1 Hyperventilation and anxiety: which ‘causes’ which?

Hyperventilation is commonly associated with anxiety. Therefore, if we think in simple terms of cause and effect, we might assume that hyperventilation ‘causes’ anxiety. However, anxiety commonly leads to hyperventilation; therefore, again, if thinking simplistically, we might assume that anxiety ‘causes’ hyperventilation. Or, if thinking more contextually, we might observe (more accurately) that anxiety and hyperventilation not only ‘feed’ each other, but can be triggered and/or aggravated by – for example: low blood sugar levels (Brostoff 1992), increased progesterone levels in the post-luteal phase of the menstrual cycle (Cimino 2000), sympathetic arousal (‘stress’) and adrenal stimulation (Nixon & Andrews 1996), metabolic acidosis, for example in pregnancy (Slatkovska et al 2006), climatic conditions, altitude, emotional stimuli, allergic reactions (Brostoff 1992), extreme fatigue, and so on. Therefore, we might conclude that anxiety and hyperventilation are part of a continuum, involving all or any of these (and numerous other) associated aetiological factors, interacting with the unique genetic and acquired biochemical, biomechanical and psychological individuality of the person affected. And we might reflect that treatment that takes account of the broader context is more likely to succeed than a simple, linear, ‘cause and effect’ assessment.

2 Possible ‘usefulness’ of trigger points

Clinical experience suggests that myofascial trigger points may, at times, form part of a functional system for sustaining tension, where this is required by the body – for instance in posturally compromised tissues, as ‘repositioners’ (e.g. for the mandible due to forward head posture), or for sustaining tension across the sacroiliac joint when it is unstable, by strategically increasing hamstring tone (Vleeming et al 1997). In such a situation the body is doing exactly what it was set up to do, as changes occur leading to trigger point development. Simons et al (1999) have shown that, in the absence of adequate levels of adenosine triphosphate (ATP), and in the presence of calcium, the actin and myosin elements of muscles are designed to lock in a shortened position. Trigger points function effectively in the absence of ATP (therefore displaying an economy of resources), and are often strategically located in tissues that are straining to accommodate dysfunctional posture, or habits of use. And trigger points often clear up spontaneously when the immediate causes (and/or other stressors such as dietary imbalance, breathing dysfunction, dehydration, etc.) are corrected (Chaitow & DeLany 2002).

Trigger points also appear to demonstrate a built-in, silent (latent) and non-silent (active) alarm mechanism, when the structures with which they are associated are being abused. Therefore, to release trigger points without regard to correcting the underlying causes (the abuse), to which they are responding, may result in a less than ideal outcome, not least of which could be a rapid, or chronic, return of the trigger point activity. Rather than always being seen as dysfunctional entities, trigger points might be considered as low-energy-consuming contractile devices, established by the absence of available ATP, to maintain a structural or localized tensional element, for immediate or long-term adaptation/compensation purposes, until no longer required. Additionally they may be seen as alarm signals when tissues are being overloaded and abused. In this way of thinking, it is the individual’s posture, patterns of daily use, or lifestyle, that are dysfunctional, not the tissues housing the trigger point, which may be doing exactly what they were designed to do. When this is true – and when we can recognize that it is – it is the context from which trigger points emerge that requires attention, not the trigger points.

Of course there are times – arguably in the majority of cases – when trigger points remain active well past their possible usefulness as stabilizing agents, or when they exist as historical remnants of previous overuse or trauma. In such instances they are nuisances, and may be disturbing normal function, and so require appropriate deactivation. Even when trigger points are potentially useful as stabilizers but are nevertheless causing pain, if more appropriate stabilization can be achieved, via (say) improved core stability, then deactivation – manually or by other means – would be seen to be appropriate.

