Recent advances in migraine research indicate that migraines are most probably a genetically caused malfunction of the neurotransmitting system in the human brain stem and diencephalon. As a consequence of a dysfunction of serotonergic and noradrenergic neurons, a disequilibrium of the vegetative nervous system occurs with sympathetic hyperexcitability. Exogenic and endogenic stress factors then precipitate migraine attacks. When biochemical substances are released, vascular spasms, vasodilatation and edema of the vascular walls are triggered. The actual migraine pain occurs via pain mediator sensitization of nociceptors in the vascular walls. A pain attack can be suppressed effectively, and in many cases even arrested, by performing manual lymph drainage at an early stage. The active mechanism can be explained by peripheral-analgesic and central sedative and analgesic effects. The interval mechanism is based on the sympathetic-suppressive effect of ML. These mechanisms will be discussed.