Selye’s (1943) general adaptation syndrome describes a process in which the individual, with his or her unique inherited and acquired characteristics, is responding to multiple variable or constant adaptive demands, resulting in:

• an initial alarm stage. An example of this is the ‘fight or flight’ (sympathetic arousal) response, which might be triggered by a single stress event or by a number of minor stressors acting simultaneously (Figure 9.3). If the stressor(s) continues to operate, the body’s defense mechanisms move to what is known as:

• the adaptation phase, which continues until the ability of the body to compensate further is exhausted. This can be expressed as homeostatic exhaustion, or a stage of heterostasis, where adaptation potential fails (think of a piece of elastic that has been stretched until it starts to fray, and eventually snaps). When this occurs we have reached:

• the stage of exhaustion. The individual’s self-regulating/self-repair potentials will be exhausted (or severely strained) and chronic symptoms and frank disease will follow. At this stage homeostatic mechanisms may fail, decompensation features emerge, and treatment to slow, modify or reverse the process is called for (Figure 9.4).

Figure 9.2 After the initial alarm phase (see Figure 9.3), if stresses continue, as they inevitably do, to one degree or another, the adaptation phase of the general adaptation syndrome (GAS) commences. This may last many years. As time passes functional changes appear (stiffness, restriction, weakness, balance problems, degrees of pain, etc.). When adaptation potential is eventually exhausted, and the phase of exhaustion starts, more obvious symptoms are experienced. At this stage homeostasis/self-regulation is no longer able to operate efficiently, and a state of heterostasis exists (see Figure 9.4B), where something (treatment, altered behavior patterns, etc.) is required in order to restore homeostasis, and improved adaptive potential, i.e. self-regulation. This is, however, not always possible, as damage (e.g., arthritis) may have progressed too far for more than modest improvement to be possible.

(Adapted from Selye 1943)

Figure 9.3 Alarm reaction.

Figure 9.4 A, B Homeostasis.

Therapeutic choices available are limited to those that reduce the adaptive load, improve the ability of the body’s systems to handle adaptive demands, or methods that treat symptoms.

WHAT HELPS?

A wide range of methods, modalities, and techniques can be usefully employed by therapists to reduce the effects of adaptation influences, or to encourage better coping with these.

Those that will be considered, later in this chapter, in relation to headache and neck pain include:

• acupuncture (what you should know about this)

• aromatherapy

• emotion/stress management and relaxation methods

• ergonomics

• high-velocity manipulation (what you should know about this)

• hydrotherapy

• lifestyle changes, including nutrition and exercise

• posture

• respiration issues

• self-care (including balance training)

• soft tissue manipulation modalities.

Scope of practice may not allow all therapists to utilize some of these methods, or to advise patients/clients specifically (e.g., about nutritional influences on their symptoms); however, knowledge of these topics is important, so that at the very least, if they seem to apply in any given case, appropriate referral can be made.

GENERAL OBJECTIVES BASED ON AN UNDERSTANDING OF THE ADAPTATION PROCESS

There is a need:

• to identify and help the individual to reduce the adaptive demands – the habits of life that are helping to create (or aggravate, or maintain) the dysfunctional state that allows minor trigger factors to activate the symptoms

• to enhance functionality by improving posture, breathing, mobility, etc.

• to ease symptoms without adding to the person’s adaptive burden, emphasizing the importance of remaining aware of just how sensitive and vulnerable this person is

• to support self-repair, self-regeneration, self-healing processes

• to take account of the whole person, the lifestyle, habits, attitudes and behavior – and not just the symptoms

• to keep in mind that the more complex the condition, and/or the more sensitive and unwell the individual is, the less that should be done therapeutically at any given time

• to try to focus on causes – and, above all,

• to do no harm.

INTERACTING CAUSES

Very few conditions – headache or neck pain as examples – arise from a single cause. That’s not to say a single ‘triggering’ event may not be identifiable – such as the draft from an air-conditioning unit, or a particular food, or sleeping with the head/neck area not appropriately supported – or whatever else might provoke a headache. However, it’s worth remembering that the same triggering event might not always produce a headache in the same individual, or ever produce a headache in another individual.

