Neurodynamics

Monika Lohkamp, Lee Herrington and Katie Small

Introduction

In 1864, Lasegue first described the straight leg raise test (SLR) as an assessment for lower back problems with nerve involvement (Butler 1991). This concept was further developed by Goddard and Reid in 1965 who described the SLR as movement of the sciatic nerve. Also, in the 1960s Alf Breig investigated the biomechanics of the nervous system in more detail and showed that nerves move independently from other tissues. This formed the basis of the concept of ‘neurodynamics’. Earlier terms for this concept were ‘neural tension’ (Breig 1978) or ‘adverse mechanical tension of the nervous system’ (Butler 1989). However, the actual term ‘neurodynamics’ was first introduced by Gifford in 1989. The concept of neurodynamics has been further developed by Grieve, Butler, Maitland and Shacklock over the last 30 years. Nowadays, although neurodynamics remains a relatively new concept within musculoskeletal clinical assessments, it is becoming more widely used and accepted as an important aspect for injury assessment and treatment.

Mechanics of the peripheral nervous system

In general terms, the nervous system can be divided into the central nervous system (CNS; brain and spinal cord), peripheral nervous system (all nerves after leaving the nerve roots within the spinal vertebrae) and autonomic nervous system (sympathetic and parasympathetic division) (Michael-Titus et al. 2007). The central and peripheral nervous system are closely connected through meninges (Butler 1991). The mechanical and physiological properties of peripheral nerves are crucial in their ability to function well.

The peripheral nerves are not only involved in conducting impulses and chemical traffic, but are also considered as dynamic tissue in the same way as muscles and joints. Along with the CNS, the peripheral nerves are designed to function while stretching and sliding (longitudinal and transverse motion) as a result of a wide variety and range of body movements (Shacklock 1995). When nerves are sliding they always slide towards the joint where movement takes place (Coppieters and Butler 2008). During movements of the body, nerves can undergo extremes of elongation, for example the spinal canal is 5–9 cm longer in flexion than extension, thus leading to an increased tensile load on the spinal cord (Breig 1978; Louis 1981 cited in Butler and Gifford 1989). Another example is the median nerve which has to adapt to a nerve bed nearly 20% longer if the shoulder is 90 degrees abducted, and the wrist and elbow are moved from flexion to extension (Millesi et al. 1986).

The nervous tissues are able to tolerate large tensile and compressive forces during movements associated with daily living and sporting activities. Nerves are strong structures owing to the surrounding connective tissue sheath helping them withstand large compressive and tensile forces (Shacklock 1995). If nerves are loaded by movement they react by moving and absorbing some of the pressure. During normal movement, as the nerve elongates the perineurium tightens, intraneural pressure increases and intrafasicular capillaries stop flowing. This occurs at 8% elongation, with intraneural microcirculation ceasing completely at 15% elongation (Ogata and Naito 1986). As the nervous system is dynamic, forces that cause a temporary disruption are easily tolerated. However, if the load becomes too excessive or persists, the maintenance of the increased local pressure to the nerve can cause local tissue ischaemia and injury.

Pathophysiology of the nervous system

Injuries involving nervous structures can either be caused by direct or indirect mechanics. A direct injury can occur from over-stretching or irritation from a repetitious activity, whereas an indirect injury can result from bleeding owing to a muscle tear through which the nerve passes. Either of these types of injury can cause extraneural dysfunction (affecting movements outside of the nerve; relative to the nerve) or intraneural dysfunction (affecting movements within the nerve (Butler (1989)). These two forms of dysfunction are not exclusive of one another and sometimes extraneural dysfunction can actually lead to intraneural dysfunction. Both, however, will be discussed separately in further detail.

Extraneural dysfunction

The term ‘extraneural’ refers to anything outside of the nerve. This refers to the ‘mechanical interface’, which is any structure surrounding the nerves and lying between them and other surrounding structures (Butler and Gifford 1989). The nervous system is surrounded by, and passes through or around, various structures, including muscle, bone, tendon, blood vessels and intervertebral discs. These help contain the nervous system and allow for its movement, so as the nerve shortens, elongates or twists during daily movement so does the mechanical interface (Shacklock 1995). The smooth and normal movement of the nervous system and mechanical interface as it interacts with the musculoskeletal system is important for injury prevention. The consequence of extraneural pathology is to subject the nerve to increased tensile, frictional or compressive load. Examples of vertebral extraneural pathology are the narrowing of the intervertebral foramina (e.g. through osteophytes) or disc protrusions irritating a nerve root. In the peripheral nervous system, examples of extraneural pathology include the sciatic nerve lying in a bed of blood from a hamstring tear, tight fascial bands across nerves and a nerve as it passes through an oedematous tunnel (tarsal tunnel, carpal tunnel).