3 Assessment of sacroiliac dysfunction

Lee (2002) reports that Hungerford & Gilleard (1998) have shown that normal individuals, performing a one-legged, standing, hip flexion (‘stork’) test, vary their motor control strategy each time they perform the test, implying that different muscles can be used to perform the same osteokinematic motion. This will vary the amount of compression each time they lift the leg, and thus vary the range of motion. Lee (2002) has written:

As if this is not enough to create hesitation as to the validity of such tests, a range of other possible influences has been noted. For example, what if:

There are multiple influences, only some of which can be controlled, during tests of this sort, suggesting that clinical reasoning as to what single tests ‘mean’ is essential. A single test result cannot define dysfunction, offering at best a shadowy indication, and becoming more relevant only when other assessment findings, and the patient’s symptom picture and history are added. Assessment is therefore a spatial exercise, not a linear one, seeking synchronous pieces of evidence that, together, lead to a working hypothesis as to what is happening – and what to do.

Conclusion

Hopefully these three examples, hyperventilation, trigger points and sacroiliac joint assessment, offer sufficient evidence to point towards a need to think contextually, to look for synchronicity, and to be cautious regarding linear thinking, especially when dealing with the complexity of the human body.

What about joints?

Soft tissue manipulation, which includes positional release methods (‘strain/counterstrain’), NMT and MET, is capable of normalizing a great many joint problems, without recourse to active manipulative effort (Schenk 1994, Wilson et al 2003, Speicher et al 2004). MET and NMT are symbiotic, and it is possible to achieve more by combining their repertoire of useful techniques than either can achieve individually. By adding the knowledge of suitable techniques by which to influence reflex activity, demonstrated by the presence of localized areas of soft tissue dysfunction (trigger points, Chapman’s points, localized fibrosis, etc.), as well as by using the tender points described by Jones, in gentle functional techniques, the scope of soft tissue manipulation methods should become apparent.

Employment of these approaches does not necessarily preclude the need for active joint mobilization and/or manipulation, in correcting restriction, but can make for a lesser need to use high-velocity thrusts, or long lever techniques, while making such manipulation simpler and far less likely to traumatize the local tissues, or the patient. By combining MET and NMT, some degree of the potential problem of avoiding tissue damage is likely to be solved. NMT, applied to a region containing fibrotic change, will allow for subsequent use of ‘normal’ MET, or of an isolytic contraction, with less discomfort or likelihood of microtrauma (see Ch. 8).

Are some musculoskeletal problems best left untreated?

The enormous privilege that the patient allows in permitting the practitioner to make physical contact also grants a degree of ‘power’ to the practitioner. Defences are lowered, and the patient is likely to be amenable to discussing areas of their emotions and thoughts, that they might resist in other situations. This presents opportunities for therapeutic intervention on levels other than the physical. The practitioner should be aware of the opportunity to exploit the potent ‘placebo’ effect that such situations allow. Suggestions, and positive guidance, can have powerful influences on the patient, and so care should be exercised, and diligent application of therapeutic techniques undertaken, knowing that the recipient is commonly receptive and highly suggestible (Pollo & Benedetti 2008).

When considering treatment of soft tissue changes that relate to an emotional or psychogenic background, it is important to realize the need for an adequate ability on the part of the practitioner/therapist to handle any emotional repercussions resulting from ‘releasing’ (or attempting to release) the soft tissue manifestations of emotional turmoil, as well as there being a need to have an adequate referral system in place to support the patient in times of crisis (Field et al 2005, Loga 2008).

If the patient is not capable of processing whatever emotional baggage is attached to a particular pattern of soft tissue dysfunction, then it is probably best left intact, until the patient is ready and equipped to process the issues that are submerged in the soma (Mancuso et al 2004).

A scenario is conceivable in which a patient with obvious musculoskeletal dysfunction, but without obvious mento-emotional problems, could be left in a fragile and vulnerable state following apparently appropriate bodywork. The oft-quoted phenomenon of ‘emotional release’, which may occur during or following treatment, is something therapists could usefully reflect upon and possibly re-evaluate. Just how beneficial – or how dangerous – is such a reaction without further support, such as counselling or psychotherapy?

Additionally, there are times when apparently purely physical symptoms, such as active trigger points in a tight hamstring, as in the example given earlier in this chapter, may best be left untreated until underlying, contextual, causes have been evaluated and dealt with.