Headaches

17.5 Headaches

Ian Wilkinson, Gopinath Musuwadi Subramanian

Headache occurs in most children at some time. In a number of these, frequent headaches are a disabling problem. In one study in primary schools in Australia, 23% of parents believed that their children suffered from ‘frequent headaches’. A population study of 4–18-year-olds in the USA, published in 2009, found that 17% had suffered from frequent or severe headaches in the previous 12 months.

Many processes result in headache. These will be considered in two major classes: ‘cranial’ headaches, where the cause of pain is a process directly involving the brain and associated structures, including meninges, cerebral blood vessels and scalp; and ‘extracranial’ headaches, where the primary cause is remote from the brain.

The mechanisms of headache are multiple, but it should be recognized that the brain itself is insensitive to pain. Some neurosurgical operations for intractable epilepsy are actually performed on the brain with the patient awake.

This chapter deals particularly with recurrent or chronic headaches and not with those that accompany acute events such as trauma, intracranial bleeds or infections of the nervous system.

Cranial causes

Migraine and stress or tension types are the most common of chronic or recurrent headaches with origins in and around the brain. The migraine subset is numerically the biggest in Australian children. Stress and tension components often interact with a predisposition to migraine. Pure stress and tension headaches are less common than in adults. Often headaches in children that are classified as ‘stress’ or ‘tension’ start out as migraine headaches but, as a consequence of recurrent pain, disability and fear of the next headache, develop strong features suggesting that stress or tension is the primary cause. Of the different headache types in children, migraine, because of its great prevalence and associated morbidity, will receive most attention in this discussion.

Migraine

Epidemiological features

• the commonest cause of recurrent headaches

• showing increasing prevalence. In a 1974 Finnish study using rigid criteria, 1.9% of 7-year-old children suffered from migraine headaches. In 1992 the study was repeated with the same criteria and the prevalence had increased to 5.7%.

• more common with increasing age of the child

• more common in males before puberty but in females after puberty

• a leading cause of referrals to paediatricians and child neurologists.

Clinical manifestations

Childhood migraines result from the same biological process as those in adults but clinical manifestations may be quite different. Some of these differences relate to the difficulty a child has in describing or explaining the features; for example, young children may not be able to describe throbbing, or lateralization, or sensory associations. Nevertheless, there are some features, such as dizziness and vomiting, that are clearly more common in children.

‘Classical’ migraine (which is a relatively uncommon type of migraine even in adults) includes aura, or transitory neurological dysfunction, especially of the visual system, and may involve sophisticated hallucinations such as fortification spectra, which often precede the onset of headache and then disappear as the headache commences. This classical sequence may occur in older children and adolescents but often instead there is a description of sensory hallucination that occurs with, or during, the headache. This may be a visual disturbance described in unsophisticated terms, such as ‘flashing lights’, ‘seeing things double’ or ‘blurry, like looking through a curtain’, or something more complex and bizarre-sounding, and often very frightening. Such hallucinations include the appearance that objects are too big or too small, or that things moving in the environment appear to be going too fast or too slow, or that body images are distorted. It is suggested that Lewis Carroll drew on personal migraine experiences in writing Alice in Wonderland when describing Alice’s distorted body perception after she ate the magic substance.

Such hallucinations can involve the auditory process, for example things sounding too loud or someone speaking too fast. At times, the aura for a child defies description but may involve a sense of unreality or depersonalization.

What can make the migraine process more difficult to unravel in a child is the not uncommon situation where the actual sensory hallucination is not accompanied (during that event) by a headache. This is referred to as migraine dissociée, and there may be more alarm and distress for a child or parent than when there is an accompanying headache.

Other variations from adult migraine involve the location of the pain. Whereas in adult migraine attacks the pain can often be lateralized (a true ‘hemi- crania’ – one origin of the word migraine), this is frequently not the case in young children, who will simply point to their forehead (without lateralization) as being the location. As the child grows older a description of pain that is unilateral and sometimes located in one or other temple becomes more common. The pain is more often in the frontal half of the head, and pain that is located only posteriorly raises the possibility of more sinister causes of headache.

