- Pharmacology
- Clinical Neurology
Background:
- Myoclonus is a disabling adverse effect of lithium therapy, occurring at various dosages.
- Previous reports noted myoclonus with lithium combinations, but lacked electrophysiologic data on its mechanism.
- No neurophysiological mechanism for lithium-induced myoclonus was previously established.
Purpose of the Study:
- To characterize the electrophysiologic features of myoclonus during lithium therapy.
- To identify the source and neurophysiological basis of lithium-induced myoclonus.
Main Methods:
- Retrospective analysis of 5 cases of myoclonus during lithium treatment.
- Review of clinical features and electrophysiologic testing, including EEG and EMG.
- Utilized multichannel surface EMG, EEG, somatosensory evoked potentials, and nerve stimulation reflexes.
Main Results:
- All patients exhibited multifocal action myoclonus, not typically occurring at rest or with reflex activation.
- Back-averaging revealed focal EEG transients over the sensorimotor cortex preceding EMG discharges.
- Discontinuation of lithium therapy resolved myoclonus in two patients.
Conclusions:
- Lithium monotherapy can induce significant clinical myoclonus.
- Characterized by short-duration EMG discharges and cortical action myoclonus without epileptiform EEG abnormalities.
- This lithium-associated myoclonus differs electrophysiologically from that seen with tricyclic antidepressants.