Disruption of iris adrenergic transmission as an index of poor endorphin modulation in headache.

Pupillometry was used to evaluate the effect of oral or topically applied adrenomimetic drugs and of local morphine on pupillary size in headache patients and controls. In headache sufferers, a disruption of adrenergic transmission is suggested since the iris adrenergic nerve terminal is apparently poor in NE; this neuron also exhibits a reduced capacity of neurotransmitter synthesis and an adrenoceptor hypersensitivity. The spontaneous reduction of pupillary size detected in headache sufferers also suggests a decreased sympathetic input. The miosis, registered after conjunctival instillation of morphine, demonstrates that iris is a possible example of an opioid-dependent adrenergic neuron in man. A poor modulation of the iris adrenergic transmission induces, in headache sufferers, a neuronal incontinence and therefore a chronic intrasynaptic leakage of NE, resulting in an exhausted empty neuron on the one hand and a compensatory hyperactivity of the effector muscular cell on the other. Since indirect evidence suggests a morphine modulation of the iris adrenergic neuron, a deficiency of endorphin modulation could be the mechanism of disruption of iris adrenergic transmission. Apart from the theoretical aspects, the exploration of iris neuroeffector junction represents a noninvasive an simple diagnostic tool in headache.