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Childhood headache
R W Newton Arch. Dis. Child. Ed. Pract. 2008;93;105-111 doi:10.1136/adc.2007.124743

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Childhood headache
R W Newton
Correspondence to: Dr R W Newton, Royal Manchester Childrens Hospital, Pendlebury, Manchester M27 4HA, UK; richard.newton797@ ntlworld.com Accepted 19 February 2008

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.

4. The trigemino-cervical complex

Involvement of the trigeminal nucleus with the dorsal horns of C1 and C2 means that neuronal activation in the upper cervical area may lead to reactivity of neurones involving intracranial blood vessels and vice versa. This explains how pain in migraine may be experienced bilaterally and is frequently referred to the back of the head.

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 6.010.0% 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.

5. Central modulation of trigeminal pain

Functional imaging shows activation of the dorsal mid-brain, including the peri-aqueduct grey matter and dorsal pons near the locus coeruleus in migraine without aura. Stimulation of neurones in these areas may reduce cerebral blood through an adreno-receptor linked mechanism (often maximal in the occipital cortex) with extracerebral vasodilation. As these elements interplay it is easy to see how one headache episode may be associated with different symptoms at different times and how between individuals, even within the same family, symptoms may vary. On a particular day, symptoms are probably a random response to a variety of environmental influences or a change in the biological neuronal substrate modulated by drug or dietary ingestion, sleep rhythm or other natural biorhythms. This explains how an individual headache experience may be associated with dysfunction of any part of the cerebral cortex (visual phenomena being most common), how a disordered sleep/wake cycle may predispose to migraine and how sleep itself may relieve the symptoms, how autonomic disturbance (anorexia, nausea, vomiting) may accompany many episodes and how parts of this presentationfor example, a visual aura or a feeling of unsteadinessmay appear with or without headache.

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.
Arch Dis Child Educ Pract Ed 2008;93:105111. doi:10.1136/adc.2007.124743

CLASSIFICATION OF CHILDHOOD HEADACHES

To study this cerebral pluripotentiality to produce symptoms we need to split symptom complexes into well-defined entities. The result is the International classification of headache disorders, now in its second edition (2004).6 This defines four main primary headache groups (migraine, tension type headache, cluster headache and other trigeminal autonomic cephalalgias and other primary headaches; eight groups of secondary headaches and two cranial neuralgias, central and primary facial pain and other headaches). Within these 14 main groups 100 types of headache phenomena are identified with a similar number of subtypes. See table 1 for the diagnostic criteria for the more common primary headache types.
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Table 1 Suggested strict criteria to be applied for various headache types
Migraine without aura diagnostic criteria: A At least 5 attacks fulfilling criteria B to D B Headache attacks lasting 1 (4 in adults) to 72 hours (untreated or unsuccessfully treated) C Headache has at least two of the following characteristics: 1. Unilateral location 2. Pulsating quality 3. Moderate or severe pain intensity 4. Aggravation by or causing avoidance of routine physical activity (for example walking or climbing stairs) D During headache at least one of the following: 1. Nausea and/or vomiting 2. Photophobia and phonophobia E Not attributed to another disorder 1.2 Migraine with aura diagnostic criteria: A At least 2 attacks fulfilling criterion B B Migraine aura fulfilling criteria B and C for one of the sub-forms 1.2.1 to 1.2.6 C Not attributed to another disorder Tension type headache. The following alternative criteria may be applied to A.2.1 infrequent episodic tension headache: A.2.2 frequent episodic tension type headache and A.2.3 chronic tension type headache A Episodes, or headache, fulfilling criterion A in main definition set and criteria B to D below B Headache lasting 30 min to 7 days C At least 3 of the following characteristics: 1. Bilateral location 2. Pressing/tightening (non pulsating) quality 3. Mild or moderate intensity 4. Not aggravated by routine physical activity such as walking or climbing stairs D No nausea (anorexia may occur), vomiting, photophobia or phonophobia E Not attributed to another disorder

