Post-hypoxic Myoclonus: Current Concepts, Neurophysiology, and Treatment

A Rare Case of Lance-Adams Syndrome: Status Post-Successful Cardiopulmonary Resuscitation

“…Neurophysiological studies, such as electroencephalography (EEG), electromyography (EMG), and somatosensory evoked potentials (SSEPs), have also been used for the evaluation of PHM [ 6 , 14 ]. These studies have been found to be particularly useful in delineating the subtypes of PHM by differentiating between cortical and subcortical myoclonus and diffuse versus focal epileptiform activity.…”

“…Medications, including lamotrigine, riluzole, and tetrahydro-nicotinic acid, which cause a decrease in the excitatory amino acid neurotransmitters, have also been found to be helpful in the treatment of LAS. According to some studies, subcortical PHM is usually treated with clonazepam, while levetiracetam or piracetam can often be used to treat cortical myoclonus following hypoxia [ 10 , 14 , 15 ]. In addition to drug therapy, rehabilitation interventions, such as gait and basic activities of daily living (ADL) training, have also been reported to slow the progression of LAS and decrease the chances of developing additional disabilities [ 16 ].…”

“…According to some studies, subcortical PHM is usually treated with clonazepam, while levetiracetam or piracetam can often be used to treat cortical myoclonus following hypoxia [10,14,15]. In addition to drug therapy, rehabilitation interventions, such as gait and basic activities of daily living (ADL) training, have also been reported to slow the progression of LAS and decrease the chances of developing additional disabilities [16].…”

Successful Control of Intractable Myoclonus in a Patient With Hypoxic Brain Injury After Intrathecal Baclofen Therapy: A Case Report

“…Myoclonus induced by various neurological abnormalities, such as severe hypoxic ischemic encephalopathy, spinal cord injury, and human immunodeficiency virus infection, still remains a challenging task. The control of movement abnormalities in LAS is chiefly achieved through the utilization of drugs such as anticonvulsants [ 1 3 7 ]. The possible mechanism of action in the case of clonazepam is the facilitation of gamma amino butyric acid (GABA)ergic transmission and a decrease in 5-hydroxytryptophan utilization in the brain [ 8 ].…”

“…The precise mechanism of post-hypoxic myoclonus is unclear. Animal studies indicate that selective vulnerability to hypoxia of purkinje cells in the cerebellar vermis leads to disinhibition of GABAergic fastigial nucleus, which in turn leads to cell death in parts of the motor thalamus and inducing neuronal injury cerebral cortex, the hippocampus, and the reticular thalamic nucleus [ 2 7 ]. As an exemplary GABAergic agent, the mechanism by which baclofen regulates myoclonus at the supraspinal level is that it stimulates the GABA-B receptor and imitates GABA effect in postsynaptic cells, resulting in maintaining stable status of GABAergic balance and controlling motor function [ 1 ].…”