A description of the quality of the pain in migraine in children is often difficult for them. The pain tends to be more of an aching type ‘like a tummy ache’ rather than sharp ‘like a needle’. A combination of the two may be described. Further, in adults with pure migraine attacks it is frequent for the pain to be described as throbbing, implying involvement of vascular structures. Children with migraine may well experience throbbing pain but may not be able to describe it as such, although, as the child becomes older, he or she may describe it as ‘beating like a drum’ or ‘like a hammer’.

Although many adults do not acknowledge headaches as being migraine unless they are severe and resulting in cessation of usual activities, in children there can be a great range in the severity of migraine events, from the situation where the child is able to continue in school or at play, to the level where all activity must cease and the child retreats to bed in misery.

Adults with migraine attacks may not change greatly in external appearance, but children are often extremely pale.

Nausea and vomiting may occur in association with adult migraine and not uncommonly continue throughout and exacerbate the headache, resulting in treatment with an antiemetic. During the attack, abdominal pain, nausea and vomiting are extremely common in children, but the sequence may be that a single vomit, often followed by a sleep, terminates the attack.

Formulating rigid diagnostic criteria for childhood migraine has proven very controversial and strict requirements for certain features to be present in combination before a diagnosis can be made may be counterproductive in clinical practice. In practice, children with headaches with some of the previously mentioned features, occurring intermittently and with symptom-free periods, who are normal to neurological examination, may be considered to suffer from migraine.

The single feature that has caused most disagreement between those studying children with headaches and those studying adults is a requirement for the headache to be of a certain duration. A diagnosis of migraine had originally required, by International Headache Society criteria, a duration of at least 4 hours. Eventually it was conceded that childhood migraine attacks may last as little as 1 hour.

Classical teaching about headaches due to tumours and other situations of raised intracranial pressure has been that they are present upon awakening, or actively cause the patient to waken. Although in reality this is not always the case, a contrast remains with childhood migraine, where the onset is more commonly later in the day, perhaps approaching midday or during the afternoon or evening.

Childhood migraine is a very cyclical condition. Patients may have a bout of recurrent headaches that lasts for weeks or months, followed by a period of remission that may last for a year or more, to be followed by another bout. Hot weather may be a factor in relapses.

Types of migraine

In the International Classification of Headache Disorders (ICHD, second edition, 2004) there are six categories and 17 subcategories of migraine. Precise classification is necessary in migraine research but is not always so important in clinical diagnosis and management, and there is often overlap between different types in children. To categorize according to the presence or absence of ‘aura’ in children can be very difficult. The ‘aura’, in children who can describe it, may often occur during the headache and not precede it, and frequently involves some sense of disequilibrium, perhaps true vertigo. Visual auras are often basic, such as blurring or double vision, and unsophisticated.

There are some conditions that are considered to be part of the migraine phenomenon, although appearing to have little relationship with adult migraine types:

• Unexplained attacks of vomiting, without associated headache, may also be precursors of migraine. These attacks can be very puzzling diagnostically and often very debilitating, possibly recurring after a predictable interval and sometimes requiring intravenous fluids and hospitalization. With the passage of time, headaches may become more of a feature of these attacks, which are labelled ‘cyclical vomiting’.

• Recurring episodes of unexplained abdominal pain defying diagnosis despite multiple investigations can also be very debilitating. There may be a family history of migraine and as time goes by the child’s pain, known as ‘abdominal migraine’ may become associated with and eventually replaced by migraine headaches.

• In early childhood, usually before the age of 5 years, patients may experience recurrent episodes of sudden onset of true vertigo. These are extremely distressing and cause the child to seek a cuddle, or lie on the ground to relieve the feeling of spinning. These events last a few minutes, sometimes hours, and may be associated with pallor, nausea and vomiting, and possibly nystagmus. In some studies up to 80% of these children, who are described as having ‘benign paroxysmal vertigo’, subsequently develop migraine headaches.

The most recent ICHD (2004) now includes a section entitled ‘Childhood periodic syndromes that are common precursors of migraine’, incorporating (1) cyclical vomiting, (2) abdominal migraine and (3) benign paroxysmal vertigo.

In infancy, ‘paroxysmal torticollis’, where the head becomes tilted strongly to one or either side for periods of hours or days, may be a precursor of migraine, although simultaneous headache may not be apparent. A similar process involving the trunk has been described. These infants have been demonstrated to be at greater risk of later developing migraine headaches.

