Document Type

Article

Publication Date

November 2004

Comments

This is the authors' final version prior to publication as clinical correspondence in Cephalalgia 24(11):1005-1006, November 2004. The definitive version is available at www.blackwell-synergy.com (http://dx.doi.org/10.1111/j.1468-2982.2004.00794.x). Copyright (c) by Blackwell Publishing, Inc.

Abstract

Cluster headache (CH) is characterized by episodes of severe unilateral headache accompanied by symptoms of cranial parasympathetic hyperactivity and sympathetic dysfunction that occur in cluster periods. Positron emission tomography (PET) studies have demonstrated evidence of a central generator of CH attacks located in the posterior-inferior hypothalamus. It has been suggested that the autonomic symptoms in CH result from reflex activation of the superior salivatory nucleus secondary to activation of the trigeminal nucleus caudalis (TNC). However, several cases of CH-like symptoms with no head pain have been documented.

We describe a patient who had suffered from typical episodic CH for two decades; it later converted into episodic autonomic dysfunction without head pain.

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