Glutamate in Migraine Neurobiology and Treatment

TY - CHAP

T1 - Glutamate in Migraine Neurobiology and Treatment

AU - Andreou, Anna P.

N1 - Publisher Copyright: © Springer Nature Switzerland AG 2022.

PY - 2022/1/1

Y1 - 2022/1/1

N2 - Migraine is a disabling chronic condition characterised by recurrent episodes of head pain accompanied by other sensory disturbances. Its pathophysiology is complex and involves both the peripheral and central nervous systems. Glutamate is believed to play an important role in migraine pathophysiology, as it is involved in multiple processes of migraine’s neurobiology. Glutamate is the main neurotransmitter of the trigeminal system and along the ascending trigeminothalamic pathways. It is also involved in the initiation and progression of cortical spreading depression, the underlying biological processes of migraine aura. Its levels are increased during attacks and in chronic migraine patients. Increased glutamate excitation is believed to be at least partly responsible for the clinical symptoms of allodynia in patients during an attack, as well as in the transformation of episodic migraine to chronic migraine. Some of the current migraine treatments include in their mechanism of action, at least partly, modulation of glutamatergic signalling. While some attempts have been made to directly block glutamate receptors, these were abandoned due to the development of significant side effects. Future glutamatergic therapeutics that could indirectly block glutamatergic signalling may present a viable effective tool in migraine patients.

AB - Migraine is a disabling chronic condition characterised by recurrent episodes of head pain accompanied by other sensory disturbances. Its pathophysiology is complex and involves both the peripheral and central nervous systems. Glutamate is believed to play an important role in migraine pathophysiology, as it is involved in multiple processes of migraine’s neurobiology. Glutamate is the main neurotransmitter of the trigeminal system and along the ascending trigeminothalamic pathways. It is also involved in the initiation and progression of cortical spreading depression, the underlying biological processes of migraine aura. Its levels are increased during attacks and in chronic migraine patients. Increased glutamate excitation is believed to be at least partly responsible for the clinical symptoms of allodynia in patients during an attack, as well as in the transformation of episodic migraine to chronic migraine. Some of the current migraine treatments include in their mechanism of action, at least partly, modulation of glutamatergic signalling. While some attempts have been made to directly block glutamate receptors, these were abandoned due to the development of significant side effects. Future glutamatergic therapeutics that could indirectly block glutamatergic signalling may present a viable effective tool in migraine patients.

KW - Aura

KW - Central sensitization

KW - CGRP

KW - Glutamate

KW - Migraine

KW - Spreading depression

KW - Trigeminal

UR - http://www.scopus.com/inward/record.url?scp=85160123260&partnerID=8YFLogxK

U2 - 10.1007/978-3-030-87480-3_6

DO - 10.1007/978-3-030-87480-3_6

M3 - Chapter

AN - SCOPUS:85160123260

SN - 9783030874797

SP - 195

EP - 228

BT - Glutamate and Neuropsychiatric Disorders

PB - Springer International Publishing

ER -