During movements, nerves take their lead from the movement of joints and muscles, needing to maintain a dynamic relationship with all non-neural tissue. For example, they must slide through tunnels of muscle and fascia, and be compressed against various structures, such as bone. Some interfacing structures make the nervous system more vulnerable to injury like, for example, tunnels (carpal tunnel, cubital tunnel, tarsal tunnel), hard interfaces (nerve on bone, passing through fascia), proximity to the surface or when nerves are fixed to the interfacing structures (e.g. common peroneal nerve at the fibular head). With abnormalities in these interfacing tissues, such as callus development, formation of bands of scar tissue, pressure from haematoma or enlarging tumour or ganglia, peripheral nerve neurodynamics and, therefore, neurophysiology may be adversely affected.

Mechanical interface dysfunctions occur when the forces exerted on the nervous system by the interfacing motion segment are abnormal or undesirable. The pressure exerted could be intermittent or sustained. These can be further divided into either ‘opening’ or ‘closing’ dysfunctions. This principle can be used throughout different neurodynamic and musculoskeletal assessments. These dysfunctions can be caused by, for example, incorrect posture, anatomical abnormalities or undesirable technique/movement.

Key point

A closing dysfunction means an alteration in the closing mechanism of the movement complex around the nervous system. You can have either too much closing (i.e. compression) or reduced closing.

Opening dysfunction involves an abnormality in the opening mechanism of the movement complex located adjacent to the nervous system. You can either have increased opening or reduced opening function (Shacklock 2005).

Intraneural dysfunction

Intraneural dysfunction refers to within the nerve itself. Entrapment of a nerve by surrounding tissues or with an intraneural fibrosis (scarring within the nerve structures) can cause pathological changes within the nerve (Butler and Gifford 1989). This may lead to a loss of range of movement or alteration in elasticity of the nerve and, as a result, enhance the normal mechano-sensitivity of the nerve during movement and thus provoke pain and reactive muscle spasm to prevent elongation.

Intraneural pathology can cause damage to the tissue of the nervous system itself, either to the conducting tissue in the form of demyelination, neuroma or hypoxia, or to the surrounding connective tissue, for example scarring of the epineurium. The possibility exists that a fibrosed nerve can cause a friction fibrosis elsewhere in the system. Tension has been taken up at one site in the nervous system thereby compromising the amount of available ‘slack’ elsewhere in the system. An example is a fibrotic length of common peroneal nerve at the head of fibular that may lead to abnormal deep peroneal nerve/interface relationships at the ankle. This may contribute to altered proprioception input from the ankle and in combination with less slack in the nervous system, influence the neurological functioning of the ankle joint, perhaps predisposing to recurrent ankle ligament sprains.

Mechano-sensitivity

The term mechano-sentitivity refers to how easily a nerve is activated following application of mechanical force (Shacklock 2005). There are a variety of causes for mechano-sensitivity; however, perhaps the most common factor is owing to pressure. This can either be applied directly or indirectly, as will be discussed.

Direct mechanical pressure can be applied to the nerve by any tissue infringing the space occupied by the nerve (e.g. ‘bulging disc’ or poorly fitted athletic knee brace). For example, compression of a disc hernia reduces blood flow in the nerve by 70% (Kobayashi et al. 2003). When loading persists, as it could from sustained un-physiological postures or maintained local pressures, damage may ensue as a result of local tissue ischaemia.

Indirect pressure is a more powerful cause of compressive load and therefore mechano-sensitivity, and is caused by immediate swelling in surrounding tissues that have been damaged. This inflammatory response also results in the release of chemical substances (histamines and enzymes) which create a chemical irritation, increasing pain, and can potentially lead to the laying down of scar tissue in and around the nerve with long-lasting negative effects on the mobility of the nerve.

Double and multiple crush syndrome

Double (DCS) or multiple crush syndrome (MCS) refers to a condition where proximal compression or elongation of a nerve decreases the nerve’s ability to withstand compression or elongation at a distal site (Upton and McComas 1973). This type of condition is caused by changes to the nerve’s axoplasmic flow. Axoplasmic flow is the term used to describe the transport mechanism of cell components in the nerve to their functional site where they help to maintain tissue health. Therefore, any pressure which is directly applied to the nerve or in the surrounding tissue following injury may cause slowing down of the axoplasmic flow and cause the nerve to ‘become sick’. If pressure is applied to two (double crush) or multiple areas (multiple crush), the nerve will be considerably more prone to injury.

Axoplasmic flow relies on a mechanically unimpeded nervous system and an uninterrupted blood flow. Changes in the flow characteristics of axoplasm could cause insidious attrition to both target tissues and neurones, and impairment in the ultrastructure of the neurone. This enables previously resistible compressive or tensile forces to cause damage, usually at the vulnerable areas of the nervous system outlined previously. For example, patients with carpal tunnel syndrome are more likely to develop a compression lesion of the ulnar nerve at Guyon’s canal and those suffering from carpal tunnel syndrome frequently have bilateral symptoms.

