1. Movement dysfunctions: According to Sahrmann (2002), faulty posture and dysfunctional movement patterns are not only the result of pain and pathology but may also cause these lesions. If the symptomatic structure alone is treated (with passive movement, for example) and the dysfunction or ‘cause of the cause’ ( Maitland 1991) is disregarded, symptoms could well reoccur. In fact, in cases of minor instability or impingement, mobilizing gently in the direction of symptoms to decrease pain may meet with limited or short-lived success. If stronger mobilizing techniques progressing into pain are applied symptoms may suddenly increase. This is a clinical indication that functional factors need be addressed. In Table 7.2 a number of disorders are listed where the functional cause assumes particular importance.

2. Overload or overuse per se may in time lead to degenerative change or stress fracture. If malalignment is also present then otherwise normal stresses may excessively load one part of the hip joint, the surrounding nerves or myofascial structures. Individuals working at heavy jobs (e.g. furniture movers) or individuals engaged in sports with poor technique or inadequate training procedures (e.g. running on hard surfaces) may subject their joints to overload. Similarly, nerve entrapments such as meralgia paraesthetica are reported to have contributing overload factors: obesity, the wearing of tight jeans and wide belts resulting in compression ( Butler 1991).

• Systemic disorders with spontaneous development of acute symptoms. Here medical care is important.

• Developmental and structural disorders: both dysplasia and Perthes’ disease may contribute to structural change and the development of femoroacetabular impingement ( Fraitzl et al. 2007, Rab 1999, Friend & Kelly 2009, Li & Ganz 2003), which in turn is said to be implicated in the development of degenerative osteoarthritis ( Ganz et al. 2003, Beck et al. 2005, Bardakos & Villar 2009). Where structural change is present, surgery may be the priority for treatment.

• Traumatic disorders where tissue healing times will affect dosage and progression of treatment.

• + Physiological movement dysfunction. Here the physiological movement is uncontrolled allowing increased end-of-range movement (hypermobility). Excessive physiological movement is generally readily observable. If neighbouring joints in the movement chain are also hypermobile, the hip may not become symptomatic as forces would be shared along the chain. However, if the neighbouring lumbar, sacroiliac and knee joints are stiff then repeated bending movements or forceful hip flexion movements during sport may traumatize the hip leading, for example, to impingement of anterior soft tissues including the labrum. According to Martin et al. (2006), labral tears have been arthroscopically identified – although not in isolation – in 90% of mechanical hip pain. A number of authors link labral damage to the development of capsular laxity and vice versa ( Schenker et al. 2005, Martin et al. 2006), suggesting that better end-range control of this movement may help reduce symptoms as well as recurrences. Other dysfunctions linked to excessive physiological movement have been listed in Table 7.2.

• + Accessory movement dysfunction. Here the translatory or gliding movement is uncontrolled resulting in a variable and undependable centre of rotation. This will also affect physiological movement and may be experienced as a lack of ‘through’ range movement control; for example, if the patient attempts to stand on one leg with his hip joint in the ‘physiological’ neutral position (neutral flexion/extension, abduction/adduction, medial rotation [MR] and lateral rotation [LR]), the hip ‘jerks’ or ‘wobbles’ and cannot remain still. These joints may not necessarily exhibit increased end-of-range movement but the ‘neutral zone’ has been shown to be increased ( Panjabi 1992) with subsequent loss of a reliable ‘translational neutral position’ (midposition of three-dimensional translation movements). This may be referred to as ‘stability dysfunction’. In addition, excessive gliding may be associated with increased end-of-range movement in the normally coupled physiological direction. A certain amount of posterior gliding is coupled with hip flexion. If this gliding is excessive the flexion movement may also seem excessive. In fact, the actual angular movement in the joint may be restricted but the disturbed gliding produces a hinge-like gapping movement and a seemingly increased flexion. Alternatively, the condition may elicit protective reactions in the effected direction resulting in decreased range of movement. However, in both situations the increased shearing movements are detrimental to the cartilage as well as irritating to the synovium and are thought to contribute to joint effusion and, in time, osteoarthritis. These joints are classed as ‘unstable’.

