Figure 1
Lance-Adams syndrome pathophysiology.
This figure illustrates Lance-Adams syndrome’s possible origins, neurotransmitter involvement, and probable causes and mechanisms underlying hypoxic myoclonus, which may affect various brain regions, consistent with prior imaging and metabolic studies [1114]. Abbreviations: GABA: gamma-aminobutyric acid. CO: carbon monoxide. PPN: pedunculopontine nucleus.
Figure 2
Lance-Adams syndrome diagnosis.
This figure presents different aspects of the diagnosis of Lance-Adams syndrome. An in-depth patient history should be obtained, as this condition usually occurs following hypoxia, and a differential diagnosis should be considered. The use of some imaging modalities may assist in the diagnosis. Even though no specific EEG findings have been reported, quantitative EEG may reveal some changes. Abbreviations: LAS: Lance-Adams syndrome. PHS: post-hypoxic seizure. EEG: electroencephalography.
Figure 3
Lance-Adams syndrome treatment and management.
This figure demonstrates possible treatments and management options for Lance-Adams syndrome. Various medications have been reported as having been used for the syndrome in past literature, including CNS depressants, anticonvulsants, CND modulators, and cannabinoids. It is controversial whether globus pallidus-deep brain stimulation is beneficial. Moreover, neuromodulation therapy has been suggested to be used in the early stages of the syndrome, as well as expiratory muscle strength training to alleviate verbal symptoms of the disease [495051525354].