Ann Rehabil Med.  2012 Aug;36(4):561-564. 10.5535/arm.2012.36.4.561.

Lance-Adams Syndrome

Affiliations
  • 1Department of Rehabilitation Medicine and Institute of Health Sciences, Gyeongsang National University Graduate School of Medicine, Jinju 660-702, Korea. yoonch@gnu.ac.kr

Abstract

It is not common for a patient who survives cardiac arrest to experience significant neurologic impairment such as acute and chronic post-hypoxic myoclonus, known as Lance-Adams syndrome. This syndrome is predominantly characterized by myoclonus that starts days to weeks after cardiopulmonary resuscitation in patients who regained consciousness. Although several cases of LAS were reported, the decisive treatment method has not been established. We report a 43 year old man with Lance-Adams syndrome who showed long-term improvement through treatment with anti-myoclonic agents and participation in a rehabilitation program.

Keyword

Cardiopulmonary resuscitation; Myoclonus; Lance-Adams syndrome

MeSH Terms

Cardiopulmonary Resuscitation
Consciousness
Heart Arrest
Humans
Myoclonus

Figure

  • Fig. 1 One day after cardiopulmonary resuscitation (CPR), the electroencephalogram (EEG) of the patient showed semiperiodic bursts of spike-and-waves and polyspike-and-wave-complexes, maximally in the frontal area.

  • Fig. 2 One month after CPR, the EEG showed no epileptiform activities.

  • Fig. 3 Three months after CPR, the EEG showed low voltage background activity though the artifacts at the multiple electrode.

  • Fig. 4 Three months after CPR, T2-weighted magnetic resonance axial images of the patient showed subtle hyperintense lesions in the both cerebral white matters, suggesting hypoxic encephalopathy.


Reference

1. Venkatesan A, Frucht S. Movement disorders after resuscitation from cardiac arrest. Neurol Clin. 2006; 24:123–132. PMID: 16443134.
Article
2. Choi HC, Song HK. Is the intensive anticonvulsant treatment for control of acute posthypoxic myoclonic status epilepticus necessary? J Korean Neurol Assoc. 2006; 24:125–130.
3. Werhahn KJ, Brown P, Thompson PD, Marsden CD. The clinical features and prognosis of chronic posthypoxic myoclonus. Mov Disord. 1997; 12:216–220. PMID: 9087980.
Article
4. Lance JW, Adams RD. The syndrome of intention or action myoclonus as a sequel to hypoxic encephalopathy. Brain. 1963; 86:111–136. PMID: 13928398.
Article
5. Kim DH, Kim SJ, Oh KI, Kwon YS, Son BK. A Case of the successful treatment of pentobarbital for posthypoxic action myoclonus (Lance-Adams Syndrome) with refractory status epilepticus. J Korean Child Neurol Soc. 2006; 14:342–347.
6. Frucht SJ, Louis ED, Chuang C, Fahn S. A pilot tolerability and efficacy study of levetiracetam in patients with chronic myoclonus. Neurology. 2001; 57:1112–1114. PMID: 11571347.
Article
7. Welsh JP, Placantonakis DG, Warsetsky SI, Marquez RG, Bernstein L, Aicher SA. The serotonin hypothesis of myoclonus from the perspective of neuronal rhythmicity. Adv Neurol. 2002; 89:307–329. PMID: 11968457.
8. Matsumoto RR, Truong DD, Nguyen KD, Dang AT, Hoang TT, Vo PQ, Sandroni P. Involvement of GABA(A) receptors in myoclonus. Mov Disord. 2000; 15:47–52. PMID: 10755272.
Article
9. Frucht S, Fahn S. The clinical spectrum of posthypoxic myoclonus. Mov Disord. 2000; 15:2–7. PMID: 10755265.
Article
10. Polesin A, Stern M. Post-anoxic myoclonus: a case presentation and review of management in the rehabilitation setting. Brain Inj. 2006; 20:213–217. PMID: 16421070.
Article
Full Text Links
  • ARM
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr