Migraine and neuropathic pain are common causes of chronic pain. The exact
pathomechanism has not been fully clarified for either disorder, but their pathophysiological
backgrounds involve several similar mechanisms. Peripheral sensitization occurs in the neuronal
elements of the dorsal root ganglion or the trigeminal ganglion, while central sensitization appears in
the second-order neurons in the dorsal horn of the spinal cord or the trigeminal nucleus caudalis. Central neuronal
hyperexcitability has been implicated in both disorders, and the emerging evidence suggests alterations in the
glutamatergic neurotransmission and N-methyl-D-aspartate-receptor activation. Migraine and neuropathic pain
additionally share certain clinical features, such as enhanced sensitivity to sensory stimuli and cutaneous allodynia. The
pharmacotherapy of both diseases is often challenging, but several antiepileptic drugs that target hyperexcitability are
beneficial for both migraine and neuropathic pain. Kynurenine pathway metabolites are capable of influencing the
glutamate receptors, and might therefore be novel candidates for future drug development.
Keywords: Allodynia, glutamate, hyperexcitability, migraine, neuropathic pain, sensitization.
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