This simple example points to the fact that symptoms (such as headache and neck pain) commonly emerge out of a background of interacting circumstances and influences, where the scene has been set for that triggering event to start the pain.

Examples of contributing factors relative to the development of headaches and neck pain might include the following:

• Being female: Women are over-represented not only in migraine but also in tension headaches (Buchgreitz et al 2006).

• Poor posture, or poor patterns of use (overuse, misuse, microtrauma, etc.) that frequently, or repetitively, stress the tissues of the head–neck–shoulder region, involving a build-up of musculoligamentous tension in the muscles, with the inevitable emergence of myofascial trigger points capable of referring pain into the head and neck (Giacomini et al 2004). Among the commonest features are tighter (‘harder’) muscles than usual (Ashina et al 1999) and a forward head posture (Moore 2004, Zito et al 2006) (see Figure 9.5, and also Figures 9.9 and 9.10).

• Residual chronic structural and functional changes affecting joint or soft tissue status, following major trauma such as whiplash, or degenerative changes such as osteoarthritis, including excessive muscle tightness/‘hardness’ (Kashima et al 2006, Zito et al 2006).

• Emotional distress, whether intermittent or constant, including anger and depression (Materazzo et al 2000), or depression (Lipchik & Penzien 2004), are all associated with increased headache incidence. Some studies have found that psychological symptoms are more related to associated symptoms (digestive, sleep, fatigue, etc.) than with the headaches themselves (Mongini et al 2006).

• Allergy: People with allergies such as eczema, who also suffered intense chronic headache, were shown to improve both in terms of their allergies as well as their headaches, when an ‘antihistamine’ diet was followed: avoiding alcohol, matured or fermented food rich in histamine (such as old cheese, fish, cured sausages), bread products containing yeast, vegetables such as spinach and tomatoes, or histamine-liberating fruits such as citrus (Maintz et al 2006).

• Nutritional imbalances (toxicity, deficiency):

b. Research has shown that a higher number of healthy eating habits corresponded to a lower frequency of headaches (as well as back and neck pain). This means that the more symptoms, such as headache, that people report, the fewer healthy eating habits they practiced. Healthy eating in a study of over 1600 people was defined as: ‘daily consumption of wholemeal bread, fresh fruit, vegetables, and salad, while avoiding daily consumption of sweets, soft drinks, meat, eggs and sausages’ (Reime et al 2000).

• Hormonal factors: Hormones such as estrogen and progesterone have long been considered as well-known migraine triggers, probably as a result of genetic predisposition (Colson et al 2006).

• Underlying pathology: Conditions such as diabetes and high cholesterol levels (hypercholesterolemia) have been shown to be closely associated with headache (Davila & Hlaing 2007).

• Pregnancy – especially if high blood pressure is also a factor (Facchinetti et al 2005).

• Sensitization: As tissues respond to a variety of ongoing or periodic adaptive demands, a degree of sensitization may occur, allowing minor stress factors (of any sort) to provoke pain. This feature of what is known as central sensitization is common to all forms of chronic pain, including headaches and neck pain, and is discussed later in this chapter (Bendtsen et al 1996).

• Breathing pattern disorders: The common habit of upper chest breathing imposes physical stress (overuse) on the accessory breathing muscles (such as scalenes, sternocleidomastoid, upper trapezius), as well as producing a wide range of biochemical and emotional changes (Figure 9.6). Breathing imbalances associated with sleep are directly linked to headaches (Chervin et al 2000). Jennum & Jensen (2002) state: ‘Primary sleep disorders such as insomnia, including sleep disordered breathing, are all associated with and may cause headache.’ They note that obstructive sleep apnea syndrome (OSAS) leads to morning headaches.

Figure 9.5 The upper crossed syndrome, as described by Janda (1996).

Figure 9.9 Seated postural stresses are demonstrated graphically by means of cogwheels which suggest the lines of force operating during(A) poor and (B) balanced sitting.

(Reproduced with permission from Journal of Bodywork and Movement Therapies 3:148.)

Figure 9.10 Postural stress in relation to guitar playing. (After Kapandji 2000.)

