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The diagnosis of entrapment neuropathies can be difficult because symptoms and signs often do not follow textbook descriptions and vary significantly between patients with the same diagnosis. Signs and symptoms which spread outside of the innervation territory of the affected nerve or nerve root are common. This Masterclass provides insight into relevant mechanisms that may account for this extraterritorial spread in patients with entrapment neuropathies, with an emphasis on neuroinflammation at the level of the dorsal root ganglia and spinal cord, as well as changes in subcortical and cortical regions. Furthermore, we describe how clinical tests and technical investigations may identify these mechanisms if interpreted in the context of gain or loss of function. The management of neuropathies also remains challenging. Common treatment strategies such as joint mobilisation, neurodynamic exercises, education, and medications are discussed in terms of their potential to influence certain mechanisms at the site of nerve injury or in the central nervous system. The mechanism-oriented approach for this Masterclass seems warranted given the limitations in the current evidence for the diagnosis and management of entrapment neuropathies.

Elevated carpal tunnel pressure is an important pathomechanism in carpal tunnel syndrome (CTS). Several invasive methods have been described for direct measurement of carpal tunnel pressure, but all have two important limitations. The pressure gauge requires sterilisation between uses, which makes time-efficient data collection logistically cumbersome, and more importantly, the reliability of carpal tunnel pressure measurements has not been evaluated for any of the methods in use. This technical note describes a new method to measure carpal tunnel pressure using inexpensive, disposable pressure sensors and reports the within and between session reliability of the pressure recordings in five different wrist positions and during typing and computer mouse operation. Intraclass correlation coefficients (ICC[3,1]) were calculated for recordings within one session for healthy participants (n = 7) and patients with CTS (n = 5), and for recordings between two sessions for patients with CTS (n = 5). Overall, the reliability was high. With the exception of two coefficients, the reliability of the recordings at different wrist angles varied from 0.63 to 0.99. Reliability for typing and mouse operation ranged from 0.86 to 0.99. The new method described in this report is inexpensive and reliable, and data collection can be applied more efficiently as off-site sterilisation of equipment is not required. These advances are likely to promote future research into carpal tunnel pressure, such as investigation of the therapeutic mechanisms of various conservative treatment modalities that are believed to reduce elevated carpal tunnel pressure.

A high prevalence of dual nerve disorders is frequently reported. How a secondary nerve disorder may develop following a primary nerve disorder remains largely unknown. Although still frequently cited, most explanatory theories were formulated many years ago. Considering recent advances in neuroscience, it is uncertain whether these theories still reflect current expert opinion. A Delphi study was conducted to update views on potential mechanisms underlying dual nerve disorders. In three rounds, seventeen international experts in the field of peripheral nerve disorders were asked to list possible mechanisms and rate their plausibility. Mechanisms with a median plausibility rating of ≥7 out of 10 were considered highly plausible. The experts identified fourteen mechanisms associated with a first nerve disorder that may predispose to the development of another nerve disorder. Of these fourteen mechanisms, nine have not previously been linked to double crush. Four mechanisms were considered highly plausible (impaired axonal transport, ion channel up or downregulation, inflammation in the dorsal root ganglia and neuroma-in-continuity). Eight additional mechanisms were listed which are not triggered by a primary nerve disorder, but may render the nervous system more vulnerable to multiple nerve disorders, such as systemic diseases and neurotoxic medication. Even though many mechanisms were classified as plausible or highly plausible, overall plausibility ratings varied widely. Experts indicated that a wide range of mechanisms has to be considered to better understand dual nerve disorders. Previously listed theories cannot be discarded, but may be insufficient to explain the high prevalence of dual nerve disorders.

Despite the high prevalence of carpal tunnel syndrome and cubital tunnel syndrome, the quality of clinical practice guidelines is poor and non-invasive treatment modalities are often poorly documented. The aim of this cadaveric biomechanical study was to measure longitudinal excursion and strain in the median and ulnar nerve at the wrist and proximal to the elbow during different types of nerve gliding exercises. The results confirmed the clinical assumption that ‘sliding techniques' result in a substantially larger excursion of the nerve than ‘tensioning techniques' (e.g., median nerve at the wrist: 12.6 versus 6.1mm, ulnar nerve at the elbow: 8.3 versus 3.8mm), and that this larger excursion is associated with a much smaller change in strain (e.g., median nerve at the wrist: 0.8% (sliding) versus 6.8% (tensioning)). The findings demonstrate that different types of nerve gliding exercises have largely different mechanical effects on the peripheral nervous system. Hence different types of techniques should not be regarded as part of a homogenous group of exercises as they may influence neuropathological processes differently. The findings of this study and a discussion of possible beneficial effects of nerve gliding exercises on neuropathological processes may assist the clinician in selecting more appropriate nerve gliding exercises in the conservative and post-operative management of common neuropathies.

Neurodynamic tests such as the straight leg raising (SLR) and slump test are frequently used for assessment of mechanosensitivity of neural tissues. However, there is ongoing debate in the literature regarding the contributions of neural and non-neural tissues to the elicited symptoms because many structures are affected by these tests. Sensitizing manoeuvres are limb or spinal movements added to neurodynamic tests, which aim to identify the origin of the symptoms by preferentially loading or unloading neural structures. A prerequisite for the use of sensitizing manoeuvres to identify neural involvement is that the addition of sensitizing manoeuvres has no impact on pain perception when the origin of the pain is non-neural. In this study, experimental muscle pain was induced by injection of hypertonic saline in tibialis anterior or soleus in 25 asymptomatic, naive volunteers. A first experiment investigated the impact of hip adduction, abduction, medial and lateral rotation in the SLR position. In a second experiment, the different stages of the slump test were examined. The intensity and area of experimentally induced muscle pain did not increase when sensitizing manoeuvres were added to the SLR or throughout the successive stages of the slump test. The findings of this study lend support to the validity of the use of sensitizing manoeuvres during neurodynamic testing.