The original DCS described neural injuries at the neck which then predisposed to carpal tunnel syndrome (Upton and McComas 1973). Alternatively, reversed DCS occurs where a distal neural injury (e.g. at the wrist) predisposes to a proximal injury, perhaps at the shoulder. MCS occurs where following initial neural injury a patient experiences multiple and related areas of symptoms. Clinical presentation of DCS or MCS may often be widespread and unfamiliar in nature. However, patients may complain of a string of injuries or multiple areas of localised pain which have common pathophysiologies that represent a minor form of DCS or MCS.

The concept of DCS or MCS therefore provides an excellent reason for clinicians to evaluate along the nerve tract when suspicious of a neurogenic lesion. This should always be considered a possibility whenever an athlete reports multiple areas of pain, for instance a distance runner who complains of tibialis anterior and buttock pain. If diagnosis is later confirmed as DCS or MCS, treatment should also be considered for all the sites involved. For the example of the distance runner, treatment of the piriformis muscle may be needed to alleviate neural symptoms at the foot by altering a site of pressure contributing to altered axoplasmic flow to the foot.

Assessment principles

Indications

The main purpose of neurodynamic testing is to load the tested neural structures to help gain an understanding of their mechanical function in relation to load and their state of sensitivity to that load. There is no set indication of when neurodynamic testing should be performed; however, some believe that it should be performed if the client presents with any form of neurological symptoms, such as pins and needles, tingling, shooting or burning pain, unexplained strength loss, paraesthesia or numbness. Alternatively, neurodynamic testing may be indicated for any overuse injury or reinjury, or if the client has sustained an injury to the vertebral region. However, in theory, neurodynamic testing could be considered for any musculoskeletal injury as nerves are closely connected to other structures (e.g. muscles, tendons and ligaments).

As well as indications, there are also contraindications and precautions to neurodynamic testing. Contraindications represent any kind of factor or condition that increases the risk or danger to cause serious harm to the client by carrying out neurodynamic testing. Therefore, if any contraindications are present the neurodynamic tests should not be carried out. Precautions are factors that you should be aware of and take additional care of when carrying out and interpreting neurodynamic tests, although this does not mean that you cannot carry out the tests. Common contraindications and precautions to neurodynamic testing are presented in Table 25.1 (Butler 1989).

Table 25.1

Contraindications and precautions to neurodynamic testing

Contraindications	Precautions
Recent onset/worsening of neurological signs	Spinal stenosis or spondolythesis	Dizziness (vertebrobasilar insufficiency)
Cauda Equina lesions	Disc protrusion	Severe, unremitting pain
Cancer of nervous system/vertebral column	Presence of neurological signs	Frank cord injury
Acute inflammatory infection	Worsening disorder	Circulatory disturbances
Osteoporosis resulting in abnormal interfacing tissues	Irritability of nervous system	General health problems (diabetes, AIDS, multiple sclerosis)
Injury to spinal cord (tethered cord)

Structural differentiation

Neurodynamic tests involve assessing the mobility of the nervous system as it interacts with the musculoskeletal system. However, this can create a problem when trying to distinguish whether reproductions of the client’s pain/symptoms during a test is as a result of the movement by nervous or musculoskeletal structures. Structural differentiation emphasises movement of the neural tissues as opposed to the musculoskeletal tissues, therefore helping to identify the damaged structure – whether neural or musculoskeletal (Butler 2000). For example, when performing the slump test by extending the knee it would cause movement, and potential tension, of both nervous (sciatic nerve) and musculoskeletal (hamstrings) tissues. To help distinguish which structure was the cause of the client’s pain/symptoms, we could get the client to release the cervical flexion. This structurally differentiating manoeuvre is unlikely to alter the strain on the lower limb musculoskeletal structures (hamstrings); however, it will change the tension on the nervous system. Therefore, if this manoeuvre resulted in reducing the client’s pain/symptoms, we could propose that their injury was related to neurological, rather than musculoskeletal, damage.

Sensitising manoeuvres

While structural differentiation is a key element for helping identify neurogenic problems, for patients with a high level of function less severe problems may remain hidden. Therefore, in order to make the test more specific to identify the problem we can add sensitising manoeuvres. This is where the normal neurodynamic technique is modified slightly to increase the test sensitivity so that it becomes more specific to the patient’s problem (Keneally et al. 1988

Key point

Once an individual joint position is achieved make sure this is maintained while other joints are moved during the test.

Gain constant verbal and visual feedback from the patient during testing.

Regularly re-test and monitor patient’s symptoms during assessment and treatment and adapt as appropriate.

). The easiest and most common way of sensitising tests is to put extra strain, or stretch, on the nerve by elongating it. A simple example of this would be to add cervical flexion when performing a SLR. Another sensitising manoeuvre would be to contract a muscle close to the nerve pathway around the affected area during the neurodynamic test, such as contracting piriformis muscle during SLR.

However, these manoeuvres cause a greater risk of pain to the patient. Therefore, sensitising manoeuvres are only recommended when previous standard neurodynamic tests have not revealed enough information to make a clear diagnosis and/or it is unlikely to cause severe pain/reproduction of symptoms, and the patient has no persistent or worsening neurological problems.

Clinical note