The distinction between the anatomy of the peripheral and central nervous systems is made, as is that between grey matter and white matter. An understanding of how the peripheral nervous system connects to the central nervous system is important and briefly described. The chapter concludes with a section on the soma, axon hillock and initial segment, which should aid appreciation of anterior horn cell activation and firing frequency.

The theoretical and practical problems of constructing normal databases within and between clinics are discussed. Pooling of data is probably a more attractive proposition in theory than in practice. The importance of standardisation of techniques is stressed, whilst caution in the over-interpretation of borderline results is counselled.

Nerve conduction velocity in degenerative disease depends on which nerve fibres are affected. If the largest diameter ones are spared, velocity will be normal. Otherwise, there will be a decrease of up to 30 per cent. The localising value of nerve conduction studies in degenerative disease is limited though hardly required after focal trauma. Electromyography will usually also be needed. An abnormal finding will always be found if either the stimulating or recording electrode lies over a region of degeneration. Preganglionic pathology occurring in radiculopathies is associated with normal sensory conduction. The degree to which sensory nerve action potentials (SNAPs) are reduced in amplitude is a useful guide to the severity of the pathology within postganglionic fibres. These concepts are illustrated with simple but helpful diagrams.

The end-plate zone of muscle contains neuromuscular junctions. This simplified account of their structure and function is designed to aid an understanding of repetitive nerve stimulation testing and single-fibre electromyography, detailed later in the book. The anatomy of the synaptic bulb containing acetylcholine-filled vesicles is described. These are discharged into the synaptic cleft by the process of exocytosis. Small quantities which occur spontaneously produce end-plate potentials but larger quantities following depolarisation of the synaptic bulb will generate a muscle action potential.

There are three types of muscle fibre: 1, 2a and 2b. Their function is determined by their size and metabolism. Type 1 fibres oxidise glucose to produce adenosine triphosphate (ATP). They are of small diameter, contract slowly, produce modest force and are resistant to fatigue. Type 2b fibres are large in diameter, produce ATP anaerobically, have fast twitch tensions, generate large force but fatigue rapidly. Type 2a fibres are intermediate. A table showing the details of the classification of muscle fibre types is provided. The chapter concludes with a brief description of cross-bridge cycling.

Slowed conduction in a demyelinated nerve is proportional to the degree of pathology. More severe pathology leads to conduction block and ultimately to degeneration of the nerve. Degeneration causes the amplitudes of the action potentials, sensory nerve action potentials (SNAPs) or compound muscle action potentials (CMAPs), to be reduced. Unfortunately, the positively skewed distribution of these severely limits their clinical usefulness in assessing the degree of pathology. The demonstration of unstable nascent potentials can be a useful sign that motor nerve regeneration is occurring but, in general, the contribution of electrophysiological techniques to the monitoring of peripheral nerve degeneration is disappointing.

Peripheral nerve classification has undergone historical changes. A table is provided giving the current synthesis of nomenclature. The functions of the different categories of sensory and motor nerves are described, including sensory and motor activity of muscle spindles, alpha-gamma coactivation and a description of the monosynaptic reflex. The importance of understanding that the conduction velocity in peripheral nerves is proportional to their diameter is stressed.

Most peripheral nerve contain both sensory and motor fibres and are called mixed nerves. It is often desirable to test these two components separately. The simple principles involved are presented. Sensory testing yields sensory nerve action potentials (SNAPs). Likewise, with motor testing we get compound muscle action potentials (CMAPs). The concept of supramaximal stimulation is discussed and important factors affecting nerve conduction are stated.

Muscle disease tends to be patchy, hence the term ‘sampling’, which is often applied to the technique of electromyographic investigation. The susceptibility of muscle pathology to electromyographic diagnosis relies on type 1 fibres being affected because motor units containing these fibres are the first to be recruited. Myelinated nerve fibres may undergo demyelination or degeneration depending upon whether the myelin or the axon is primarily affected. Severely demyelinated nerves are unstable and degenerate. Disease of nerve cell bodies cause centripetal degeneration in the longest axons, the so-called dying-back neuropathy. Severe trauma to a nerve causes distal degeneration, also known as Wallerian degeneration.

The mechanisms underlying F-wave and H-reflex studies are described in detail and accompanied by simple diagrams and clinical examples. The H-reflex is analogous to the familiar tendon reflex. These tests, whilst sometimes useful, tend to provide more aesthetic than diagnostic satisfaction.

Diagnostic methods share the same common objectives: what is the location of the disorder? What is the pathology? What is the severity and prognosis? Can the abnormality be monitored? The way in which these questions are related to muscle, the neuromuscular junction and the peripheral nervous system are described. The techniques used in these diagnoses are electromyography and nerve conduction studies. The structures and the application of the techniques to them are shown diagrammatically.

Electromyography is used to differentiate primary muscle disease (myopathy) from abnormalities within the muscle resulting from pathology of its nerve supply (neuropathy). The diagnosis rests on the assessment of motor unit size and an estimate of motor unit numbers during voluntary activity, the recruitment pattern. That motor unit size is reflected in motor unit potential duration is explained and illustrated. Excessive polyphasic motor unit potentials are abnormal but do not, by themselves, distinguish between neuropathy and myopathy. The limitations of assessing motor unit numbers are acknowledged. Potentials may also be recorded from resting muscles. These may be normal as in end-plate potentials or end-plate noise, or abnormal as in fibrillation potentials, positive sharp waves, fasciculation potentials, myotonia, myokymia or complex repetitive discharges. Elegant examples of all of these are included.