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• Vol.53 No.11
• CLINICA NEUROL, 53: 1125−1127, 2013
• Vol.53 No.11 contents

Symposium 2

The recent pathophysiology of cluster headache (trigeminal autonomic cephalalgias; TACs)

Tomokazu Shimazu, M.D., Ph.D.¹⁾

¹⁾Neurology, Saitama Neuropsychiatric Institute

Background
Cluster headache (CH), known as one of the trigeminal autonomic cephalalgias, is a stereotyped primary pain syndrome characterized by unilateral severe pain, the pathophysiology of which are not well understood.

Pathophysiology
The underlying pathophysiology of CH is incompletely understood. The periodicity of the attacks suggests the involvement of a biologic clock within the hypothalamus which controls circadian rhythms, with central disinhibition of the nociceptive and autonomic pathways, the trigeminal nociceptive pathways. Positron emission tomography and voxelbased morphometry have identified the posterior hypothalamic gray matter as the key area for the basic defect in CH. Functional hypothalamic dysfunction has been confirmed by abnormal metabolism based on the N-acetylaspartate neuronal marker in magnetic resonance spectroscopy. A recent case study demonstrated the release of both trigeminal and parasympathetic neuropeptides during a bout of pain in the same pattern previously described in CH. It is hypothesis that trigeminal activation leads to reflex autonomic activation. At a clinical level, there should be a pain threshold above which autonomic symptoms occur, modified by the highly somato- topic and functionally organized central connections of the trigeminovascular system.
Full Text of this Article in Japanese PDF (1259K)

(CLINICA NEUROL, 53: 1125−1127, 2013)
key words: cluster headache, trigeminal autonomic cephalalgias (TACs), pathophysiology, hypothalamus, neuropeptide

(Received: 30-May-13)