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The reaction of peripheral nerves to injury
Main nerve trunks contain many thousands of axons. When a trunk is stretched, but not ruptured, by dislocation of, say, the femoral or humeral heads, or by the nearby passage of a bullet, the axons within that nerve may respond in different ways. The degree of injury may vary along the length of a particular nerve or transversely across its cross-section: some axons will remain intact, some will sustain conduction block but recover rapidly, and yet others will degenerate throughout their entire extent distal to the injury because they have been ruptured. A proportion recover spontaneously whilst the remainder never recover.
introduced the terms neurapraxia for conduction block, axonotmesis for a degenerative lesion of favourable prognosis, and neurotmesis for a degenerative lesion of unfavourable prognosis. expanded this classification to five degrees of peripheral nerve injury by subdividing neurapraxia according to the degree of connective tissue disruption, and subsequently added a sixth category. However, the fundamental distinction between neurapraxia and either axonotmesis or neurotmesis remains the persistence of conduction in the distal segment of the nerve in neurapraxia, and the absence of conduction in axonotmesis or neurotmesis. In clinical practice, neurotmesis usually signifies transection of an entire nerve trunk, its constituent fascicles and their surrounding investments of perineurium and epineurium; the proximal and distal nerve stumps are frequently separated by an inter-stump gap of varying length ( Fig. 1.5.1 ). The early disappearance of conduction indicates impending or actual critical ischaemia and is probably the most important indicator that a lesion is deepening (see below).
Axonotmesis (centre) and neurotmesis (bottom) at the moment of injury. Note the preservation of the Schwann cell basal lamina in axonotmesis.
Courtesy of Rolfe Birch, all rights reserved, published in Birch R, Surgical Disorders of the Peripheral Nerve. 2nd edition, 2011. Springer-Verlag, London.
Neurapraxia/conduction block
Conduction block exhibits certain characteristic features: paralysis exceeds loss of sensation; proprioceptive nerves are more deeply affected than those responsible for light touch; sympathetic nerves to the smooth muscles of the blood vessels and sweat glands are least affected. There are distinct patterns of conduction block. Anoxia is important in all of them and there are often elements of mechanical deformation, inducing alterations of the nodal and paranodal apparatus in myelinated axons, and subsequent demyelination of whole internodes or of paranodes.
Transient ischaemia
Lying in one position without moving for a long time (e.g. during coma, inebriation or anaesthesia), prolonged sitting with the legs crossed or prolonged leaning on the elbows are all situations in which a limb nerve may be transiently compressed against a bone or a hard surface. The ischaemia thus induced in the compressed nerves causes an anoxic, physiological, block of both axoplasmic transport and ion channel functions along affected axons. This is seen during operation for the exposure of limb nerves with an inflated cuff in position: stimulation of a nerve evokes a brisk muscular response by transmission through the neuromuscular junction, which then diminishes before disappearing after about 30 minutes, whereas conduction within the nerve itself can be detected for about another 30 minutes. On the other hand, direct stimulation of the muscle provokes a twitch that can be elicited for about another 2 hours; loss of this direct response signals impending muscle death. The selective vulnerability of different populations of nerve fibres is demonstrated by the classical experiment of applying an inflated cuff about the arm ( ). The observer experiences first a loss of superficial sensibility, then a graduated loss of muscle power. The first pain response is lost soon after superficial sensibility fails; the delayed pain response is still detectable after 40 minutes of ischaemia. Large myelinated axons are first affected; unmyelinated axons and autonomic fibres escape, and pilomotor and vasomotor functions are scarcely affected. All modalities recover within a few minutes of release of the cuff; the unpleasant quality of the residual delayed pain sensation, and the burst of painful ‘pins and needles’ after release of the cuff, give an insight into the feelings of patients affected by dysaesthesiae.
Slowly progressing ischaemia
Conduction block caused by a haematoma or aneurysm, or by bleeding into compartments, produces early and deep autonomic paralysis and loss of power that extends over hours or days, whilst deep pressure sense and some joint position sense persist. These symptoms are seen in war wounds, when nerves become compressed and strangled by scar tissue or by the cicatrix deep to split skin grafts, and may progress over a period of weeks or months. The recovery of function and relief of pain are rapid – at times, dramatic – after removal of the cause in most of these cases.
Prolonged conduction block associated with focal demyelination
Severe prolonged pressure causes local demyelination and a conduction block that is not directly attributable to anoxia and that may last for weeks or months ( Fig. 1.5.2 ). Compression-induced focal paranodal myelin deformation may be involved; experimental studies using a cuff inflated to high pressure around a limb produced slippage of paranodal myelin at nodes of Ranvier lying under the edges of the cuff, i.e. where the pressure gradient between compressed and non-compressed portions of the nerve was likely to be greatest ( , ) . Clinically, local demyelination and conduction block will persist until the source of the external irritation, e.g. a bony projection, is removed ( ). Relief of pain and recovery follow rapidly in lesions that have persisted for many months, or even years. Mechanical deformation is the likely explanation for the conduction block seen in cases of ‘hourglass’ constriction of fascicles within a nerve trunk, where axons may be focally constricted within affected fascicles ( Fig. 1.5.3 ).
Prolonged conduction block of war wounds
The characteristic features of classical neurapraxia (see above), caused by the nearby passage of a missile, are likely to be provoked by a momentary displacement or stretching of the nerve trunks. However, a different pattern of conduction block may occur in recent conflicts, where the patient is exposed, at close range, to the shock wave of an explosion (e.g. blast injury), in addition to penetrating injury to the bony and soft tissues at the level of the nerve lesion. In these cases, the smallest fibres are most deeply affected and they may not recover. Pain may vary in both of these variants of conduction block ( ).
Non-freezing cold injury (trench foot)
Trench foot, or non-freezing cold injury (NFCI), is caused by exposure to cold of sufficient severity and duration but above the freezing point. It results in abnormalities of the small sensory nerve fibres and associated vascular abnormalities which may persist for years. Based on observations of trench foot in World Wars I and II, the condition was described as a vaso-neuropathy ( ). It is associated with marked degeneration of cutaneous intraepidermal nerve fibres with regeneration of disproportionate and abnormal nerve fibres along subepidermal blood vessels, causing a ‘painful vaso-neuropathy’ ( ).
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