title: Cortical myoclonus during lithium exposure.
abstract: BACKGROUND
  Myoclonus can occur in association with lithium therapy at toxic and therapeutic dosages, and can be a predominant and disabling adverse effect. Moreover, myoclonus has been reported when lithium has been combined with cyclic antidepressants and with the neuroleptic clozapine. Although clinical case reports exist, no electrophysiologic data are available that provide a source or a neurophysiological mechanism for the myoclonus seen in lithium therapy.
  
  
  OBJECTIVE
  To describe the electrophysiologic characteristics and source of the myoclonus associated with lithium therapy.
  
  
  METHODS
  We retrospectively analyzed 5 cases of myoclonus during lithium therapy. We reviewed the clinical features and results of previous electrophysiologic testing. Four patients received lithium monotherapy; and 1, sertraline hydrochloride and nefazodone hydrochloride in addition to lithium. The electrophysiologic data that had been gathered included multichannel surface electromyographic (EMG) recordings with simultaneous electroencephalography (EEG), somatosensory evoked potentials, and elicitation of long-latency EMG reflexes to median and digital nerve stimulation.
  
  
  RESULTS
  All 5 patients showed multifocal action myoclonus without reflex activation and only rare occurrence at rest. In each case, back-averaging created a focal EEG transient over the contralateral sensorimotor area preceding the myoclonus EMG discharge. In 2 of the patients receiving lithium monotherapy, the therapy was discontinued and the myoclonus disappeared.
  
  
  CONCLUSIONS
  Lithium, by itself, can be associated with prominent clinical myoclonus, short-duration (<50-millisecond) myoclonus EMG discharges and cortical action myoclonus without the presence of epileptiform abnormalities on the routine EEG. This myoclonus is different from the most common form that is well documented to occur with tricyclic antidepressant therapy by clinical and electrophysiologic means.
authors.affiliation: Department of Neurology, Parkinson's Disease and Movement Disorders Center, Mayo Clinic Scottsdale, 13400 E Shea Blvd, Scottsdale, AZ 85259, USA. jcaviness@mayo.edu
authors.forename: John N
authors.initials: JN
authors.lastname: Caviness
authors.forename: Virgilio G H
authors.initials: VG
authors.lastname: Evidente
mesh_terms: D000328:Adult; D000368:Aged; D001714:Bipolar Disorder / Q000188:drug therapy*; D002540:Cerebral Cortex / Q000187:drug effects / Q000503:physiopathology*; D003865:Major Depressive Disorder / Q000188:drug therapy; D004569:Electroencephalography / Q000187:drug effects; D004576:Electromyography / Q000187:drug effects; D005260:Female; D006801:Humans; D008094:Lithium / Q000009:adverse effects*; D008297:Male; D008875:Middle Aged; D009207:Myoclonus / Q000139:chemically induced* / Q000175:diagnosis / Q000503:physiopathology*; D012189:Retrospective Studies
chemical_list: D008094:Lithium