Abstract
Psychiatric comorbidities are common among patients with migraine. These comorbidities can compromise the quality of life of patients and may affect the result of treatment. The prevalence is higher in patients with migraine who overuse abortive medication. The mechanisms underlying these comorbidities remain unclear, but the amygdala is likely to be involved in their pathogenesis. This brain area has important functions in integrating sensory experiences with unpleasant emotions. The central amygdala plays a general integrative role in autonomic functions related to pain, and receives input from the outer layers of the trigeminal nucleus caudalis via the lateral parabrachial nucleus. A recent study showed that neurons in lateral parabrachial nucleus are activated more strongly by noxious stimulation of the face than of the hind paw. Increased excitability of laterocapsular division of the central nucleus of the amygdala has been observed in animals with cortical spreading depression, an electrophysiological phenomenon underlying the aura phase of migraine. Chronic treatment with analgesics further increases the neuronal excitability in the central nucleus of the amygdala and increases cortical spreading depression-evoked expression of Fos in the trigeminal nucleus caudalis and amygdala. These preclinical evidences imply the role of amygdala in pathogenesis of comorbid depression and anxiety commonly observed in patients with migraine.
Original language | English |
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Title of host publication | Amygdala |
Subtitle of host publication | Mechanisms, Structure and Role in Disease |
Publisher | Nova Science Publishers, Inc. |
Pages | 69-103 |
Number of pages | 35 |
ISBN (Electronic) | 9781536138962 |
ISBN (Print) | 9781536138955 |
Publication status | Published - 1 Jan 2018 |