Unlocking the Mystery: Double Crush Syndrome

Double crush syndrome mechanism

The first description of double crush syndrome was in 1973⁽¹⁾. There are typically central and peripheral areas of symptoms (see table 1). The hypothesis is that there is a disruption of axoplasmic flow or neural elasticity that causes nerves that have been compromised at one site to become more susceptible to compromise at another location.

Table 1: Common areas implicated in double crush syndrome in the upper and lower limb⁽²⁾

Repetitive strain or overuse is often a contributing factor, but sometimes trauma precedes a double crush syndrome presentation. For example, in the lower limb, hip dislocation and acetabular fracture with sciatic nerve involvement may present later with peroneal nerve involvement.

Mechanical compression of a nerve in one area adversely affects neural mobility in another area. For example, anatomical anomalies that cause mechanical compression, like a cervical rib, are sometimes present. Or spondylosis of the spine with osteophytes encroaching on the nerve root could cause mechanical compression. Likewise, scarring from an old injury like a hamstring strain could cause tethering of the sciatic nerve, compromising its mobility. Or an old fracture of the neck fibula with a bony callus could mechanically compromise the common peroneal nerve. All of these will affect the mobility or neurodynamics of the nerve either proximally or distally to the mechanical compression.

RED FLAG WARNING

It is critical to exclude systemic diseases such as multiple sclerosis, diabetes, thyroid disease, and chemotherapeutic agents that could be causing nerve damage.

The key is to identify all of the areas of compromise along the path of the nerve during the assessment, and treatment aims to improve the mobility of the nerve in each area. There are two systems in the body that stretch from the head to the toes: the myofascial and neural systems.

The myofascial system

Myofascia surrounds all our bodies’ muscles, tendons, ligaments, organs, nerves, joints, and bones. Healthy myofascia is flexible and stretches as the body moves. A mobile and flexible myofascial system allows other structures to move freely. This includes the neural system. When myofascia tightens up, it restricts movement and can cause pain. Releasing and ensuring a fully mobile myofascial system will improve neural mobility and help alleviate pain.

The neural system

The neural system conductance is tested clinically with a neurological examination that includes muscle power, sensation, and reflex testing. These clinical tests, as well as nerve conductance studies, are generally normal in double crush syndromes. A clear neural examination in the instance of a central area of symptoms with a peripheral area of symptoms strengthens the hypothesis of a double crush syndrome. Neural mobility testing provides essential information in double crush syndrome; the same tests become a valuable part of treatment^(3-6). 

Table 2: The difference between a neurological and neurodynamic examination.

Table 3: Areas where nerves are least mobile and are often implicated in double crush syndrome⁽⁷⁾.

Clinical presentation

Typically double crush syndrome presents in similar patterns. For example:

• A golfer presents with “tennis elbow” and medial scapular pain.
• A rugby player presents with a hamstring strain and lower back pain.
• A cyclist complains of neck and elbow pain and numbness along the outside of the little finger.
• A long jumper complains of buttock and dorsal foot pain.

All of these are typical examples of patients with double crush syndrome. It is common for patients to describe two distinct areas of pain that do not appear to be connected. Often the onset of one area of pain precedes the other by weeks or months.

Nerve root compression pain is very specific, unremitting, and in a dermatomal distribution, often worse distally than proximally. In addition, with nerve root pain, there are commonly other neurological symptoms of numbness, pins and needles, and weakness.

The description of the pain associated with compromised neural mobility is different. It is non-specific and vague in intensity and distribution. It is not dermatomal and switches around from one area to another. Other neurological symptoms may or may not be present with neurodynamic pain.

On physical examination, neural tension tests will be positive. and tension points are tender. There will be some compromise to the mobility of the nerve in both or all areas that the patient describes in the subjective examination.

Poor posture is often a contributing factor. For example, forward head posture adversely affects the mobility of the nervous system. Therefore, posture correction in the workplace and during sports is important.

Aims of Physiotherapy Treatment

• Release centrally
• Release peripherally
• Restore full neurodynamics
• Correct posture
• Rehab, including slider and tensioner exercises

Physiotherapy management

1. Central joint and soft tissue mobilization

Clinicians can mobilize the central spinal regions to reduce the tension. Maitland accessory mobilization techniques are useful for improving the tiny glides and mobility at each motion segment. Anteroposterior (AP) unilateral mobilizations work especially well in the cervical spine to release neural tethering and restore neural mobility. Furthermore, any other spinal levels with known disc degeneration or spondylosis should be mobilized. For example, mobilizing the first rib and releasing the scalenes has a marked positive impact on brachial plexus mobility (see figure 1).

Figure 1: Structures that compress the brachial plexus