Colás et al found chronic daily headache (CDH) with analgesic overuse common in the general population. [1] With 70% of CDH
patients in the general population not overusing analgesics, [1] it is
essential to reconsider the theory that chronic analgesic consumption can
transform episodic migraine or tension-type headache (TTH) into CDH.
Evidence for the role of analgesics in the development of CDH is
purely circumstantial: [2]
1.) There is no evidence to support the
suggestion [1] that analgesics interfere with the efficacy of prophylactic
headache medications.
2.) We know of no central neuronal process possibly
relevant to migraine or TTH pathophysiology that might be affected by
chronic analgesic consumption. Since drugs that do not cross the blood-
brain barrier also remit migraine, a primary involvement of central
neuronal processes in idiopathic headaches is arguable. [3]
3.) Improvement of headache following analgesic withdrawal is regarded as the
principal basis of this causal assumption. [4] While analgesic abuse is a
self-determined unsupervised activity, analgesic withdrawal is a medically
controlled activity; every therapeutic intervention -- including
supervised analgesic withdrawal -- involves a placebo effect. [2]
4.) Analgesic withdrawal in clinical practice is commonly accompanied by other
interventions undertaken simultaneously. [5]
5.) No particular temporal pattern has emerged between regular analgesic use and development of daily
headache in migraine patients. [2]
6.) A mean of 5.4 years (range, 2 to 10 years) of analgesic consumption preceded onset of daily headache in 62.5%
(5 of 8) of migraine patients; [4] a very tardy speculative pathogenetic mechanism needs to be invoked. [2]
7.) Relevance of the tendency of
headache-prone patients to develop daily headaches if put on analgesics
for a non-headache indications1 must be considered in the context of the
inevitable pain-stress nexus as stress frequently precipitates migraine.
8.) The subtle semantic distinction between CDH and transformed
migraine is based entirely on phenomenology. [2,3]
9.) We do not know why
only very few patients regularly using analgesics develop CDH. [2]
Natural transformation of an episodic primary headache into CDH1
appears to be an uncommon but logical outcome of primary headache
disorders. [2,5] A small subset of primary headache (migraine or tension-
type) patients – over-represented in subspecialty clinics -- might
progress spontaneously from episodic headaches of lower frequency to
episodic headaches of a higher frequency up to daily recurrences. The call
for public health interventions in CDH patients with analgesic overuse [1]
must be preceded by better mechanistic comprehension.
References
1. Colás R, Muñoz P, Temprano R, et al. Chronic daily headache with
analgesic overuse. Epidemiology and impact on quality of life. Neurology
2004;62:1338-1342.
2. Gupta VK. De novo headache and analgesic consumption:
pathophysiological insights from nosologic complexity? Headache 2004;44:375.
3. Gupta VK. Classification of primary headaches: pathophysiology versus nosology? Published electronic response to: Peatfield R. A revised classification of headache disorders. Available at:http://bmj.com/cgi/content/full/328/7432/119?etoc (22 January 2004).
4. Bahra A, Walsh M, Menon S, Goadsby PJ. Does chronic daily headache arise de novo in association with regular use of analgesics? Headache
2003;43:179-190.
5. Lipton RB, Bigal ME. Chronic daily headache. Is analgesic overuse a
cause or a consequence? Neurology 2003;61:154-155.