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17 Headaches

Matthew D. Holmes

image Clinical cases for thought

Case 17.2

A 7-year-old boy presents with constipation and colicky pain. His mother reported he had always had periods of abdominal pain; however, the details on frequency and duration were hazy. He described the pain as a combination of sharp and achy. Nothing appeared to make it worse. Developmentally, he was normal except having ‘poor spatial hearing’. He had a strong sense of smell and tended to get travel sickness, especially on longer drives. Conventional medical evaluation had failed to find a cause for his symptoms.

Examination revealed decreased pursuit and saccade eye movements on optokinetic nystagmus to the right. His right pupil responses fatigued quicker than the left. He had a slight ptosis and decreased facial muscle tone on the right. Topagnosia (finger identification) was less accurate on the left hand. His ability to perform tandem gait with eyes closed was poor. Palate elevation and gag reflex was decreased on the left versus the right. Smooth pursuit in the plane of movements facilitated by the left (more than the right) anterior and posterior canals (up to the left, down to the right) showed saccadic intrusions. Posturography on a compliant surface revealed a tendency to fall posteriorly. Aberrant joint motion was noted in the cervical, thoracic, and lumbar spine regions.


Headaches can be due to a variety of causes but are generally categorised into primary and secondary headaches (Box 17.1). The primary headaches, the main focus of this chapter, are headaches that are not caused by another disease or condition, unlike secondary headaches. The International Headache Society (IHS) maintains a list of conditions that can produce headache symptoms secondary to the disorder (International Headache Society 2004). This list is extensive and the clinician managing the headache patient needs to be familiar with these conditions and include or exclude them as appropriate. Such causes may include intracranial mass, vascular lesions, systemic disorders or infection. In particular, the clinician needs to be aware of the following danger signs that may indicate the need for aggressive investigation.

Adapted from IHS 2004, with permission.

Clinicians managing patients with headache should ensure they are familiar with these danger signs and the subsequent management needed.

The main body of this chapter, however, will focus mainly on the major primary headaches as defined by the IHS, and discuss their pathophysiology and management from a functional neurology perspective. The approach of functional neurology has much to offer the headache sufferer, as many of the headaches are due to physiological dysfunctions in discrete brain areas. These areas can then be targeted using either their presynaptic neuronal pools or embryological relationships to cause an improvement in the health or central integrative state of the area. The functional neurologist should also consider the overall homeostatic environment of the body, evaluating whether it is conducive to neuronal health and, if not, taking steps to improve it.


Migraine is a common disabling condition that is ranked nineteenth by the World Health Organization amongst worldwide diseases causing disability (IHS 2004). Approximately 15–20% of the general population suffers from migraine headaches (Bolay et al. 2002). It has considerable social and economic impact; hence effective treatment strategies have the ability to make significant improvements in the quality of life of the sufferer, and have positive social benefit as well. In this chapter we will discuss the two most common forms of migraine, migraine with aura and migraine without aura, along with the childhood syndromes that are often the precursor of migraine.

Migraine without aura (MWOA)

Migraine without aura was previously known as common migraine.

The International Headache Society (2004) describes MWOA as: ‘Recurrent headache disorder manifesting in attacks lasting 4–72 hours. Typical characteristics of the headache are unilateral location, pulsating quality, moderate or severe intensity, aggravation by routine physical activity and association with nausea and/or photophobia and phonophobia’.

To be diagnosed with MWOA the individual must have had at least five attacks lasting 4–72 hours with at least two of the following characteristics: unilateral pain location, pulsating quality, moderate to severe pain intensity and/or aggravated by routine activity. It must also be accompanied by either nausea and/or vomiting or phono- and photophobia (Box 17.2) (IHS 2004).

Central sensitisation

Accompanying peripheral sensitisation is the phenomenon of central sensitisation. Activation of trigeminovascular nociceptors leads to an increase in activity in the second-order neurons in the trigeminocervical nucleus (Bolay et al. 2002). Furthermore, activation in the trigeminocervical nucleus occurs with stimulation of both meningeal afferents and those from the greater occipital nerve (a branch of the C2 dorsal root), and that stimulation for just 5 minutes can lead to an increase in response in the nucleus for over an hour to other nociceptive stimuli, including if that stimulation is received from the C2 innervation (Goadsby 2005). This is particularly relevant for manual therapy practitioners with their focus on removal of pain generators from the cervical spine. It is likely that this sensitisation involves the activation of NMDA receptors in the nucleus as in vitro application of sumatriptan, an antimigraine drug, is effective in blocking NMDA receptor activation (Buzzi & Moskowitz 2005).

