This theory suggests that a multifaceted succession of neural and vascular activities commences migraine. At the normal state, even in the absence of a headache the cerebral cortex, mainly the occipital cortex of a migraineur’s brain is in a state of hyper excitability. These findings are proven in studies involving transcranial magnetic stimulation with functional magnetic resonance imaging (MRI). This finding justifies the distinctive vulnerability of the brain of patients with migraine to headaches.
The cortical spreading depression (CSD) theory defines the process involving in MA. CSD is a precise ripple of neuronal excitation in the cortical gray matter that sweeps from its starting point at the rate of two- six millimeters (mm)/ minute (min). This cellular depolarization produces the aura phases and thereby triggers trigeminal fibers resulting in the phase of headache. The discharge of potassium or the excitatory amino acid glutamate from neural tissue causes depolarization of the nearby tissues leading to the discharge of more neurotransmitters thereby disseminating