Figure 9.6 Negative health influences of a dysfunctional breathing pattern such as hyperventilation.

BACKGROUND

We can see that headaches, and their associated symptoms, may emerge from a background involving very different stressors, interacting with the unique genetic, biomechanical, biochemical, and psychosocial characteristics of the individual.

Clearly any person whose system is coping with multiple types, levels, and degrees of compensation and adaptation is likely to be susceptible to provocation by a variety of further stress factors – ‘triggering’ events or influences – including, as examples, additional physical and/or psychological strain, or a change in atmospheric pressure (such as occurs before a thunderstorm), or a draft from air-conditioning, or an infection, or an allergic response, or … a host of other possibilities.

In such cases, when a headache develops, what’s the real cause? What’s the real ‘trigger’? Is the trigger really a ‘cause’, or is it just a final straw? Or are the many interacting stresses the ‘causes’ – the biochemical, psychosocial, biomechanical factors to which the local area (cervical muscles for example) and the person as a whole are adapting – that have led to the stage where a single additional stress (the trigger) can start the headache, or initiate neck pain? Much depends on just how long adaptive stressor demands have been operating – weeks, months, years, or a lifetime.

THE SENSITIZATION MODEL

Bendtsen (2000) has described a model that explains the process leading to tension-type headache. He points to a process of central sensitization (facilitation) that occurs in both spinal and pericranial tissues, after prolonged bombardment of pain messages from pain receptors (nociceptors) in distant myofascial tissues.

This increased pain input to supraspinal structures ‘sensitizes’ (or ‘facilitates’) them, leading to increased pericranial muscle activity, which can continue even after the triggering factors have been normalized, resulting in episodic or chronic tension-type headaches. At its simplest this means that nerves have become hyperirritable, so that even minor stimuli, which would previously not have caused any discomfort, can lead to a great deal of pain. This does not mean that the person is imagining the pain, but that the sensations reaching the brain are interpreted as being far stronger than would be the case under ‘normal’ conditions, before sensitization.

The research supporting this model demonstrates the need to understand how, over time, a reversible problem may become entrenched and chronic.

Once they exist, areas of facilitation/sensitization appear to be capable of being irritated by stressors of all types – physical, chemical or psychological – even if there is no direct or obvious impact on the sensitized area (Bendtsen & Ashina 2000).

An adaptation example – leg length and headaches?

Janda (1988) describes the adaptive changes resulting from the presence of a significant degree of leg shortness (say ¾ inch/2 cm):

Janda’s point is that after all the adaptation that has taken place, treatment of the most obvious cervical restrictions, or local soft tissue changes, where the person might be aware of pain and reduced range of motion, would offer only limited benefit.

Whether the short leg is anatomic or functional (i.e., where there is a primary sacroiliac dysfunction that alters the position on the ilia, and therefore creates an apparent change in leg length), the changes described by Janda will occur. The difference is that with a functional change, correction of the sacroiliac joint problem should reduce the chain reaction of adaptational modifications, whereas with a true anatomic short leg, choices would be far more limited (e.g., requiring a heel and sole lift) (see Figure 9.7 for an example of a short-leg-induced scoliosis corrected by a heel lift).

Figure 9.7 A scheme of the palpation findings (posterior aspect) in a young woman with a lateral pelvic tilt, upwards on the right side, and right unilateral dorsal pain from pelvis to occiput. Virtually all her chronic symptoms were relieved within 12 days by a simple unilateral heel raise. Note: The degree of scoliosis has been exaggerated.

(Reproduced with permission from Journal of Bodywork and Movement Therapies 6:187.)

Another example

Liem (2004) has explained a sequence that results from a degree of malocclusion, involving, as an example, the first molar on the left, where premature contact occurs on bringing the teeth together.

Figure 9.8 shows something of the chain reaction of adaptations resulting from this apparently minor structural imbalance, in which cranial modifications absorb the stresses of this dental misalignment, followed by bodywide muscular and fascial adaptations that also include osseous changes involving the left clavicle, humerus, radius, ilium, patella, tibia, and foot.

