The effects of cardiac sympathetic nerve stimulation on coronary inflow were studied in previously operated conscious dogs, using electromagnetic flowmeters. Stimulation caused an increase of coronary inflow which was due mainly to an augmentation of flow during diastole. In systole, inflow changes were smaller and variable according to the strength of stimulation. The data presented indicate that an arteriolar dilatation may play a role in augmenting coronary inflow. In several instances, the increase of coronary inflow was preceded by a phase of reduction which suggested the possibility of coronary vasoconstriction as a primary direct effect of cardiac sympathetic activation.

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Cluster headaches have an incidence of 1-3 per 10,000 with a 2.5:1 male-to-female gender ratio. Although not life threatening, the impact of the attacks on the individual patient can result in tremendous pain and disability. The pathophysiology of the disease is unclear, but it is known that the hypothalamus, the brainstem, and genetic factors, such as the G1246A polymorphism, play a role. A distinction is made between episodic and chronic cluster headaches. In a controlled setting, we treated 29 patients with cluster headaches (13 with chronic cluster and 16 with the episodic form), who had been refractory to conventional treatments, with a low dose of ketamine (an NMDA receptor antagonist) i.v. over 40 min to one hour every 2 weeks or sooner for up to four times. It was observed that the attacks were completely aborted in 100 % of patients with episodic headaches and in 54 % of patients with chronic cluster headaches for a period of 3-18 months. We postulated neuroplastic brain repair and remodulation as possible mechanisms.

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