Bilateral oculosympathetic paresis associated with loss of nocturnal melatonin secretion in patients with spinal cord injury

Bilateral oculosympathetic paresis associated with loss of nocturnal melatonin secretion in patients with spinal cord injury
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DOI:
10.1080/10790268.2005.11753798
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发表时间:
2005-01-01
影响因子:
1.7
通讯作者:
Brown, R
Brown, R
中科院分区:
医学4区
文献类型:
--
作者:
Zeitzer, JM;Ayas, NT;Brown, R

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背景:沿着交感神经通路到眼睛的病变可引起眼交感神经麻痹(OSP,霍纳综合征)。眼交感神经通路从下丘脑向下通过颈脊髓并向上到达上级颈神经节(SCG),其支配同侧面部和眼睛中的交感神经靶。该通路似乎与从下丘脑通过颈脊髓和SCG到松果体的类似的视网膜-松果体神经通路密切共定位。因此,沿着该共享通路的病变沿着,例如发生在颈脊髓的神经学完全损伤(四肢瘫痪)中,将被预测为导致同时的OSP和松果体褪黑激素产生的损失。褪黑激素的产生损失可能会导致广泛的睡眠中断观察患者tetraplegal.Methods:我们评估的存在OSP的摄影文件的上睑下垂和瞳孔扩张反应可卡因滴眼液在5个人的神经功能完全损伤,他们的上胸或下颈脊髓。我们将这些结果与分析模式的褪黑激素的生产在这些相同的individual.Results:双边OSP是存在于个人与颈脊髓损伤,每个也缺乏显着的褪黑激素的生产。在2例胸段脊髓损伤低于眼交感神经通路水平的患者中未观察到OSP的证据。两者都有正常的昼夜节律的褪黑激素的生产,与正常parameters.Conclusion的节奏的时间和幅度:双侧眼交感神经麻痹的存在可以预测的夜间生产的褪黑激素的完全丧失。
Background: Lesions along the sympathetic pathway to the eye produce oculosympathetic paresis (OSP, Horner's syndrome). The oculosympathetic pathway descends from the hypothalamus through the cervical spinal cord and ascends to the superior cervical ganglion (SCG), which innervates sympathetic targets in the ipsilateral face and eye. This pathway appears to closely co-localize with a similar retino-pineal neural pathway from the hypothalamus through the cervical spinal cord and SCG to the pineal gland. As such, lesions along this shared pathway, such as occur in neurologically complete injury to the cervical spinal cord (tetraplegia), would be predicted to result in simultaneous OSP and loss of pineal melatonin production. Loss of melatonin production may contribute to the pervasive sleep disruption observed in patients with tetraplegia.Methods: We assessed the presence of OSP by photographic documentation of ptosis and pupillary dilation response to cocaine eye drops in 5 individuals with neurologically complete damage to their upper thoracic or lower cervical spinal cord. We correlated these results with an analysis of the pattern of melatonin production in these same individuals.Results: Bilateral OSP was present in individuals with cervical spinal cord injury; each also lacked significant production of melatonin. No evidence of OSP was observed in the 2 individuals with thoracic spinal cord injury below the level of the oculosympathetic pathway. Both had normal circadian rhythms of melatonin production, with timing and amplitude of the rhythm within normal parameters.Conclusion: The presence of bilateral oculosympathetic paresis can be predictive of the complete loss of the nocturnal production of melatonin.