third and largest group had bilateral headaches (pulsating or pressing) with nausea and vomiting but few other symptoms. Classifications developed from adult practice may not always be helpful for the paediatrician. We should do our best to think this way clinically but the unclassified group is likely to be large and this has a bearing on the explanatory words we use (see below). Chronic daily headache. This is rare in my practice but has been reported in 0.9% of UK children2 and up to 4% in the USA.8 An impressive study of 7900 Taiwanese children aged 1214 years showed a prevalence of 2.4% in girls and 0.8% in boys where symptoms were being experienced at least 15 days a month with an average of two hours per day for more than three months.9 Almost 75% had chronic tension type headache and nearly 7% had chronic migraine. These families present a diagnostic and management challenge. We need to consider a spaceoccupying lesion and idiopathic intracranial hypertension. Shorter histories may make one think of a chronic lymphocytic meningitis. In my experience, however, probably the commonest formulation is that of illness behaviour, where the young person concerned is experiencing a physical symptom as an expression of some inner conflict or fear. Chronic analgesia over use may contribute to symptoms.

OTHER IMPORTANT CHILDHOOD HEADACHE SYNDROMES

Early recognition of these syndromes will allow you to minimise investigations and give a reassuring explanation. The periodic syndromes are commonthe others representing no more than 1% of referrals. The childhood periodic syndromes are commonly precursors of migraine.10 11 Cyclical vomiting describes recurrent stereotyped episodes of vomiting and intense nausea associated with pallor and lethargy. The child is well in between. Abdominal migraine is an idiopathic recurrent disorder characterised by episodic midline abdominal pain manifesting in bouts lasting 172 hours. Pain is moderate to severe in intensity and associated with vaso-motor symptoms, nausea and vomiting. The child is well in between episodes. Benign paroxysmal vertigo of childhood is a heterogeneous disorder characterised by recurrent brief episodes of vertigo occurring without warning and resolving spontaneously in otherwise healthy children. Between episodes, neurological examination, audiometric and vestibular function tests are normal.

COMMON PRIMARY HEADACHE TYPES

Migraine without aura (previously known as common migraine). This classification acknowledges that in children attacks may last 172 hours, the headache is commonly bilateral and it is unusual in the occipital area. Migraine with aura (previously classical migraine, ophthalmic hemi-paraesthetic, hemiplegic or aphasic migraine, complicated migraine). The absence of interictal signs and the frequent presence of a prodrome (tiredness, difficulty concentrating, autonomic features, etc) is emphasised. Infrequent episodic tension type headache. These infrequent episodes of headache last from minutes to days. Strict definitions of caseness are required for scientific study, but few children seem to have read them before coming to clinic! Cluster analysis of headache symptoms in 150 children attending our Manchester clinic identified three groups of symptom clustersnone of which matched the diagnostic IHS classification.7 One group typically had unilateral pulsating headaches with nausea and vomiting, phonophobia and photophobia. Another cluster typically had bilateral headaches, (from dull to stabbing) and commonly with nausea, vomiting, blurred vision, diplopia and flashing lights. The
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Cluster headache; chronic paroxysmal hemicrania

Both are uncommon in childhood. Cluster headache describes distressing episodes of severe unilateral pain, which is orbital, supra-orbital, temporal (or any combination of these) lasting up to three hours and occurring up to eight times a day. The episodes

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are associated with at least one of the following, all of which must be ipsilateral: conjunctival injection, lacrimation, nasal congestion, rhinorrhoea, forehead and facial sweating, myosis, ptosis, or eyelid oedema. In chronic paroxysmal hemicrania the episodes show pain with a similar characteristic but they tend to be shorter lasting and more frequent. The bouts may occur at the same time each day with a striking therapeutic response to indomethacin.12

CLINICAL ASSESSMENT
Before each consultation children and their families should be encouraged to write down their main concerns.13 After identifying what is worrying the family most, the childs pain should be assessed: site, duration, frequency, character, relieving and exacerbating factors for each headache type and record any associated symptoms. Ask about duration of symptoms and any recent change in behaviour, personality or educational performance. Red flag features14 identify the need to investigate further (see box 1). Be careful with language. Waters15 drew attention to the fact that the word throbbing in general parlance often means very severe rather than pulsatile and many people conceptualise the head to have five sides rather than two (top, front, back, left and right), so it is better to sit back and then clarify than lead children and their families with specific questions.