• − Physiological movement dysfunction. If specific ranges of movement are not used, adaptive restriction may occur in time. Disuse may result from habitual patterns or protective reactions. Habitual patterns may be due to restricted movement in non-symptomatic neighbouring joints (see the arrow in Figure 7.1). In the case of pathological disorder (e.g. ankylosing spondylosis), protective reactions may be appropriate and some movement restriction unavoidable. In other cases, a restrictive pattern may remain because the patient failed to fully use the joint although the disorder was no longer irritable.

• − Accessory movement dysfunction – the blocked joint. If gliding movement (e.g. anterior glide) is excessive in one direction it may in time become restricted in the opposite direction (posterior glide) (see the curve in Figure 7.1). Since hip flexion is coupled with posterior glide, the flexion may become restricted. Patients often describe a bursting feeling at end of range.

 Where excessive physiological movement (hypermobility) is found in the symptomatic direction active stabilizing exercise may be the treatment of choice (e.g. better end-range control of lateral rotation for specific labral lesions, or athlete’s groin). If pain occurs during low-level activity, correcting the movement pattern by tonically recruiting and shortening the global stabilizer and inhibiting overactivity in the global mobilizer will help achieve a pain-free movement pattern. For excessive lateral hip rotation, for example, recruiting the anterior gluteus medius and minimus and the short adductors while inhibiting the piriformis and superior gluteus maximus may achieve this aim.

 If the hip is compensating with excessive movement for restriction in neighbouring joints these joints can be mobilized at some stage (e.g. excessive hip external rotation during a golf swing may compensate for lumbar spine or knee rotational restrictions).

 Where excessive gliding movement (minor instability) contributes to dysfunction in the symptomatic direction, pain-free tonic recruitment of the segmental stabilizers while maintaining normally painful positions and performing normally painful activities may help restrain excessive gliding. Similarly, passive accessory mobilization in the opposite direction to pain may be necessary if this direction has become stiff.

 Where restriction in the coupled gliding direction is found to block the physiological movement, passive accessory joint mobilization, may be the treatment of choice. Because gliding and physiological movements are coupled (Matles 1975, Simoneau G, Hoenig K Lepley J et al 1998 cited in Sims (2003), mobilizing an accessory movement such as posteroanterior glide may restore extension movement. Sims (2003) states that the migratory ‘up and out’ presentation of osteoarthrosis may lack longitudinal caudal motion whereas the medial migratory presentations may lack lateral gliding motion.

 Restriction in physiological movement may be helped by a combination of muscle lengthening, trigger-point techniques or fascial techniques, etc.

• Walking on level surfaces: 30° flexion, 10° extension, 5° abduction, 5° adduction, 5° medial rotation, 5° lateral rotation

• Ascending stairs: 65° flexion, 5° extension

• Descending stairs: 65° flexion, 5° extension

• Sitting: 90° flexion

• Tying shoelaces: 50° flexion.

 according to Maitland et al. (2001), an intra-articular disorder with a degree of inflammation might be suspected if symptoms are more constant in their behaviour, are perceived as deeply localized and more restricting in daily life activities and if regular changes in resting positions are needed. Systemic inflammatory disease such as rheumatoid arthritis may occur more spontaneously and episodically with morning pain and stiffness lasting longer than an hour. Concomitant multi-joint involvement is a feature.

 labral tears: here forceful rotation is often involved and may be accompanied by a clicking sensation in the groin.

 Tendinopathies and muscle lesions: pain is clearly pinpointed by the patient and reproduced on stretching or contracting the muscle or during stop-and-go activities ( Agre 1985).

 Joint surface of the hip: reproduction of symptoms occurs during weight-bearing activities, particularly sustained standing. Sudden loading of the joint surface, for example, when moving out of sustained positions such as sitting may also produce symptoms ( Arnold et al. 1972).

 Capsular tightness: end-of-range movements may aggravate symptoms.

 Fascia: under tension, burning or prickling symptoms may occur.

 Nerve entrapment (e.g. meralgia paraesthetica): burning pain during the night is typical.

 The symptomatic activity and subsequent analysis of the movement direction together with type and area of symptoms ( Fig. 7.5) will help establish the dysfunction. It also helps the therapist focus on the movement direction requiring careful assessment and later treatment. Direction-specific aggravating activities with their typical movement dysfunctions are listed in Table 7.7.