5th Edition of International Neurology Conference 2026

Abstract

Lance-Adams Syndrome (LAS) is a rare form of chronic post-hypoxic myoclonus that presents days to weeks after successful resuscitation from cardiac arrest. With fewer than 150 cases described in the literature and no established diagnostic criteria, differentiating LAS from acute myoclonic status epilepticus (MSE) remains a major clinical challenge.

We describe a man in his twenties who developed severe, persistent generalised myoclonic seizures following two in-hospital cardiac arrests secondary to hypoxia. Initial neuroimaging and biochemical findings were unremarkable, and repeated electroencephalograms (EEGs) demonstrated evolving epileptogenic activity but not the continuous discharges expected in MSE. The patient’s preserved cognition and responsiveness during seizure episodes raised suspicion for LAS.

Despite treatment with multiple antiepileptic agents, including levetiracetam, clonazepam, sodium valproate, phenytoin, thiopentone, and phenobarbitone, seizure control was not achieved. A ketamine infusion ultimately terminated the generalised myoclonus within 24 hours. His long-term antiepileptic regimen was optimised to sodium valproate, levetiracetam, piracetam, and clonazepam, resulting in significant symptom improvement.

Rehabilitation focused on managing intention myoclonus and intensive physiotherapy to address critical illness-related weakness. Weighted limb exercises and gamified physiotherapy were incorporated to improve engagement and voluntary motor control. Breathing and anxiety-management techniques were used to address stress-induced worsening of myoclonus.

At seven months post-cardiac arrest, the patient remains in a neurorehabilitation setting. He demonstrates progressive recovery of gross and fine motor function and improved independence in activities of daily living, though mild intention myoclonus persists.

LAS is often misdiagnosed as MSE, leading to premature withdrawal of care. The key distinguishing feature is preserved awareness once sedation is lifted. Our case emphasises the importance of structured sedation holds in all post–cardiac arrest patients presenting with myoclonus to avoid diagnostic error.

Neuroimaging and electrophysiological findings are frequently nonspecific. In this case, serial CT and MRI scans were normal, and EEG results varied across stages of illness, reflecting the poor diagnostic reliability of these investigations in LAS. MRI remains the preferred imaging modality to exclude hypoxic-ischaemic encephalopathy (HIE), though diagnosis ultimately remains clinical.

Pharmacological management of LAS is empiric, with no universally accepted regimen. In this case, ketamine was uniquely effective for drug-resistant myoclonus, aligning with emerging case reports supporting its use. Long-term symptom control was best achieved with a multidrug approach combining sodium valproate, levetiracetam, clonazepam, and piracetam—agents consistently cited in the literature.

Physiotherapy plays a central role in functional recovery, though evidence guiding specific interventions remains limited. Incorporating engaging, patient-centred therapy improved compliance and outcomes in this case, highlighting the interplay between mental state and rehabilitation success