Page 109 - The clinical aspects and management of chronic migraine Judith Anne Pijpers
P. 109

Introduction
Migraine is a common, multifactorial brain disorder, characterized by recurrent headache attacks with nausea, vomiting and hypersensitivity to movement, light and sound, and sometimes with aura symptoms. Most patients have the episodic form, with a median attack frequency of 1-2 per month 1. However, every year 3% of these patients convert from less-frequent episodic migraine to high-frequent chronic migraine (≥ 15 headache days per month, of which ≥ 8 migraine days), a process called migraine chronification 2,3. Frequent use of acute headache medication is a major risk factor for migraine chronification, and as such, the majority of chronic migraine patients have medication overuse. Discontinuation of the overused medication is an important therapy, which is effective in the majority, but not of all patients 3–5.
Migraine chronification is hypothesised to be a decreased threshold problem, in which patients have increased susceptibility for migraine attacks. This increased susceptibility may be a consequence of central sensitisation, a state of ongoing excitability and hyper-responsiveness of central regions of the brain 3,6–8. During the headache phase of a migraine attack, the trigeminal afferents surrounding meningeal blood vessel become activated 6,9. Recurrent activation of these trigeminal afferents induces sensitisation of the trigeminal nucleus caudalis. Due to convergence of sensory input from both the dura and the periorbital skin, sensitisation of the trigeminal nucleus caudalis results into referred ipsilateral cephalic cutaneous allodynia, i.e. the perception of pain due to a normally non- painful stimulus. Subsequently, thalamic neurons become sensitised, leading to referred extended cephalic and extracephalic cutaneous allodynia, as all sensory input from the skin converges in the thalamus 6–8.
Thus, cutaneous allodynia, and especially the spatial distribution of cutaneous allodynia, may be used as a clinical marker of the presumably sequential central sensitisation processes. Cutaneous allodynia can be perceived upon thermal or mechanical stimuli. Hence, it is experienced during daily activities, such as combing hear, exposure to cold, wearing tight clothes, and resting the head on a pillow 10–13. Cutaneous allodynia is associated with a higher prevalence of depression in migraine patients 14 and is an (independent) predictor for migraine chronification 10. Preclinical and clinical studies suggests that central sensitization of the trigeminal nociceptive system is a reversible phenomenon
6
Allodynia as predictor for treatment response
107
 



























































































   107   108   109   110   111