Cranial neuralgias and central causes of facial pain

These are rarely seen in childhood but trigeminal neuralgia can occur. It is characterised by unilateral, brief, electric shock-like pains, abrupt to start and finish, limited to the distribution of one or more trigeminal nerve divisions. They are often triggered by a trivial stimulus but can also occur spontaneously. The disorder may remit without intervention and is often alleviated by carbamazepine or gabapentin. Tolosa-Hunt syndrome also presents with unilateral peri-orbital pain (rarely bilateral). There is usually a history of a preceding upper respiratory viral infection. Within a few days of the onset of the pain (up to two weeks), paralysis of the third, fourth or sixth cranial nerve occurs. The optic, facial or acoustic nerves may be involved. This rare disorder has been associated with granulomatous material in the cavernous sinus or supra-orbital fissure. Steroids can lessen the severity and duration of bouts and the risk of permanent cranial nerve paresis. Ophthalmoplegic migraine represents recurrent bouts of headache associated with paresis of one or more ocular cranial nerves (most commonly the third). Paresis often lasts up to four days and may be a mild variety of Tolosa-Hunt syndrome (see above) rather than a migraine. This disorder does remind us, however, that a number of paroxysmal headaches in children may occasionally be associated with infarction. Therefore any child presenting with focal neurological signs needs careful consideration for further investigation.

PHYSICAL EXAMINATION
Carry out a quick neurological examination (see box 2). In particular look at stature, visual fields and cranial bruits. Note any Fogs test asymmetry that could represent hemisphere dysfunction; check the blood pressure.

MANAGEMENT
The single most important thing for families is an explanation of childhood headache that makes sense. Try to teach some simple biology (see box 3 for a suggested approach). The importance of explaining things in this way is that you alter family expectation. For about 50% the tendency to recurrent headache will be life long,16 with good and bad spells. So make it clear that your intention is not to rid them of the problem but to allow them to adjust to it and live life successfully in spite of it, minimising the inconvenience of the episodes when they arise.

WHAT SHOULD WE CALL THESE HEADACHES?

We have noted how the IHS classification is very precise and how an individual childs symptoms may not to fit exactly.7 This creates a difficulty for the study of headache but does not mean we need relay uncertainty to the family. Your child has unclassified headaches is not an assuring message. Judith Hockaday rather pragmatically defined migraine as recurrent paroxysmal headaches, with a return to normal physical and mental health in between, continuing normal development and other causes excluded.17 In 2008 this is too imprecise for scientific studies but the principle of this pragmatic approach should allow us to say to parents that their childs headaches do represent a form of migraine, thus avoiding unclassified. Migraine is a familiar term, allowing a simple biological explanation and the avoidance of confusion. One source of confusion is the term tensiontype headache because the lay public (and many doctors!) associate tension-type headache with
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Box 1 Red flag features leading to serious consideration of further investigation

Headache worse in recumbency or with coughing and straining. Headache waking up child (note the difference between headache present on awakening which is not uncommon in migraine).* c Associated confusion, and/or morning or persistant nausea or vomiting. c Recent change in personality, behaviour or educational performance. c Physical signs to include field defect, short stature or cranial bruit; cerebellar signs and signs of raised intracranial pressure. *Many people with a migraine wake and then feel the gradual onset of head pain as opposed to being woken by severe pain which could well represent a spaceoccupying lesion.
c c

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Box 2 Hints for a quick neurological examination
Cranial nerves: c Pupillary reaction to light and accommodation (II, III) and view optic fundi (II) c Eye movements (III, IV, VI) c Bite and waggle jaw from side to side (V) c Screw up eyes and show teeth (VII) Say agh (IX) c Shrug shoulders (XI) c Put out tongue (XII) c Temporal visual fields (rare to have nasal field defect without temporal field defect) c Visual/hearing acuity when indicated by history. Then, patterns of movement: is it central nervous system (CNS) or neuromuscular (weakness)? If it is CNS, is it pyramidal, extrapyramidal, or cerebellar? c Hold arms outstretched c Finger-nose test c Alternating movement c Touch each finger in turn c Walk: look for toe-heel (or heel-toe?) gait-width of base/asymmetry-waddle of proximal weakness? c Fogs test c Gowers sign. Note: Routine sensory testing is unnecessary unless the history has a sensory component or there are motor signs. Supplementary tasks: c Reflexes/plantar response (if indicated) c Neurocutaneous features c Dysmorphism c Signs of a storage disorder: visceromegaly; heart murmur; skeletal signs of storage
given the great overlap of symptoms between children and in the same child over a period. Hence the modern term tension-type headache (with previously misleading terms tension or tension-like headache discarded).

