Child Migraine Spectrum

Review Article

Austin J Clin Neurol 2015; 2(9): 1076.

Child Migraine Spectrum

Recep ALP*

Department of Neurology, Namık Kemal University, Turkey

*Corresponding author: Recep ALP, Department of Neurology, Namık Kemal University, Turkey

Received: June 22, 2015; Accepted: August 08, 2015; Published: August 10, 2015

Abstract

Migraine is a heterogeneous disorder and prevalence of migraine increasing. Migraine phenotype differs somewhat in the developing brain, and childhood episodic syndromes may arise before typical migraine headache. Some studies showed abnormalities in the maturation of brain functions in migraine children and adolescents. Migraine has two major subtypes but migraine is spectrum that involved different clinical face from headache to hemiplegia. Migraine without aura is a clinical syndrome characterized by headache with specific features and associated symptoms. Migraine with aura is primarily characterized by the transient focal neurological symptoms that usually precede or sometimes accompany the headache. Hemiplegic migraine description is migraine with aura including motor weakness. Retinal migraine is repeated attacks of monocular visual disturbance, including scintillations, scotomata or blindness, associated with migraine headache. Migraine and epilepsy are prototypical examples of paroxysmal brain disorders. Although migraine-like headaches are quite frequently seen in the epileptic postictal period, sometimes a seizure occurs during or following a migraine attack. Childhood episodic syndromes such as recurrent gastrointestinal disturbance, cyclical vomiting syndrome, abdominal migraine, benign paroxysmal vertigo, benign paroxysmal torticollis that may be associated with migraine although historically noted to occur in childhood, they may also occur in adults. Migraine preventive strategies are particularly important in children. The first essential step is to explain the condition to the child and his or her parents. Explanation and reassurance may be the only treatment needed in some cases. As with migraine, the best treatment is prevention. The aim was to establish the occurrence of migraine spectrum in child neurology practice and among migraine, and to discuss their presentation.

Keywords: Migraine; Childhood; Headache; Neurology

Introduction

Migraine is a heterogeneous disorder: attacks vary in pain intensity, duration, pattern of associated features, and frequency of occurrence. Some migraineurs have recurrent attacks without remission periods; others experience symptom-free intervals lasting several years; a third group becomes free of attacks for the rest of their life. Migraine is the second most common cause of chronic recurrent headache in school children [1,2].

Migraine without aura and migraine with typical aura are common in pediatric neurology, but migraine variants occur rarely [3]. Migraine variants represent migraine attacks, characterized by serious neurological or gastrointestinal signs but with mild or absent headache [4].

The aim of this study was to establish the occurrence of migraine variants among all patients in pediatric neurology practice, as well as among migraine, and also to discuss their presentation and their place in the ICHD-III [5].

Epidemiology

The prevalence of migraine has been studied across all ages starting in early childhood. There is a slight predominance in boys in the pre-pubertal years, and the overall occurrence increases throughout adolescence into young adulthood when there is a transition to predominance in girls [1,2,6]. Subsequent epidemiological studies have continued to show the high frequency of headaches in children and adolescents, with migraines being the most common disabling type various criteria have been used to define migraine, although most recent studies from several countries and geographical locations have used the second edition of the International Classification of Headache Disorders (ICHD-II) [7,8]. Epidemiological studies have documented its high prevalence and high socio-economic and personal impacts. Migraine is a frequent disease with a prevalence of 3-15% in children and adolescents [8-11]. Positive family history for headache is commonly reported with a frequency of 60–77.5% [8,12].

Pathophysiological Mechanisms of Migraine

Migraines are self-limiting dysfunctions of grey matter. It is primarily a neuronal sensory dysfunction which secondarily involves the vascular systems. Involvement of the sensory nerve fibers within meningeal blood vessels gives rise to head pain [13,14].

The exact mechanism of the central nervous system pathophysiologic dysfunction in migraine is unclear. It is generally accepted that spreading of neuronal depression, neurogenic inflammation, and the activation of trigeminovascular system are involved [15-19].

The neurophysiologic investigation of the pathophysiological mechanisms subtending migraine in children and adolescents could be particularly interesting, since during the developmental age the migrainous phenotype is scarcely influenced by many environmental factors that can typically act on adult headache patients. The neurophysiologic abnormality most frequently found in adult migraineurs, that is the reduced habituation of evoked potentials, was confirmed also in migraine children. Some studies showed abnormalities in the maturation of brain functions in migraine children and adolescents. While the visual system maturation seems slowed in young migraineurs, the psychophysiological mechanisms subtending somatosensory spatial attention in migraine children are more similar to those of healthy adults than to those of age-matched controls. There are some still unexplored fields that will have to be subjects of future studies. The nociceptive modality, which has been investigated in adult patients with primary headaches, should be studied also in pediatric migraine. Moreover, the technique of transcranial magnetic stimulation, not yet used in young migraineurs, will possibly provide further elements about brain excitability in migraine children [20].

Regional cerebral blood flow imaging shows no changes suggestive of cortical spreading depression (CSD) during attacks of migraine without aura, although blood flow changes may occur in the brainstem, as may cortical changes secondary to pain activation. This contrasts with the pathognomonic spreading oligaemia of migraine with aura. Although the bulk of the literature suggests that CSD does not occur in migraine without aura, some recent studies disagree. Furthermore, it has been suggested that glial waves or other cortical phenomena may be involved in migraine without aura. The messenger molecules nitric oxide (NO), 5-hydroxytryptamine (5-HT) and calcitonin gene-related peptide (CGRP) are involved. Although the disease was previously regarded as primarily vascular, the importance of sensitization of pain pathways, and the possibility that attacks may originate in the central nervous system, have gained increasing attention over recent decades [20].

Classification of Migraine

The International Classification of Headache Disorders, 3rd edition (ICHD-3) has been released by the ‘International Headache Society’ in May 2013 [5]. As this version is based on a large body of research on headache, in contrast to previous editions that were mostly based on opinion of experts, it is being considered as a major step forward in the diagnosis and management of headache [21]. Migraine has two major subtypes but migraine is spectrum that involved different clinical face from headache to hemiplegia.

Migraine without aura is a clinical syndrome characterized by headache with specific features and associated symptoms. Migraine with aura is primarily characterized by the transient focal neurological symptoms that usually precede or sometimes accompany the headache. Some patients also experience a premonitory phase, occurring hours or days before the headache, and a headache resolution phase. Premonitory and resolution symptoms include hyperactivity, hypo activity, depression, cravings for particular foods, repetitive yawning, fatigue and neck stiffness and/or pain [21] Table 1.