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Childhood headache
  1. R W Newton
  1. Dr R W Newton, Royal Manchester Children’s Hospital, Pendlebury, Manchester M27 4HA, UK; richard.newton797{at}ntlworld.com

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Few adults have never had a headache yet the condition in childhood, particularly when recurrent, commonly causes irrational fear of serious illness among parents and primary care physicians, leading to referral to paediatric services.

HOW COMMON IS IT?

Headache is common in humans. Population-based studies1 2 show an equal sex prevalence of about 2.5% (or slight male predominance) under 12 rising to 6.0–10.0% thereafter with a female preponderance. Although at times alarming, it rarely represents serious underlying disease (3 of 815 children in one study3) and we ought to emphasise this to the families involved.

WHAT CAUSES HEADACHE AND ASSOCIATED SYMPTOMS?

With its 100 000 million neurones, each with about 100 000 dendritic connections there is little wonder that brain malfunction may lead to a myriad of possible associated experiences. What follows is what we know from migraine research.4

1. The genetic basis of migraine headache

Many young people with headache have a first degree relative with a similar problem. Migraine without aura (see below) is probably a multifactorial disorder caused by genetic and environmental factors. Familial hemiplegic migraine (FHM-I) is associated in about 50% with mutations involving voltage-gated calcium channel CACNA1A gene and in about 20% the ATP1A2 gene. This suggests a channelopathy may cause aura and other neurological manifestations of childhood headache.

2/3. The trigeminal innervation of pain-producing intracranial structures; activation of the peripheral branches of the ophthalmic branch of the trigeminal nerve

Large cerebral vessels, pial vessels, the venous sinuses and dura mater are all innervated by small diameter myelinated and unmyelinated neurones serving nociception. Moskowitz showed in rats that migraine pain may be a form of sterile neurogenic inflammation with plasma extravasation with mast cell degranulation and platelet aggregation.5 Cortical spreading depression may activate trigeminal neurones, particularly the ophthalmic division, release substance P and calcitonin gene-related peptide. This sterile inflammatory response may lead to allodynia (perceived pain from a normally non-painful stimulus) in the trigeminal area, sensitisation of thalamic neurones and an important central nervous system role.

4. The trigemino-cervical complex

Involvement of the trigeminal nucleus …

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