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丛集性头痛无症状患者的睫脊反射增强是由于节前交感神经机制所致。

The enhanced ciliospinal reflex in asymptomatic patients with cluster headache is due to preganglionic sympathetic mechanisms.

作者信息

Havelius U, Heuck M, Milos P, Hindfelt B

机构信息

Department of Ophthalmology, University Hospital MAS, Malmö, Sweden.

出版信息

Headache. 1997 Sep;37(8):496-8. doi: 10.1046/j.1526-4610.1997.3708496.x.

DOI:10.1046/j.1526-4610.1997.3708496.x
PMID:9329232
Abstract

An amplified ciliospinal reflex response has been documented in patients with cluster headache, lacking a Horner-like syndrome. The mechanism is unknown. Tentatively, it may be due to an increased release of monoamines from post-ganglionic sympathetic nerve endings or an increased density of postsynaptic adrenergic receptors in the dilatator muscle of the iris. The instillation of a 1% phenylephrine solution into the conjunctival sac induces mydriasis by stimulating postsynaptic adrenergic receptors in the dilatator muscle of the iris, while the instillation of a 2% tyramine solution causes mydriasis by releasing noradrenaline from the presynaptic sympathetic nerve terminals in the iris. According to these premises, a positive correlation should be expected between the ciliospinal reflex response and the pupillary response to tyramine, if the enhanced ciliospinal reflex response was due to an increased presynaptic release of monoamines. No such correlation was found. Nor was there any positive correlation between the ciliospinal reflex response and the pupillary response to phenylephrine, contradicting an increased density of postsynaptic monoaminergic receptors in the dilatator muscle of the iris as the explanation. However, there was a significant positive correlation between the pupillary responses to phenylephrine and tyramine, ruling out any functionally caused "denervation" hypersensitivity in the dilatator muscle of the iris. It is concluded that the amplified ciliospinal reflex response in cluster headache patients (lacking a Horner-like syndrome) reflects compensatory pathophysiological mechanisms proximal to the third-order sympathetic neuron.

摘要

在丛集性头痛患者中已记录到睫脊反射反应增强,且无霍纳氏综合征样表现。其机制尚不清楚。初步推测,这可能是由于节后交感神经末梢单胺释放增加,或虹膜开大肌中突触后肾上腺素能受体密度增加所致。向结膜囊滴入1%的去氧肾上腺素溶液,通过刺激虹膜开大肌中的突触后肾上腺素能受体诱发瞳孔散大,而滴入2%的酪胺溶液则通过从虹膜突触前交感神经末梢释放去甲肾上腺素导致瞳孔散大。根据这些前提,如果增强的睫脊反射反应是由于单胺突触前释放增加所致,那么睫脊反射反应与对酪胺的瞳孔反应之间应存在正相关。但未发现这种相关性。睫脊反射反应与对去氧肾上腺素的瞳孔反应之间也没有正相关,这与虹膜开大肌中突触后单胺能受体密度增加的解释相矛盾。然而,对去氧肾上腺素和酪胺的瞳孔反应之间存在显著正相关,排除了虹膜开大肌中任何功能性导致的“去神经”超敏反应。结论是,丛集性头痛患者(无霍纳氏综合征样表现)中增强的睫脊反射反应反映了三级交感神经元近端的代偿性病理生理机制。

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