Abstract
Rise of intracranial pressure (ICP) is currently presumed to underlie benign cough headache (BCH). Cough normally increases ICP but very few patients develop BCH. Children, young adults and females are rarely affected. Reduction of ICP by lumbar puncture (LP) or indomethacin offers variable therapeutic success. BCH can persist for several months or years but LP lowers ICP for few hours only and has significant morbidity. Choroidal blood volume and intraocular pressure (IOP) are instantaneously responsive to cough. Mechanical deformation of pressure-sensitive ocular structures by sudden experimental IOP elevation generates transient neural traffic in ocular trigeminal nerve fibres. Homeostatic mechanisms normally limit effect of cough-induced intraocular venous congestion. I propose that in a few patients, ocular sympathetic hypofunction significantly alters intraocular pressure–volume relation and predisposes to exaggerated choroidal venous congestion and fluctuation of IOP in response to cough, that, in turn, results in sudden transient cephalalgogenic antidromic trigeminal nerve discharge. Known variations in ocular hydrodynamics, ocular rigidity, and forced expiration rationalize epidemiology of BCH. This hypothesis can be tested by study of pupillary function and facial sweating in patients with BCH.
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