WHO SHOULD WE INVESTIGATE?

The purpose of the consultation is to assure the child and their family that we are dealing with a common biological and harmless phenomenon. It is important not to undermine this reassurance with unnecessary investigations. To say something is harmless on the one hand and then proceed to arrange imaging is to dilute that message and confuse. There are no biological markers for the spectrum of headache in childhood. The single most useful investigation is an MRI scan and I reserve this for those children showing red flag features (box 1) or if the family insist. Occasionally more complex investigation is required, particularly if the differential diagnosis includes transient ischaemic attacks (a situation that can arise in migraine with aura, with/or without headache). My own practice is not to offer regular follow-up to children with headache but rather to offer open access by telephone or appointment as an opportunity to answer further questions or address another clinical need.

TREATING CHILDHOOD HEADACHE

Ryan has reviewed migraine treatment with a commentary on the drugs included in the British National Formulary for Adults and Children.18 Remarking on difficulties with classification he states, In clinical practice a more liberal interpretation of symptomatology is likely to be helpful and increases the number of children who might benefit from medical intervention. In other words it is justifiable to try migraine treatments for other childhood headache disorders.

psychiatric disturbance of some sort. It is commonly believed that stressors bring them on (see most simple analgesia advertisements). In effect they are yet another paroxysmal headache type whose pathophysiology is yet to be defined. It is likely that the pathophysiological substrate for migraine and tension-type headache are the same

Box 3 Suggested biological explanation

DRUG TREATMENT Many children will have learnt about cells in their school science. Tell them the brain is made up of tiny things called nerve cells (suggest you use simple illustrations), about 100 000 million in all. Each of these cells has 100 000 connections so there are more connections in the average human brain than there are telephone connections in Greater London. It is the job of a nerve cell to make messages and if the flow of messages around the brain is tidy then we will have a smooth pattern of seeing, moving, thinking and so on. So, if nerve cells are sending an unusual pattern of messages we will experience symptomsthe pattern of symptoms reflecting the part of the brain that is involved at that time. Headache is one symptom produced in this way. It is no surprise to learn therefore that most people on earth will get a headache from time to time and that for up to one in six of us it may be a recurrent problem. About half the children we see in clinic have a first degree (close) relative with a headache tendency but about half do not. So genetic factors clearly play an important role but are not the whole story. For at least four out of 10 children with a tendency to recurrent headache, the tendency is life long.11 However, that is not the bad news it sounds. For most people with a headache tendency there are good spells and bad spells, with periods of months or even years in between the bad spells. There is nothing medicine can do to cure this problem but there is much it can offer to make the bad spells more bearable.
The review by Goadsby4 and that of Villalon and colleagues19 relates our knowledge of the underlying pathophysiology to rational intervention with therapeutic agents. 5-hydroxy-triptamine (5HT), ergotamine, di-hydro-ergotamine and other anti-migraine agents produce vasoconstriction in the external carotid circulation and relieve some migraine symptoms. Propanolol suppresses midbrain adrenergic mid-brain centres. Sumatriptan inhibits neurogenic plasma protein extravasation and second generation triptans (zolmitriptan, rizatriptan and naratriptan) are all 5-HT receptor agonists acting in different locations with the central nervous system to cause vasoconstriction. There are now emerging data on how antiepileptic drugs may help migraine symptoms. Few child-specific data are available. Victor and Ryan20 identified only 18 studies with reasonable methodological quality, but for no individual drug were comparable data reported in more than one study, making meta-analysis impossible. Two

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placebo-controlled studies showed a beneficial effect on the primary outcome measure headache frequency. They were for the drugs propranolol and flunarizine. Nimodipine, timolol, papavarine, pizotifen, trazodone, L-5HTP, clonadine, metachlopromide and domperidone showed no efficacy in the reduction of frequency of attacks. Studies on ciproheptadine, phenobarbitone, phenytoin, amitriptyline, metoprolol and piracetam were excluded for various reasons. The findings from a Drug and Therapeutics Bulletin, Managing migraine in children21 are summarised beside recent Cochrane reviews all with study populations largely incorporating adults.

decision-making process. Once remission is induced it is good to withdraw therapy within the next six weeks or so.

