Abstract
Pediatric headache is a common condition that often results in frequent outpatient visits. There are two broad etiological groups of headaches—primary and secondary headaches—with the former being more prevalent. Migraine, a type of primary headache, shares similarities with those experienced by adults, albeit with some variations in diagnostic criteria. The secondary causes of headache should be differentiated from the primary headaches with proper clinical evaluation and focussed investigations. The management of migraine focusses on lifestyle modifications, behavioral therapy, and pharmacotherapy for acute episodes and long-term preventive therapy. There are many novel promising treatment modalities. This review article provides an overview of pediatric headache epidemiology, classification, and pathophysiology and then elaborates on management and prevention strategies.
From the article:
1. Etiology
Headaches in children can be categorized into primary, where pain is a result of the headache condition itself, and secondary, where pain serves as a symptom of an underlying condition. Migraine and tension-type headaches are the most frequently encountered types of primary headaches in children. Cluster headache, a type of primary headache in children, exhibits similar characteristics to headaches in adults but is rare among young children. Upper respiratory tract infections are the commonest cause of secondary headaches that prompt emergency visits. Meningitis, hydrocephalus, and intracranial tumours are common etiologies of life-threatening headache in children. Frequently, no diagnosis can be reached despite an extensive evaluation. In a study involving 48,575 children aged 5 to 17 years who had headache disorders, about 19% were identified with primary headaches, 1.1% were diagnosed with secondary headaches, and 79.7% did not receive a formal diagnosis.
2. Pathophysiology
The pathophysiology of headaches is intricate, with genetic and environmental factors playing crucial roles in the development of migraine, tension-type headache, and cluster headache. However, identifying the specific genes involved has proven to be a challenging task. Familial hemiplegic migraine, which is linked to mutations in the calcium voltage-gated channel subunit alpha1 A (CACNA1A), ATPase Na+/K+ transporting subunit alpha 2 (ATP1A2), and sodium voltage-gated channel alpha subunit 1 (SCN1A) genes, and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), which is associated with a notch receptor 3 (NOTCH3) gene mutation, stand out as the most extensively studied headache disorders with a genetic foundation.
The vascular theory of migraines, according to which migraine stems from blood vessel dilation and that the aura is a result of vasoconstriction, is now deemed invalid, as evidenced by magnetic resonance angiography studies. A typical migraine episode consists of four phases: the prodromal or premonitory phase, the aura phase, the headache phase, and the post-dromal phase. The premonitory phase is characterized by irritability, fatigue, difficulty in concentration, nausea, or pallor. Functional neuroimaging studies suggest involvement of the hypothalamus in the premonitory phase, as well as during the migraine attack phase. The migraine aura constitutes a reversible neurological phenomenon impacting approximately one-third of all migraine sufferers and occasionally overlapping with the headache phase. The underlying mechanism of this phase is thought to involve cortical spreading depolarization (CSD) across the cortex. CSD is marked by a brief excitation period, followed by a prolonged depression of cortical activity. Originating from the occipital lobes, it propagates anteriorly, dissipates at the central sulcus, and influences neurotransmitter levels, ionic balance, and blood flow. The headache phase is characterized by the activation of the trigeminocervical complex. Neuropeptides, particularly calcitonin gene-related peptide (CGRP), are involved in trigeminal activation and have emerged as a potential target for therapeutic interventions in migraine patients.
The development of cluster headaches involves interactions among the trigemino-vascular pathway, trigeminal autonomic reflex, hypothalamus, and the neuropeptides CGRP and pituitary adenylate cyclase-activating polypeptide. In tension-type headaches, the pain is thought to stem from myofascial structures and is heightened by central sensitization mechanisms. This central sensitization involves an imbalance in neurotransmitters such as CGRP, nitric oxide, neurokinin-A, glutamate, substance-P, serotonin, and endogenous peptide systems...
Conclusion
Pediatric headache is a prevalent condition in children, leading to substantial morbidity and frequent healthcare visits. The primary culprits are often primary headaches and acute viral infections. The initial assessment is essential for identifying potential warning signs, excluding secondary or life-threatening causes of headaches, and minimizing unnecessary investigations. Migraine is the most significant and common type of headache in children and adolescents. Prompt acute management of migraines involves supportive care and analgesics, but there is a lack of clear evidence-based recommendations for preventive therapy in children, highlighting a need for further research in this area. Newer modalities including non-invasive neuro-simulation botulinum toxin and CGRP antagonists are promising and emerging therapies.
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