The cutaneous allodynia is often associated with migraine and is thought to be another symptom of this central sensitisation of the trigeminocervical nucleus. The allodynia usually occurs on the ipsilateral forehead to the headache, but has been documented to occur over the ipsi- and contralateral hands as well (Dalkara, Zervas et al. 2006).

Brainstem dysfunction and disinhibition

Brainstem dysfunction has also been implicated in migraine, both as a primary migraine generator, and through failure of brainstem pain inhibition mechanisms. Goadsby (2005) reports activation of the locus ceruleus and periaqueductal grey (PAG) in migraine without aura, and that these correspond to areas that have generated migraine-like symptoms in patients when stimulated electrically. Similarly, Goadsby reports excess iron has been found in the PAG of episodic and chronic migraineurs, and lesions in this area have been known to cause migraine. The notion of brainstem dysfunction is further supported by the presence of measured balance deficits, vestibular changes (Akdal et al. 2007; Akdal et al. 2009; Asai et al. 2009), and subclinical cerebellar deficits in migraineurs (Sandor et al. 2001).

The PAG is involved in descending pain control mechanisms, along with the locus ceruleus and raphae nuclei. In 2001, Knight and Goadsby (2001) published research that suggests that it is dysfunction in the PAG that leads to disinhibition of the trigeminocervical nucleus and hence pain.

The combination of brainstem dysfunction along with balance and cerebellar deficits presents many opportunities for intervention by the functional neurologist. This could also explain the anecdotal reports from clinicians who have found that cerebellar and vestibular rehabilitation programmes are useful in the treatment of migraine.

Mechanisms leading to initial trigeminovascular activation

The brain of the migraineur displays different neurophysiological behaviours to that of the normal individual. Evoked potential and transcranial magnetic stimulation (TMS) studies have shown that the cerebral cortex of the migraine sufferer shows an impaired ability to habituate to sensory stimulation across all sensory modalities (Schoenen 2006; Brighina et al. 2009). This is thought to be due to impaired functioning of inhibitory networks in the cortex, and it has been suggested that this dysfunction occurs in a manner similar to the GABA circuit down-regulation that occurs in sensory deafferentation (Brighina et al. 2009). Interestingly, Brighina et al. (2009) report that repeated trains of TMS have been shown to improve the functioning of the inhibitory networks that could have long-term effects. This is consistent with the functional neurology paradigm that it is possible to improve neuronal functioning by repeated stimulation within the tolerance of fatigue, thereby promoting gene expression, protein synthesis, and thus building plasticity.

It is logical to assume that this inability to habituate to sensory stimulation could predispose the cortex to excitotoxic events, and evidence suggests that this is the case (Dalkara et al. 2006). This is further supported by evidence that there is impaired energy metabolism in migraineurs (Lodi et al. 2006), which will predispose to anaerobic metabolism. Anaerobic metabolism is toxic to neurons and the metabolic by-products associated with it such as lactic acid are able to activate nociceptive fibres. Functional neurological interventions to promote aerobic metabolism and to protect from anaerobic metabolism should be considered by the clinician. Interventions that may be considered include:

It is also thought that the migraineurs have immunological changes that predispose them to the activation of the inflammatory cascade, which in turn leads to the migraine attack. These triggers may be infections, foods, or other environmental factors (Longoni & Ferrarese 2006). Any management plan for the migraineur should include the identification and, as far as possible, the removal of the triggers. Headache diaries including diet and environmental exposures can be useful for identifying the triggers.

Migraine with aura (MWA)

Migraine with aura was previously known as classic migraine.

The International Headache Society (2004) describes MWA as: ‘Recurrent disorder manifesting in attacks of reversible focal neurological symptoms that usually develop gradually over 5–20 minutes and last for less than 60 minutes. Headache with the features of migraine without aura usually follows the aura symptoms. Less commonly, headache lacks migrainous features or is completely absent’ (Box 17.3).