Pizotifen
Pizotifen is a histamine (H1) and serotonin receptor antagonist licensed for migraine prevention in children aged over 2 years in doses up to 1.5 mg daily, usually in divided doses. Common unwanted effects of the drug include anti-muscarinic effects (dry mouth, constipation), increased appetite, weight gain and sleepiness. It is probably the drug most commonly used by UK paediatriciansbut here is no evidence to suggest it works! A randomised placebo-controlled crossover trial involving 47 children aged 714 years showed that Pizotifen (11.5 mg daily) did not reduce the number of episodes, the total or mean duration of episodes, or the duration of the longest episode.20 30

TREATING ACUTE EPISODES

Drugs should be given as early in an individual episode as possible22 and probably not be used for more than two days a week in order to avoid the risk of medication over-use headache.23 A study of 416-year-olds showed pain alleviation was about twice as likely with paracetamol or ibuprofen as with placebo with no clear difference in efficacy between the two active drugs.24 A single dose of ibuprofen (7.5 mg/kg) resulted in more responders at two hours than placebo.25 Sumatriptan nasal spray, 10 mg, is licensed in the UK for adolescents aged 1217 years for the acute relief/treatment of migraine with or without aura. If symptoms respond but recur the dose may be repeated after at least two hours (not to exceed 20 mg in 24 h). One trial involving 653 children showed a 5 mg (but not 10 or 20 mg) improved headache relief at two hours. Taste disturbance was the most common unwanted effect.26 Nasal sumatriptan (20 mg) showed pain scores improved over placebo (86% vs 43%) in a trial involving 14 children aged below 10 years.27 However, oral sumatriptan appears ineffective in this group28 (in accordance with a recent Cochrane review29).

Propranolol
Propranolol is licensed for the prophylaxis of migraine in children at a dose of 20 mg two or three times a day in those under 12 years, and in a starting dose of 40 mg two or three times a day in the over 12s, but contraindicated in asthma. There are three trials comparing propranolol with placebo in childhood migraine. In a crossover trail propranolol (16120 mg daily divided into three doses) reduced the average frequency of episodes.31 However, in a second study there was no difference in headache frequency between propranolol (80120 mg daily) and placebo, and the average duration of headache progressively increased in children taking propranolol with a small decline on placebo.32 In a third trial propranolol (3 mg/daily for three months) showed no reduction in the number of migraine episodes compared with and placebo.33 Unwanted effects included bradycardia, hypotension, peripheral vasoconstriction, bronchospasm, gastrointestinal disturbances, tiredness, sleep disturbance and nightmares. A recent systematic review included 58 trials involving 5072 participants of all ages, many with poor methodology, showed propranolol is more effective than placebo in the short-term interval treatment of migraine, but that no longterm benefit is conferred.34

Opiodes
There are no published studies on the use of opiodes in childhood migraine, which should generally be avoided due to the risk of addiction. Unwanted effects include nausea, vomiting and constipation.

Anti-emetics
Metaclopromide should be avoided, particularly in young children, because of the risk of inducing a dystonic attack. Domperidone is only licensed in the UK for use following radiotherapy and chemotherapy but may be helpful (if it is retained). Prochlorperizine is available as a nasal spray or suppository.

Antiepileptic drugs
There is growing evidence that antiepileptic drugs help migraine prevention. In a systematic review of 23 papers with 2927 participants those treated with antiepileptic drugs were more than twice as likely to have migraine frequency reduced by 50% or more compared with placebo.35 Valproate and topiramate in particular were shown to be effective but acetazolamide, clonazepam, lamotrigine and vigabatrin were not superior to the placebo. More work is required on gabapentin. If symptoms warrant it, dosage can slowly be escalated to an initial target dose of 30 mg/kg/day
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Prophylactic therapy
Use this only as a last resort where frequent symptoms are becoming very intrusive in a young persons life and make them part of the
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for valproate or 4 mg/kg/day for topiramate over a three-week period or so, stopping the escalation if episodes arrest. The treatment should be continued until remission has been sustained for about a sixweek period and then the drug might be tailed over six weeks. chocolate or cheese may trigger migraine at one time but a few weeks later may not induce the event. So, before condemning any child to a life without chocolate or cheese, it is wise to explain this fluctuating vulnerability and exclude a trigger only if it consistently acts as one over time. It is the counsel of perfection anyway to suggest that a young person should attempt to live a life free of heat, light, noise, excitement, lack of sleep, etc. Indeed a doctor may lose a lot of credibility in a young persons eyes by doing so. Our job is rather to raise these issues for the young person to consider and for them to take an informed decision.

