Boucetta Soufiane, Montplaisir Jacques, Zadra Antonio, Lachapelle Francis, Soucy Jean-Paul, Gravel Paul, Dang-Vu Thien Thanh
Center for Studies in Behavioral Neurobiology and Department of Exercise Science, Concordia University, Montreal, Quebec, Canada.
PERFORM Centre, Concordia University, Montreal, Quebec, Canada.
Sleep. 2017 Oct 1;40(10). doi: 10.1093/sleep/zsx140.
Idiopathic hypersomnia is characterized by excessive daytime sleepiness, despite normal or long sleep time. Its pathophysiological mechanisms remain unclear. This pilot study aims at characterizing the neural correlates of idiopathic hypersomnia using single photon emission computed tomography.
Thirteen participants with idiopathic hypersomnia and 16 healthy controls were scanned during resting wakefulness using a high-resolution single photon emission computed tomography scanner with 99mTc-ethyl cysteinate dimer to assess cerebral blood flow. The main analysis compared regional cerebral blood flow distribution between the two groups. Exploratory correlations between regional cerebral blood flow and clinical characteristics evaluated the functional correlates of those brain perfusion patterns. Significance was set at p < .05 after correction for multiple comparisons.
Participants with idiopathic hypersomnia showed regional cerebral blood flow decreases in medial prefrontal cortex and posterior cingulate cortex and putamen, as well as increases in amygdala and temporo-occipital cortices. Lower regional cerebral blood flow in the medial prefrontal cortex was associated with higher daytime sleepiness.
These preliminary findings suggest that idiopathic hypersomnia is characterized by functional alterations in brain areas involved in the modulation of vigilance states, which may contribute to the daytime symptoms of this condition. The distribution of regional cerebral blood flow changes was reminiscent of the patterns associated with normal non-rapid-eye-movement sleep, suggesting the possible presence of incomplete sleep-wake transitions. These abnormalities were strikingly distinct from those induced by acute sleep deprivation, suggesting that the patterns seen here might reflect a trait associated with idiopathic hypersomnia rather than a non-specific state of sleepiness.
特发性嗜睡症的特征是尽管睡眠时间正常或较长，但白天仍过度嗜睡。其病理生理机制尚不清楚。这项初步研究旨在使用单光子发射计算机断层扫描来表征特发性嗜睡症的神经关联。
13名特发性嗜睡症患者和16名健康对照者在静息觉醒状态下使用配备99mTc-乙基半胱氨酸二聚体的高分辨率单光子发射计算机断层扫描仪进行扫描，以评估脑血流量。主要分析比较了两组之间的局部脑血流分布。局部脑血流与临床特征之间的探索性相关性评估了这些脑灌注模式的功能关联。在进行多重比较校正后，显著性设定为p < 0.05。
特发性嗜睡症患者在内侧前额叶皮质、后扣带回皮质和壳核区域脑血流量减少，而杏仁核和颞枕叶皮质血流量增加。内侧前额叶皮质较低的局部脑血流量与较高的白天嗜睡程度相关。
这些初步发现表明，特发性嗜睡症的特征是参与警觉状态调节的脑区功能改变，这可能导致该疾病的白天症状。局部脑血流变化的分布让人联想到与正常非快速眼动睡眠相关的模式，表明可能存在不完全的睡眠-觉醒转换。这些异常与急性睡眠剥夺引起的异常明显不同，表明此处所见的模式可能反映了与特发性嗜睡症相关的一种特质，而非非特异性的嗜睡状态。
