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Minimal Mesopontine Neuronal Loss In Disordered Rapid-Eye-Movement Sleep

Idiopathic rapid-eye-movement sleep behaviour disorder is not characterised by marked mesopontine neuronal loss, nor are metabolic disturbances detectable by proton magnetic resonance spectroscopy, say Spanish researchers.

Rapid-eye-movement sleep behaviour disorder was thought to result from dysfunction of the brain stem structures which regulate physiological rapid-eye-movement sleep muscle atonia, the researchers note.

At a university hospital sleep laboratory centre in Barcelona, Spain, the researchers investigated whether proton magnetic resonance spectroscopy, a non-invasive way of detecting in vivo neuronal dysfunction in localised brain areas, could detect brainstem abnormalities in patients with idiopathic rapid-eye-movement sleep behaviour disorder.

Spectroscopy centered on the midbrain and the pontine tegmentum was acquired in 15 untreated patients with the disorder and in 15 healthy controls matched for age and sex.

The patients were diagnosed by history and video-polysomnography, normal neurological examination and normal cranial magnetic resonance imaging. The controls had no sleep complaints and normal polysomnography and brain imaging.

The researchers evaluated the metabolic peaks detectable with proton magnetic resonance spectroscopy, N-acetylaspartate, creatine-phosphocreatine, choline-containing compounds and myoinositol in the mid-brain and pontine tegmentum. They also evaluated the ratios of N-acetylaspartate, choline-containing compounds and myoinositol to creatine-phosphocreatine.

No significant differences were found in these ratios between patients and controls.
Sleep 2002;25:8:867-870. "Proton Magnetic Resonance Spectroscopy in Idopathic REM Sleep Behavior Disorder"

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