Lance-Adams Syndrome in the Intensive Care Unit: A Case Report

Lance-Adams syndrome (LAS), or chronic post-hypoxic myoclonus, is a myoclonic disorder following acute cerebral hypoxia after successful cardiopulmonary resuscitation (CPR). LAS is distinct from acute post-hypoxic myoclonus (acute PHM), presenting with myoclonic jerks and cerebellar ataxia after regaining consciousness. However, the overlap at the onset complicates differentiation and may lead to the withdrawal of life-sustaining measures, especially in sedated ICU patients. The presented case involves a 77-year-old male diagnosed with LAS post-CPR. Despite the presence of early myoclonic jerks EEG, laboratory testing, and neuroimaging showed no definitive proof of irreversible neurological damage. Once diagnosed, treatment involved sequential antiseizure medications and physical therapy when the patient achieved full consciousness. However, the patient ultimately faced severe disabilities and was unable to recover. This case report emphasizes the importance of limiting sedation, comprehensive clinical examination, and the use of complementary tests when no definitive proof of irreversible neurological damage is present after acute cerebral hypoxia. While LAS has a better vital prognosis than acute PHM, it is associated with poor neurofunctional recovery and chronic disability in most cases. Further research is essential for evidence-based management.