Background: A modified straight leg raise test for the sural nerve (SLRSURAL) has been proposed to assist in the differential diagnosis of sural nerve pathology in people with posterior calf or ankle pain, or lateral foot pain. The biomechanical rationale is that strain in the dorsolateral ankle and foot structures following dorsiflexion-inversion can be selectively increased in the sural nerve with hip flexion. There are however no studies which have investigated whether hip flexion can increase strain in the sural nerve at the ankle. Objectives: To measure strain and longitudinal excursion of the sural nerve and Achilles tendon during a modified SLR. Design: Cross-sectional cadaver study, with a repeated-measures design. Method: Strain and excursion were measured unilaterally in seven embalmed cadavers using differential transducers and a digital calliper. Data were analysed with repeated-measures ANOVAs (pSURAL. The relatively small changes in strain and excursion were most likely due to limited available ankle mobility in the tested cadavers. Further research is required to establish the diagnostic accuracy of SLRSURAL in a clinical setting.

Treatment-related clinical prediction rules (CPRs) can potentially help clinicians choose a treatment for a particular patient. The recent publication of several systematic reviews illustrates the increased interest in CPRs for physiotherapy treatments (Beneciuk et al., 2009; May and Rosedale, 2009; Stanton et al., 2010). This editorial discusses how methodological issues may affect the information that can be taken from a study on a physiotherapy treatment CPR.We hope this discussion will help clinicians feel more comfortable about interpreting this type of research. © 2010 Elsevier Ltd. All rights reserved.

It is assumed that strain in a nerve segment at the end of a neurodynamic test will be greatest if the joint nearest that nerve segment is moved first in the neurodynamic test sequence. To test this assumption, the main movements of the median nerve biased neurodynamic test were applied in three different sequences to seven fresh-frozen human cadavers. Strain and longitudinal excursion were measured in the median nerve at the distal forearm. Strain and relative position of the nerve at the end of a test did not differ between sequences. The nerve was subjected to higher levels of strain for a longer duration during the sequence where wrist extension occurred first. The pattern of excursion was different for each sequence. The results highlight that order of movement does not affect strain or relative position of the nerve at the end of a test when joints are moved through comparable ranges of motion. When used clinically, different neurodynamic sequences may still change the mechanical load applied to a nerve segment. Changes in load may occur because certain sequences apply increased levels of strain to the nerve for a longer time period, or because sequences differ in ranges of joint motions.

Plantar heel pain is a symptom commonly encountered by clinicians. Several conditions such as plantar fasciitis, calcaneal fracture, rupture of the plantar fascia and atrophy of the heel fat pad may lead to plantar heel pain. Injury to the tibial nerve and its branches in the tarsal tunnel and in the foot is also a common cause. Entrapment of these nerves may play a role in both the early phases of plantar heel pain and recalcitrant cases. Although the contribution of nerve entrapment to plantar heel pain has been well documented in the literature, its pathophysiology, diagnosis and management are still controversial. Therefore, the purpose of this article was to critically review the available literature on plantar heel pain of neural origin. Possible sites of nerve entrapment, effectiveness of diagnostic clinical tests and electrodiagnostic tests, differential diagnoses for plantar heel pain, and conservative and surgical treatment will be discussed.

One of the signs advocated for monitoring during neurodynamic testing in the assessment of patients with upper quadrant disorders, is the response of the shoulder girdle. It is stated that a protective rising of the shoulder girdle is present when patients with neurogenic disorders are assessed and that the elevation is absent in asymptomatic subjects. As sensory responses are elicited in the majority of asymptomatic subjects and as the range of motion (ROM) is often limited during neurodynamic testing, it is questionable whether the elevation of the shoulder girdle would be absent in asymptomatic subjects. The aim of this study was to measure the shoulder girdle elevation force during five variants of the neural tissue provocation test for the median nerve. Thirty-five asymptomatic male subjects were assessed. A load cell was used to measure the amount of shoulder girdle elevation force and two electrogoniometers were used to measure the ROM at the elbow and wrist. When the ROM at the end of the test was restricted, a gradual increase in shoulder girdle elevation force could be observed throughout the test. Compared to the initial force at the start of the test, all variants resulted in a significant increase in force. It is concluded that a gradual increase in shoulder girdle elevation force should not be regarded as an abnormal sign in the interpretation of neurodynamic tests.

The 'feel through range' and the 'end-feel' of the elbow extension, and the elevation of the shoulder girdle during the upper limb tension test for the median nerve are considered important in clinical decision making. As no objective measurements have been published regarding these parameters, a special device was designed in order to obtain objective information on the force by which the shoulder girdle is elevated during the test. The purpose of this technical note is to describe the technical aspects of the device and its practical application. In a pilot study, five asymptomatic subjects have been assessed. The relationship between the elevation of the shoulder girdle and the range of elbow extension has been analysed. The data of five subjects and representative curves of one subject are presented. All five subjects demonstrate a considerable increase in force elevating the shoulder girdle. The results show that the device can be used to measure the force by which the shoulder girdle is elevated throughout the test. Although the number of subjects and the number of repetitions is limited, the data suggest that the method is accurate and that the phenomenon of shoulder girdle elevation during the upper limb tension test in asymptomatic subjects is consistent.