Altered functional connectivity in lesional peduncular hallucinosis with REM sleep behavior disorder.
Altered functional connectivity in lesional peduncular hallucinosis with REM sleep behavior disorder.
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DOI：
10.1016/j.cortex.2015.10.015
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发表时间：
2016-01
期刊：
影响因子：
--
通讯作者：
Whitfield-Gabrieli S
中科院分区：
文献类型：
--
作者：
Geddes MR;Tie Y;Gabrieli JD;McGinnis SM;Golby AJ;Whitfield-Gabrieli S
脑干病变引起脚幻觉症（PH）产生生动的幻视，偶尔伴有睡眠障碍。重叠的脑干区域通过丘脑皮层网络的门控来调节视觉通路和REM睡眠功能。一名66岁的阵发性房颤患者出现了突发性复杂幻视，并保留了洞察力和暴力的梦境行为。脑部MRI显示左侧脑桥头背侧弥散受限，提示急性缺血性梗死。多导睡眠图诊断为REM睡眠行为障碍（RBD）。我们研究了脑桥-膝状体-枕叶回路的完整性，并与46名对照者进行了基于种子的静息态功能连接MRI（rs-fcMRI）。与对照组相比，RS-fcMRI显示病变与外侧膝状体核（LGN）之间以及LGN与视觉关联皮层之间的功能连接显著减少。相反，脑干和视觉联合皮层之间的功能连接，以及视觉联合皮层和PFC之间的患者显着增加。在人类中，左侧头背侧脑桥的局灶性损伤足以引起RBD和PH，这表明两种综合征的机制重叠。这种病变产生了一种改变功能连接的模式，与通过丘脑皮质通路的去传入干扰视觉皮层连接一致。
Brainstem lesions causing peduncular hallucinosis (PH) produce vivid visual hallucinations occasionally accompanied by sleep disorders. Overlapping brainstem regions modulate visual pathways and REM sleep functions via gating of thalamocortical networks. A 66-year-old man with paroxysmal atrial fibrillation developed abrupt-onset complex visual hallucinations with preserved insight and violent dream enactment behavior. Brain MRI showed restricted diffusion in the left rostrodorsal pons suggestive of an acute ischemic infarct. REM sleep behavior disorder (RBD) was diagnosed on polysomnography. We investigated the integrity of ponto-geniculate-occipital circuits with seed-based resting-state functional connectivity MRI (rs-fcMRI) in this patient compared to 46 controls. Rs-fcMRI revealed significantly reduced functional connectivity between the lesion and lateral geniculate nuclei (LGN), and between LGN and visual association cortex compared to controls. Conversely, functional connectivity between brainstem and visual association cortex, and between visual association cortex and PFC was significantly increased in the patient. Focal damage to the left rostrodorsal pons is sufficient to cause RBD and PH in humans, suggesting an overlapping mechanism in both syndromes. This lesion produced a pattern of altered functional connectivity consistent with disrupted visual cortex connectivity via de-afferentation of thalamocortical pathways.