In restless legs syndrome, the neural substrates of the sensorimotor symptoms are also normally involved in upright standing posture and biped walking.

Restless legs syndrome (RLS) exhibits sensorimotor symptoms. In familial cases, a gene at chromosomal location 9p-24-22 is linked to RLS and the expressed mutation is Dopamine Receptor Specific Individual Sensitivity (DRSIS). The symptoms are triggered during changes in alertness, generally at sleep hours, resulting from insufficient dopamine transmission.

In restless legs syndrome, during changes in vigilance, the forced EEG shifts from alpha activity to delta or high alpha may lead to the altered states of dopamine receptor function and the symptoms.

RLS cases may carry a genetic vulnerability called EEG alpha activity gate dyscontrols which appear during changes in vigilance and generally during sleep. It is triggered by forced EEG shifts either from alpha activity to delta or high alpha. Expressions of alpha activity gate dyscontrols may have a gate effect that trigger a second vulnerability-dopamine receptor specific individual sensitivity (DRSIS) and this leads to a deficiency in dopamine transmissions at diencephalospinal dopamine system (DSDS).