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Headache is a common chief complaint in the pediatrician’s practice. During the initial intake, important information to gather includes headache onset, frequency, timing, duration, quality, location, radiation, and associated symptoms. Determining factors that are likely contributing to the headache or identifying “triggers” may aid in prevention or even stop the headaches. By asking these pertinent questions, the provider will achieve accurate classification (primary vs secondary and episodic vs chronic), resulting in more consistent and positive outcomes for patients. Referral to a headache specialist is indicated when headaches appear refractory to standard treatments or if the appropriate classification is in question. Of the multitude of headache types presenting in children, only a handful of commonly encountered headaches are discussed in this chapter. A complete list of headache types and detailed diagnostic criteria may be found in the International Classification of Headache Disorders, 3rd edition (ICHD-3).


A variety of headache types affect a majority of the pediatric population at least once during childhood. Most epidemiologic studies of pediatric headaches focus on migraine headache. Approximately 10% of children meet criteria for migraine headache, with half experiencing significant headache-related disability. This results in school absence, decreased socialization, and time away from work for parents caring for an ill child, which translate to a substantial economic impact from headache. In fact, the Global Burden of Disease Study 2013 reports recurrent tension-type headache and recurrent migraine as the second and seventh most prevalent chronic disorders worldwide.


The pathogenesis of headache varies by type of headache. Although migraine was previously regarded as primarily vascular in origin, the importance of sensitization of pain pathways and the possibility that attacks may originate in the central nervous system have gained increasing attention during recent decades. The circuitry of migraine pain is complex and involves the trigeminovascular system and several aspects of its neurotransmission peripherally and centrally to the trigeminal nucleus caudalis, the central mesencephalic gray, and the thalamus. Both peripheral and central aspects of the trigeminovascular system are altered in migraine. Peripheral components, including meningeal nociceptors, are hyperexcitable and may be conditioned to respond to a lower level of stimulation. Neurons from the spinal trigeminal nucleus transmit signals to central sites, including the brainstem, cortex, thalamus, hypothalamus, and basal ganglia. Repeated attacks lead to sensitization of these sites, resulting in cortical changes. The state of this system is affected by variations in homeostasis caused by changes in hormones, stress response, dehydration, sleep patterns, and hunger.

In migraine with aura, regional cerebral blood flow is decreased in the cortex corresponding to the clinically affected area and often over a wider area. Reduction in blood flow usually starts posteriorly in the visual cortex, spreads anteriorly, and is usually above the ischemic threshold. After 1 to several hours, gradual transition into hyperemia occurs in the same regions. Cortical spreading depression of Leao is ...

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