NERVE COMPRESSION SYNDROMES

Michael Tonkin

After studying this chapter you should be able to:

1. Understand normal peripheral nerve anatomy and function including electrophysiological testing.

2. Appreciate the aetiopathogenesis of the most common entrapment syndromes.

3. Assess the risk factors commonly associated with carpal tunnel syndrome.

4. Understand the general principles of medical and surgical treatment of entrapment neuropathies and their complications.

Introduction

Nerve compression (entrapment) syndromes are a common cause of limb pain. The most common of these is the carpal tunnel syndrome in which the median nerve is compressed at the wrist. Other examples include the cubital tunnel syndrome due to compression of the ulnar nerve at the elbow, the tarsal tunnel syndrome due to entrapment of the posterior tibial nerve at the ankle and meralgia paraesthetica due to entrapment of the lateral cutaneous nerve of the thigh in the inguinal region. Understanding these syndromes requires knowledge of nerve anatomy, the classification and pathophysiology of nerve injury and the causes of nerve injury. Electrophysiological examination is the main investigation used to support or clarify clinical diagnoses based upon precise history taking and careful examination. Treatment of individual patients may vary according to the duration and severity of symptoms and signs, age and general medical condition. When present, reversible causes must be addressed.

This chapter will focus on nerve compression syndromes in the diagnosis of hand and upper limb pain and will review normal peripheral nerve anatomy and physiology.

Peripheral nerve anatomy

Peripheral nerves emerge from the spinal intervertebral foramina and travel to their endpoint structures, sensory receptors and neuromuscular junctions. The axon is a peripheral process from the nerve cell body in the anterior horn of the spinal cord (motor neuron) or the dorsal root ganglion (sensory neuron). Excitable cells such as neurons and muscle fibres communicate with each other at special regions called synapses. The first cell communicates with the second by releasing chemicals called neurotransmitters. The synapse between a motor neuron and a skeletal muscle fibre is called the neuromuscular junction, and the neurotransmitter is acetylcholine (see Ch. 8 for further discussion).

Case 3.1 Carpal tunnel syndrome: 1

Case history

Mrs Fotini, aged 55, is a production line worker in a factory with a packaging company. She works an 8-hour day in four shifts divided by half-hour rest periods between shifts.

She presented complaining of pins and needles in both hands, which wake her at night and occur intermittently during the day. She also describes neck stiffness and discomfort with pain radiating from her left shoulder to her hand and swelling in both hands, more so in the early mornings.

She was diagnosed as having late-onset diabetes 2 years earlier, which has been reasonably controlled by diet and oral hypoglycaemic medication. She also takes non-steroidal anti-inflammatory medications for osteoarthritis affecting the small joints in her hands, neck and back.

Examination of her hands reveals no swelling of her joints and a normal range of movement. However, sustained wrist flexion for 1 min reproduced her symptoms of numbness affecting both hands.

The history and examination findings suggest a diagnosis of bilateral carpal tunnel syndrome and her GP recommended she wear a wrist splint at night to keep her wrist in the neutral position.

The axon is surrounded by Schwann cells and, together, axon and Schwann cells make up a nerve fibre. Myelinated fibres are those in which each axon is surrounded by single Schwann cells arranged longitudinally to form a continuous chain. Non-myelinated fibres contain multiple axons within the cytoplasm of a surrounding Schwann cell.

Peripheral nerve fibres are usually classified into three types in relation to their conduction velocity, which is generally proportionate to size (Table 3.1).

Table 3.1

Classification of nerve fibres

Nerve fibres are gathered into groups called fascicles and are surrounded by a mechanically strong membrane, the perineurium. Within the fascicles, nerve fibres lie within connective tissue called endoneurium. The fascicles themselves are embedded in an internal epineurium surrounded by an external loose epineurial connective tissue layer (Fig. 3.1). Nerves, such as the sciatic nerve, contain a greater percentage of connective tissue in relation to axonal substance. However, most people experience the sensation of leg and foot numbness following prolonged periods of sitting, especially on unyielding objects, when the protective benefit of the connective tissue cushion is overcome.

Fig. 3.1 Microanatomy of a peripheral nerve and its components. (A) Fascicles surrounded by perineurium are embedded in a loose connective tissue, the epineurium. The outer layers of the epineurium are condensed into a sheath. The expanded views show the appearance of (B) unmyelinated and (C) myelinated fibres.

The nerve trunk receives a segmental vascular supply. Extrinsic vessels run parallel to the nerve providing branches that lie within the epineurium, perineurium and endoneurium in a longitudinal pattern in each layer, with interconnecting branches between layers. Those vessels passing through the perineurium into the endoneurium often lie obliquely, creating a valve mechanism, which is vulnerable to pressure (Fig. 3.2).

Fig. 3.2 Vascular supply of a peripheral nerve. Vessels are abundant in all layers of the nerve; extrinsic vessels support, via regional feeding vessels, the epineurium, perineurium and endoneurium.