Hemiplegic migraine may present with unilateral weakness, and possibly unilateral sensory disturbance, and this often precedes the actual headache.

Expressive or receptive language difficulties also may be a presenting feature of some attacks, with the headache not occurring till an hour or so later.

In acute confusional migraine the patient is quite disoriented and distressed, with short-term memory loss. This condition raises concerns about more sinister neurological processes, or drug intoxication, often leading to invasive investigations. Again, the headache may not become apparent until later in the event.

Clinical example

Jarrod, aged 13 years, was sitting in class when he developed tingling in his right arm. He tried to put his arm up to tell the teacher but it was too weak. When he tried to call his teacher, he could not find the words to say. He became very distressed and confused. An ambulance took him to hospital where he was found to have a right hemiparesis. He had developed a headache on the left side and underwent computed tomography of his head, and lumbar puncture. Both were normal. The weakness, numbness and confusion resolved over the 3 hours from onset, but the headache lasted for 6 hours. It was discovered that his father had suffered similar attacks of hemiparesis and headache when he was a teenager. This is an example of familial hemiplegic migraine.

Aetiology

The causative mechanisms for migraine are very complex and much researched, and it is beyond the scope of this textbook to go into great detail.

At a chemical level, both noradrenergic and serotonergic transmitter pathways are implicated, and this has relevance to drug therapy.

Certainly genetics plays a major role and as many as 90% of children with migraine will have parents or siblings with the same condition.

Many different mechanisms of inheritance have been postulated. In recent years there has been clear evidence that familial hemiplegic migraine is associated with mutations on three different chromosome sites (chromosomes 19, 1 and 2), although they all present with similar clinical features. The sites on chromosomes 19 and 2 disrupt calcium and sodium channel function respectively.

In 1944 Leao described ‘spreading depression of activity in cerebral cortex’. The slow spread of this electrical change across the visual cortex was synchronous with the spread of the visual aura accompanying the migraine attack. It was thought that this spreading depression was produced by ischaemic changes resulting from vasoconstriction, and that the subsequent vasodilatation of innervated blood vessels produced the pain response.

This vascular theory of migraine held sway for 50 years, but in the last decade a new theory has arisen, which proposes that the cortical depression results from an abnormal excessive depolarization of neurons, which spreads across the cortex producing neurological dysfunction. This has been well demonstrated during the march of depolarization across the motor cortex that accompanies the spreading weakness of hemiplegic migraine, but can also occur in sensory and cerebellar cortex.

This neurogenic theory postulates that the depolarization producing the motor or sensory dysfunction sends afferent (or inward) messages into brainstem centres that interact, reach a critical threshold, and then send efferent (or outward) messages via the trigeminovascular system to blood vessels in pain-sensitive structures, which undergo dilatation as well as sterile inflammatory change, resulting in headache.

Given that some children are at risk genetically of developing migraine, it is clear that there may be provoking factors for individual attacks. These include head injuries, not necessarily severe ones. The head injury may be the commencing point for recurrent bouts of migraine headache, and this may have legal ramifications. Other provoking factors are:

• intercurrent systemic infections, particularly with fever

• strenuous physical exercise

• hot weather

• dehydration

• worry and stress, either domestic, social or educational in origin. While these factors remain, they may greatly complicate treatment. The distinction from ‘stress’ or ‘tension’ headaches without an underlying migraine basis may be very difficult

• foodstuffs. This is a very controversial area, with evidence for and against. Citrus fruit, cheese, chocolate and processed meat have been implicated

• food additives, such as monosodium glutamate, sodium nitrite, benzoic acid, tartrazine.

Treatment

Treatment can be divided into the following tiers:

• avoidance of triggers

• non-specific analgesia for attacks

• specific anti-migraine medication for attacks

• prophylactic medication

• non-medication treatments.

Avoiding specific triggers in childhood migraine can be difficult. In many, they do not exist. In Australia, hot weather and exercise are common precipitants that are part of a normal childhood lifestyle. Ensuring adequate hydration in the above situations may be helpful.

The role of restrictive diets is controversial. If it is evident that certain foodstuffs or drinks regularly provoke attacks then they should be avoided. Placing children on very limited diets is not only unpleasant and difficult to enforce, but may even have nutritional consequences.