Selective serotonin reuptake inhibitors

To date, the review by Moja and colleagues indicates that selective serotonin reuptake inhibitors, over two months of treatment, are no more efficacious than placebo in people with migraine.36

Feverfew (unlicensed in the UK)

A systematic review showed Feverfew (50143 mg) may reduce the frequency and severity of migraine and nausea and vomiting compared with placebo.37 However, only one trial included children (all over 9 years). Pittler and Ernst concluded there was insufficient evidence from randomised double blind trials to suggest a beneficial effect for Feverfew over placebo for preventing migraine, but they noted it presented no major safety problems.38

SUMMARY OF CLINICAL APPROACH

Following careful clinical assessment the majority of families would be best helped by a simple understandable explanation of their childs paroxysmal headaches as a common, benign, biological phenomenon. Although many may retain a lifelong tendency there will be long spells of remission lasting months or even years. Further investigation should be confined largely to those with red flag features; or those with the rare non-benign headache disorders. Studies on relevant genes, trigeminal innervation of intracranial structures, the trigemino-cervical complex and central pain modulation has improved our knowledge of headache disorder pathophysiology. This offers a rationale for intervention. Simple analgesia, possibly with an anti-emetic, should be administered as early in an individual episode as possible so as to curtail its effect. Prophylactic therapy should be reserved for those children in whom the headache is truly intrusive in their lives. Propranolol or the antiepileptic drugs are the only drugs to date with an evidence base to justify their usage. It is probably worthwhile not to complicate the consultation too much with too rigid an interpretation of the international classification (a tool really aimed at the scientific study of pathophysiology and intervention). The term migraine or migraine variant with a biological explanation is enough to give families the understanding and reassurance they need.
Competing interests: None.

Behavioural interventions
A meta-analysis of 17 studies (9 controlled, 2 randomised) involving a total of 292 children (aged 518 years) investigating a range of behavioural interventions suggested that thermal biofeedback, progressive muscle relaxation or a combination of the two was more effective at reducing headache than placebo or waiting list control conditions, and that biofeedback alone or in combination with progressive muscle relaxation was apparently more effective than all the other treatments.39 However, the studies were small (556 participants each) and only six were considered to carry good methodological quality. This comment was echoed in Melchart and colleagues40 systematic review of acupuncture for idiopathic headache which nonetheless suggested some benefit; Bronfort and colleagues review of non-invasive physical treatments for chronic/ recurrent headache showed a few non-invasive physical treatments may be effective as prophylactic treatments, including spinal manipulation for cervicogenic headache (rare in children), the use of pulsating electromagnetic fields and a combination of transcutaneous electrical nerve stimulation (TENS) and electrical neurotransmitter modulation).41 Again the methodology was poor and these results cannot be relied upon.

REFERENCES
1. 2. 3. Bille, Bo. Migraine in school children. Acta Paediatrica Suppl 1962;51:4151. Abu-Arefeh I, Russell G. Prevalence of headache and migraine in schoolchildren. BMJ 1994;309:7659. Abu-Arafeh I, Macleod S. Serious neurological disorders in children with chronic Headache. Arch Dis Child 2005;90:93740. Goadsby PJ. Migraine pathophysiology. Headache 2005;45(Suppl 1):S14S21. Moskowitz MA. Basic mechanisms in vascular headache. Neurol Clin 1990;8:80115. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders. Cephalalgia 2004;24(Suppl 1):1160. Viswanathan V, Bridges SJ, Whitehouse W, et al. Childhood headaches: discrete entities or continuum? Dev Med Child Neurol 1998;40:54450. Mack KJ. An approach to children with chronic daily headache Dev Med Child Neurol 2006;48:9971000.

LIFESTYLE ISSUES
The British National Formulary for Children suggests that we advocate the avoidance of common headache triggers: heat, light, noise, strong smells, lack of sleep, lack of water, lack of food (such as breakfast), excitement, travel, exercise and (infrequently) types of food. Taking the latter it is my experience that the brains propensity/vulnerability to migraineous phenomena fluctuatesprobably related to endogenous biorhythms. Thus,
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4. 5. 6.

7.

8.

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