Figure 9.8 Bodywide adaptations in response to a left first molar malocclusion. Ant. fascial lat., anterior fascial lateral; ER, external rotation; IR, internal rotation; SBS, sphenobasilar symphysis; TFL, tensor fascia lata.

(Reproduced with permission from Liem 2004.)

This individual might therefore display a range of symptoms involving the foot, knee, pelvis, spine, neck, and/or head. Although there is no certainty that headache would be one of the symptoms, it would be surprising if it were not. Treatment of the areas of adaptation might offer short-term relief to such symptoms; however, until the primary area of imbalance is addressed – the malocclusion – results would almost certainly be short term.

Janda’s example of adaptation and facial pain

Janda (1982) describes a typical postural pattern in an individual with temporomandibular joint (TMJ) problems, involving changes in upper trapezius, levator scapulae, scalenii, sternocleidomastoid, suprahyoid, lateral and medial pterygoid, masseter and temporalis muscles. In this pattern (described below) all these muscles will show a tendency to tighten and/or to develop tendencies to spasm, tenderness, and the evolution of trigger points.

The postural pattern associated with TMJ dysfunction might therefore involve:

1. hyperextension of the knees

2. increased anterior tilt of the pelvis

3. flexion of the hips

4. lumbar hyperlordosis

5. rounded shoulders and winged (rotated and abducted) scapulae

6. cervical hyperlordosis

7. compensatory overactivity of upper trapezius and levator scapulae

8. forward head position resulting in opening of the mouth and retraction of the mandible

9. intervertebral joint stress in the cervical spine

10. …and almost certainly, neck and head pain.

The message that can be drawn from these examples is that dysfunction patterns first need to be identified before they can be assessed for the role they might be playing in the person’s pain and restriction conditions, and certainly before these can be successfully and appropriately treated.

What’s short? What’s tight? What’s weak? What’s loose? What’s affecting neighboring structures negatively? What’s causing these changes, and what can be done about it without aggravating the situation?

WHAT’s TO BE DONE?

In any given case your role is to try to identify what can be done to help ease the current headache (see previous chapters, and also Box 9.1), as well as what might be done, or what the person might do, to reduce the likelihood of further symptomatic episodes.

Box 9.1 Soft tissue modalities in a clinical management sequence

1. Identify local and general imbalances that may be contributing to the symptoms being presented (posture, patterns of use, local dysfunction).

2. Identify, relax, and stretch overactive, tight muscles, using massage and possibly muscle energy techniques (MET), positional release techniques (PRT), myofascial release techniques (MRT) and others.

3. Mobilize restricted joints (possibly using MET, PRT).

4. Facilitate and strengthen weak muscles.

5. Re-educate (exercises, training, etc.) movement patterns, posture and/or breathing function.

This sequence is based on sound biomechanical principles (Jull & Janda 1987, Lewit 1999) and serves as a useful basis for care and rehabilitation of the patient with musculoskeletal problems that may be contributing to neck pain or headache. A variety of soft tissue normalization methods can be incorporated into this model (DiGiovanna 1991, Greenman 1989).

In these examples, using a biomechanical model of care, incorporating massage and appropriate soft tissue modalities (see Box 9.1) and rehabilitation strategies (posture, breathing, etc.) should certainly help to alter/improve the soft tissue status, enhance circulation and lymphatic drainage, and – if appropriate – assist in the deactivating of trigger points that may be contributing to the headache.

A broader model of care

The biomechanical model outlined in Box 9.1 is one way of managing such problems. Other proposed models for effective care of musculoskeletal dysfunction incorporate somatic, as well as behavioral, features. For example, Langevin & Sherman (2006) have described a model in which a broader therapeutic approach to musculoskeletal dysfunction in general can be understood. This is an ‘integrative mechanistic’model that addresses both behavioral and structural aspects, as well as pain psychology, postural control, and neuroplasticity.

This model emphasizes the need, in many instances, for multidisciplinary treatment protocols – possibly incorporating direct biomechanical/manual approaches including massage, movement re-education, psychosocial interventions, and, where necessary, pharmacologic and/or nutritional treatment methods and modalities – that meet the particular needs of the individual.

In this way long-term preventive approaches might also include: