The sympathetic nervous system is responsible for responding to stressful situations with involuntary actions, which will increase the neuronal activity in order to maintain body homeostasis. Stress is one of the most common causes of migraines. When it occurs for a prolonged period, there will be an over-stimulation of the sympathetic nervous system that will lead to dysautonomia, generating the rapid consumption of the neurotransmitter norepinephrine at the same time that adenosine, dopamine. It is believed that before the headache, the levels of norepinephrine are elevated, causing a vasoconstriction of extracranial vascularization, followed by a vasodilation resulting from the release of the other hormones previously mentioned, thus instituting the painful phase of migraine. Thus, migraine acts on the vascular system through changes in its homeostasis, predisposing the occurrence of future ischemic and/or hemorrhagic episodes to the brain and cardiac levels. The disruption of this system with the multifactorial mechanisms of migraine manifestation can then result in an increased risk of coronary heart disease and other changes in cardiac functioning, acquiring highly harmful potential for the human body. The interest in this study started in view of the numerous uncertainties within the scientific sphere regarding the possible systemic impacts caused by migraines after detailed research on the subject. The same becomes relevant, as it will contribute to the development of knowledge about headaches.
