Page 16 - The clinical aspects and management of chronic migraine Judith Anne Pijpers
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Chapter 1
Chronification of migraine may be considered as a threshold problem, in which patients have an increased susceptibility for migraine attacks.10 This increased susceptibility might be a consequence of specific factors, such as medication overuse or depression,10 stable intrinsic factors such as genetics susceptibility,17 and fluctuating intrinsic (eg. hormonal changes) and extrinsic factors (eg sleep deprivation), leading to enhanced pain facilitation (pro-nociception) or lack of pain inhibition (anti-nociception). 1,10,15,18–20
Central sensitisation: enhanced pain facilitation
Enhanced pain facilitation, also known as central sensitization, is a state of ongoing excitability and hyper-responsiveness of central regions in the brain, even in the absence of the initial stimulation from peripheral neurons. In migraine, the initial peripheral stimulation is the activation of the trigeminal vascular system (elaborated on previously, see also figure 1), causing intracranial hypersensitivity. This is experienced by patients as pulsating pain in the head, aggravating by activity (Figure 2A).1,14,15
Activation of the trigeminovascular system results into stimulation trigeminal nucleus caudalis (TNC) and subsequently the thalamus (Figure 1). Recurrent activation induces sensitisation of the TNC, in which CGRP might play an important role.1,14 Due to convergence of sensory input from both the meninges and the periorbital skin, sensitisation of the TNC results into referred ipsilateral cephalic cutaneous allodynia, i.e. the perception of pain due to a normally non-painful stimulus (Figure 2B).15,20 Subsequently, thalamic neurons become sensitised by stimulation from the TNC, resulting into extended cephalic and extracephalic cutaneous allodynia (Figure 2C).15,20





























































































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