Nerves span joints with varying ranges of motion. On the outside of the nerve trunk, a conjunctival adventitia allows movement of the nerve trunk within its soft tissue surroundings. In deeper layers, fascicles can slide against each other. This allows movement of approximately 50 mm within the brachial plexus during abduction and adduction of the shoulder, 10 mm of the ulnar nerve at the elbow during flexion and extension, and 9 mm of the median nerve at the carpal tunnel with wrist flexion and extension.

Pathophysiology and classification of nerve injury

The endoneurial environment of the nerve is preserved by a combination of a blood–nerve barrier, in which the endoneurial vessels do not allow extravasation of proteins, and by the diffusion barrier of the perineurial sheath. The tissue pressure inside fascicles is slightly positive, providing a normal and healthy mechanical stiffness of fascicles.

When oedema is introduced into the endoneurial space of the nerve trunk, this may not escape easily owing to the diffusion barrier of the perineurial membrane. Consequently, axonal transport of substances from nerve cell bodies down axons (anterograde axonal transport) and from the periphery to the nerve cell body (retrograde axonal transport) is impaired.

A local metabolic conduction block may be induced by mild compression but is physiological only and without consequences for the structure of nerve fibres. Provided the compression is mild and limited in time, such a metabolic block is reversible. With extended compression, there may be oedema within the fascicles resulting in a local conduction block lasting longer than the duration of the precipitating cause. The myelin sheath is damaged but axonal continuity is preserved. This is termed neurapraxia and is usually spontaneously reversible within 3 months (termed a Sunderland type I lesion).

More severe compression or traction may disrupt the continuity of axons. Provided the endoneurium is intact, regenerating axons are maintained within the correct tubes and are guided to the appropriate sensory receptors and neuromuscular junctions. This lesion is classified as an axonotmesis or a Sunderland type II lesion.

Loss of continuity of axons and connective tissue components result in neurotmesis. This usually is a consequence of an acute stretching of the nerve, a severe crush or traumatic division. Sunderland has subdivided these more severe lesions into three types:

1. Loss of the endoneurial layer (type III)

2. Loss of the perineurial layer (type IV)

3. Complete transection of the nerve with loss of the epineurial layers (type V).

Surgical repair is the only method of returning some function in the last of these. The degree of internal disorganization in types III and IV may result in very poor nerve regeneration and minimal return of function without surgical repair.

Electrophysiology

Nerve conduction studies and electromyography often provide the only objective evidence of a neuropathic condition. It is necessary to understand the concepts and terminology of nerve physiology, pathology and methods of electrodiagnostic studies in order to evaluate the results of these studies.

Electrodiagnostic studies can help confirm the clinical compression of a compression neuropathy with a high degree of sensitivity and specificity, but there are some pitfalls.

Both nerve and muscle cells have a relative negative electrical charge inside them compared with the extracellular environment by virtue of a much higher concentration of potassium within the cells and a lower concentration of sodium and chloride. Electrical stimulation of the cells causes depolarization and generates an action potential. During depolarization, there is an opening of sodium channels in the cell membrane leading to an increase in sodium permeability and creation of an electric current by this rush of positively charged ions into the cell. Current then flows along the path of least electrical resistance, the length of the axon. Myelinated nerve fibres provide a mechanism for regenerating the charge of current (saltatory conduction). The myelin acts as an insulator to prevent current leakage. The myelin sheath indents at intervals, creating tight gaps that expose the axon, called nodes of Ranvier (Fig. 3.1). The action potential is propagated down the axon and exits at the node completing the electrical circuit through the extracellular fluid. This repeats the process of depolarization and perpetuates regeneration of the longitudinal current. However, there is a delay in the process at each node. Conduction velocity is faster with fewer nodal delays, the large-diameter nerves having the greatest internodal distances and therefore the fastest conduction speeds. These fibres include the alpha motor neurons and the sensory fibres transmitting light touch and proprioceptive (joint position) sensations. Pain and temperature and autonomic functions are conducted by slower, smaller myelinated or unmyelinated fibres.

When the action potential from the motor neuron arrives at the neuromuscular junction, it is transmitted chemically to the muscle. The electrical current is measurable and allows objective measurements of nerve function.

Nerve conduction studies

Motor nerve conduction studies

Motor nerve conduction studies assess the lower motor neurons from the level of the anterior horn to the muscle. The principle will be illustrated by reference to the median nerve (Fig. 3.3). A supramaximal electrical stimulus depolarizes all axons of the nerve and results in an action potential that travels in the normal physiological direction (orthodromically) down the nerve and is measured by recording electrodes overlying the thenar muscle belly. The distal motor latency is the time in milliseconds that it takes the impulse to travel from the stimulation point at the wrist to the recording electrode, say 3 milliseconds (ms). If the nerve is then stimulated at the elbow and the response follows after 7 ms, the motor conduction velocity is estimated by subtracting the distal motor latency from the proximal motor latency (i.e. 7−3=4 ms) and dividing the result by the distance between the two stimulating points (240 mm), i.e. a motor conduction velocity of 60 m/s. The shape of the wave is also important. A drop in amplitude indicates a conduction block, whereas an increase in duration indicates a lack of uniform conduction along the axons.