The use of non-specific analgesics in attacks is the simplest means of treatment. The most commonly used is paracetamol, best given in an initial dose of 20 mg/kg. Unfortunately, children may not seek medication, or as a result of being at school may not be able to access medication, until the attack is advanced. The paracetamol may not be effective at this time, or may be vomited. There may be a role for rectal paracetamol in this latter situation.

A recent study has indicated that ibuprofen in a dose of 10 mg/kg may be more effective than paracetamol. Other non-steroidal anti-inflammatory drugs (NSAIDs) may be helpful.

In recent years aspirin has been avoided in childhood because of concerns about its relationship with Reye syndrome, a rare but severe acute encephalopathy with potentially fatal outcome. Nevertheless, aspirin in doses of 15 mg/kg may be employed in older children with recurrent headaches.

The use of codeine and powerful narcotics in childhood headache is not usually necessary and is potentially hazardous, although restricted infrequent use of combinations of paracetamol and codeine in older children may be necessary and effective.

Ergotamine has long been a useful antimigraine drug in adults, particularly at the beginning of the attack. Although some studies have shown efficacy of oral dihydroergotamine in children, ergotamines have had limited use because children often delay seeking treatment and also because they may produce side-effects such as vomiting and abdominal discomfort.

Triptans are serotonin agonists with multiple methods of action against migraine attacks, and may be useful in children and adolescents. Sumatriptan has been the most employed in this age group, and the nasal spray, either 10 or 20 mg has been shown to be effective in patients aged 12–17 years. It should be administered as early as possible in the course of the attack.

Sumatriptan and other triptans have little proof of efficacy when given orally or subcutaneously to children and adolescents.

Antiemetics such as promethazine, prochlorperazine and metoclopramide may be useful in situations where the migraine attack is associated with pernicious vomiting, but this is unusual in children, and often a vomit followed by a sleep brings about the end of the particular attack. Antiemetics may produce significant drowsiness, and metoclopramide in particular may be associated with acute dystonic reactions.

Prophylactic treatment to prevent migraine attacks may be indicated when there is significant suffering and disruption of the patient’s lifestyle. It is difficult to define what frequency of attacks should dictate a decision to implement prophylaxis; opinions vary between two and four events per month. The decision process should combine the frequency of the attacks with the negative impact on the young person’s lifestyle. Many commonly used medications may have significant side-effects.

One of the problems in managing migraines in this age group is the difficulty in obtaining proof that individual medications are effective. Controlled trials are complicated by the cyclical nature of migraine in the young, with bad bouts being followed shortly afterwards by periods of temporary or permanent remission, and by the very high placebo response rates.

A 2008 revision of a Cochrane database study again concluded a lack of evidence for the benefit of prophylaxis in childhood migraine. The only proven treatments were for propranolol (in a study, subsequently contradicted) and flunarizine in repeated studies. Unfortunately flunarizine is not readily available in Australia, although it is used widely in Europe.

Nevertheless, the following medications are commonly used in clinical practice:

• Cyproheptadine, an antihistamine with serotonin-blocking and calcium channel-blocking properties. Side-effects include drowsiness (which may be minimized with a single night-time dose regimen) and increased appetite. Effective doses range from 0.1–0.3 mg per kg per day, given either once or twice daily.

• Propranolol, a β-adrenergic blocking drug, also blocks release of serotonin from platelets. It is contraindicated in asthma. Doses range from 0.5 to 2.0 mg per kg per day in two or three equal doses. The value of propranolol and similar drugs has been proven in adults, but trials in children have produced conflicting results.

• Pizotifen, with antiserotonin and antihistamine properties, has side-effects of increased appetite, weight gain and drowsiness. The last may be avoided by a single night-time dose. Doses are limited by the single-size pill format (0.5 mg) but range from one to three at night.

• Clonidine, a vasoactive drug, has been trialled in a range of conditions in children but lacks good evidence for use in migraine and has significant potential side-effects.

• Amitriptyline, originally marketed as an antidepressant, has been used for migraine prophylaxis in children. It may be particularly useful where there are stress and depressive features, but care must be taken to avoid provoking cardiac arrhythmias.

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Aug 4, 2016 | Posted by admin in PEDIATRICS | Comments Off

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