SYMPATHETIC VASOCONSTRICTOR OUTFLOW TO EXTREMITY MUSCLES IN CLUSTER HEADACHE - RECORDINGS DURING SPONTANEOUS AND NITROGLYCERIN-INDUCED ATTACKS

search for evidence of sympathetic dysregulation during cluster headac he attacks, microneurographic recordings of muscle nerve sympathetic a ctivity (MSA) were obtained from the peroneal nerve. In three recordin gs commenced after the onset of spontaneous attacks, MSA was about twi ce as high during the attack as afterwards. In four nitroglycerin-indu ced attacks, MSA showed a rise paralleling the pain, preceded by an in itial peak. The latter accompanied hypotension, whereas the rise coinc iding with cluster headache was associated with rising blood pressure. The normal baroreflex-governed pulse synchrony of MSA was preserved b oth during spontaneous and provoked attacks. In seven cluster headache patients in whom nitroglycerin did not cause an attack, only an initi al peak in MSA occurred. Nor was any late nitroglycarin-induced rise i n MSA observed in nine healthy subjects; the initial peak in MSA and h eart rate was followed by a rapid return to normal despite a falling b lood pressure. It is concluded that cluster headache attacks are assoc iated with an increase in MSA that elevates blood pressure by causing vasoconstriction, and that this increase, rather than indicating sympa thetic dysregulation, is a normal pain-evoked secondary phenomenon. Th e findings in healthy subjects support the notion that nitroglycerin h as a central sympatho-inhibitory affect.