Sweating and vascular responses in the face: normal regulation and dysfunction in migraine, cluster headache and harlequin syndrome.
At least four neural mechanisms influence facial blood flow. Firstly, sympathetic vasoconstrictor fibres exert a tonic constrictor influence on the vasculature of the ears, lips and nose, and sparsely supply other parts of the face. Secondly, the sympathetic nervous system actively dilates the cutaneous vasculature of the face during heat stress and emotion. Thirdly, parasympathetic vasodilator reflexes in the facial and glossopharyngeal nerves increase blood flow to the exocrine glands and tissues of the eyes, nose and mouth when these tissues are irritated. Fourthly, axon reflexes release vasoactive peptides from sensory fibres, which participate in local inflammatory responses. The sympathetic nervous system normally controls facial sweating. However, after injury to postganglionic sympathetic fibres, parasympathetic fibres sometimes make functional connections with sweat glands, so that parasympathetic reflexes provoke pathological sweating. In this review, new information about the neural pathways and stimuli which influence facial sweating and blood flow is summarized, and this is followed by a discussion of the pathophysiology of extracranial vascular disturbances and facial sweating in migraine, cluster headache and harlequin syndrome.
Drummond
P D
PD
Division of Psychology, Murdoch University, Western Australia.
D001808:Blood Vessels / Q000503:physiopathology; D003027:Cluster Headache / Q000503:physiopathology*; D005145:Face / Q000098:blood supply*; D005483:Flushing / Q000503:physiopathology*; D006801:Humans; D008881:Migraine Disorders / Q000503:physiopathology*; D012016:Reference Values; D013546:Sweating; D013577:Syndrome