This study suggests that there is a continuum of reduced striatal dopamine transporters involved in the pathophysiologic mechanisms causing increased muscle activity during REM sleep in patients with subclinical RBD.

Striatal D2/D3 dopaminergic receptors have been proposed to play a role in cataplexy. The authors studied the striatal presynaptic dopamine transporter and postsynaptic D2-receptors in seven patients with narcolepsy and seven control subjects using [123I](N)-(3-iodopropene-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl)tropane and [123I](S)-2-hydroxy-3-iodo-6-methoxy-([1-ethyl-2-pyrrolidinyl]methyl)benzamide SPECT. D2-receptor binding was elevated in narcolepsy (p = 0.017) and correlated with the frequency of cataplectic and sleep attacks (R > or = 0.844, p < or = 0.017). The human striatal dopaminergic system is altered in vivo in narcolepsy/cataplexy.

Polysomnography and needle electromyography were performed on three members of a family with hereditary geniospasm. Electromyography showed simultaneous bilateral discharges exclusively in the mentalis muscle. In one subject we documented a paroxysm of geniospasm during sleep phase 2. This activity ceased with the onset of REM sleep. In view of the mechanism of REM atonia and the bilateral chin EMG discharges, our findings support a supranuclear origin of the peculiar mentalis muscle paroxysms.