| pubmed-article:2050515 | pubmed:abstractText | A large number of clinical and neurophysiological observations are reviewed that clearly indicate that the symptoms of migraine aura result from a spread of an excitatory wave along the cortex from a primary focus. This excitation may start as a consequence of information overload to a low threshold cortical area. The transient neuronal excitation is followed by a long-lasting period of reduced cortical flow, which involves a substantial component of active constriction of resistance vessels, even persisting for several hours during the headache phase. When the excitatory wave has reached and activated free pain fiber endings in sufficiently many cortical vessels, off-branching peripheral motor endings of these fibers may become activated via axon reflexes. These motor endings may be located in cortical microvessels or in small vessels around large dural vessels. This leads to a neurogenic inflammation in the vessel walls, experienced as headache by the sufferer. The wall of dural sinuses offers a rational explanation for the beneficial effect of most medications used in migraine. | lld:pubmed |
