Ocular sympathetic function, facial flushing and the presence or absence of lachrymation and rhinorrhoea were examined in 30 patients during spontaneous or nitroglycerin-induced cluster headache. In 27 cases measurements were also obtained during the headache-free interval. Ocular sympathetic function was impaired on the symptomatic side between cluster attacks and function was reduced further during cluster headache. Greater heat loss from the orbital region on the symptomatic side was associated with ocular sympathetic dysfunction both during and between attacks, and with lachrymation during attacks. Heat loss from the cheek and side of the nose was greater on the symptomatic side in patients whose attack was accompanied by lachrymation, but heat loss from these areas was unrelated to the extent of ocular sympathetic deficit. These findings suggest that parasympathetic overactivity in the greater superficial petrosal nerve provokes facial flushing and lachrymation. Parasympathetic overactivity could also cause dilatation of the internal carotid artery and compression of the periarterial plexus of sympathetic fibres, producing a sympathetic deficit with release of vasoconstrictor tone in the eye. Thus autonomic disturbances in cluster headache may be explained by the unitary hypothesis of parasympathetic hyperactivity being responsible for ocular sympathetic deficit.