• peripheral neuropathy
• diagnosis
• polyneuropathy

The diagnosis of a peripheral neuropathy is one of topographic localisation within the nervous system; not of aetiology. It is not a diagnosis in isolation as peripheral nerves are damaged consequent to some other condition, such as systemic exposure to exogenous agents in the environment and workplace. In subjects at risk, it is important to determine if and when peripheral nerves become affected, hopefully before clinical dysfunction and permanent damage occur. Many studies have employed clinical, electrophysiological, quantitative psychophysical sensory, and pathological procedures in the investigation of peripheral nerve disease. Their success has been less than optimal, mostly because of complexities in the peripheral nervous system and inherent procedural limitations.

Peripheral neuropathies can be divided into:

• Those which are bilaterally symmetrical—polyneuropathies (for example, most neurotoxins, diabetes mellitus)

• Those which are focal—mononeuropathies (nerve entrapment)

• Multiple mononeuropathies (vasculitidies, leprosy, multifocal motor).

Other subdivisions are based on the predominant site of dysfunction:

• Axons—axonopathies (diabetes, organophosphates)

• Nerve cell bodies—neuronopathies (poliomyelitis, pyridoxine)

• Schwann cells and/or their myelin sheaths—demyelinating neuropathies (Guillain-Barré syndrome, acute arsenic poisoning).

There are also different types of peripheral nerve fibres: motor, sensory, and autonomic. Sensory fibres are divided into at least three groups anatomically, physiologically, and functionally:

• Aα (or Aαβ)—large diameter, myelinated, fast conducting; mediating vibration, position, and touch sensations

• Aδ—small diameter, myelinated, slow conducting; mediating cold sensation

• C fibres—very small diameter, unmyelinated, very slow conducting; mediating hot and pain sensations.

Not all fibre types are affected in all peripheral …