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The Nerve Lesion in the Carpal Tunnel Syndrome J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.7.615 on 1 July 1976. Downloaded from Journal of Neurology, Neurosurgery, and Psychiatry, 1976, 39, 615-626 The nerve lesion in the carpal tunnel syndrome SYDNEY SUNDERLAND From the Department of Experimental Neurology, University of Melbourne, Parkville, Victoria, Australia SYNOPSIS The relative roles of pressure deformation and ischaemia in the production of compres- sion nerve lesions remain a controversial issue. This paper concerns the genesis of the structural changes which follow compression of the median nerve in the carpal tunnel. The initial lesion is an intrafunicular anoxia caused by obstruction to the venous return from the funiculi as the result of increased pressure in the tunnel. This leads to intrafunicular oedema and an increase in intrafunicular pressure which imperil and finally destroy nerve fibres by impairing their blood supply and by compression. The final outcome is the fibrous tissue replacement of the contents of the funiculi. Protected by copyright. In 1862 Waller described the motor, vasomotor, (Gasser, 1935; Allen, 1938; Bentley and Schlapp, and sensory changes which followed the com- 1943; Richards, 1951; Moldaver, 1954; Gelfan pression of nerves in his own arm. His account and Tarlov, 1956). carried no reference to the mechanism In the 1940s Weiss and his associates (Weiss, responsible for blocking conduction in the nerve 1943, 1944; Weiss and Davis, 1943; Weiss and fibres, presumably because he regarded it as Hiscoe, 1948), who were primarily concerned obvious that pressure was the offending agent. with the technical problem of uniting severed Interest in the effects of nerve compression nerves, observed that a divided nerve enclosed was not renewed until the 1920s when cuff or in a tightly fitting arterial sleeve became swollen tourniquet compression was used to produce a proximal and distal to the constriction. The reversible conduction block in the nerve. These proximal swelling was attributed to obstruction investigations were confined to a study of the to axoplasmic flow and the distal to degenerative physiological effects of compression and, though changes following division of the nerve. Weiss they were not concerned with the pathological (1943) observed changes in the vascularity of the http://jnnp.bmj.com/ changes in the nerve responsible for them, they nerve but regarded these as transient. Swellings inevitably led to speculation on possible mech- at the margins of a constriction were also anisms and raised the question of whether the observed by Causey (1948) who attributed them block was due to mechanical deformation or to to the displacement of axoplasm. ischaemia introduced by the compression. The first experimental investigation directed Many concluded that ischaemia was the to the histopathology of nerve compression responsible agent (Lewis et al., 1931; Clark et al., injury was undertaken by Denny-Brown and on September 28, 2021 by guest. 1935; Gasser, 1935; Grundfest, 1936; Thompson Brenner (1944a, b). They compressed nerves in and Kimball, 1936; Wortis et al., 1942; Weddell the cat by tourniquet and spring clip at pressures and Sinclair, 1947; Causey and Palmer, 1949; and for periods that were sufficient to produce Merrington and Nathan, 1949). Others reported a transient conduction block. Signs of damage characteristic differences between nerve block appeared early in the compressed segment due to pressure and that due to ischaemia which became oedematous and infiltrated with lymphocytes and macrophages. In the spring Address for correspondence and reprints: Professor Sir Sydney clip experiments the compressed segment was Sunderland, Department of Experimental Neurology. University of Melbourne, Parkville, Victoria, 3052, Australia. greatly narrowed with oedematous tissue on (Accepted 3 March 1976.) either side of the constriction. The affected 615 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.7.615 on 1 July 1976. Downloaded from 616 Sydney Sunderland nerve fibres showed swelling, notching, and et al., 1974) and against underlying bone by a vacuolation of the axons, and a change in their loop of nylon cord with a weight attached staining qualities. The myelin showed granula- (Rudge et al., 1974). From the histological tion, fissuration, and vacuolation, particularly changes observed in and about the compressed in the vicinity of the nodes and Schwann cells. segment, it was concluded that the conduction These changes finally resulted in parts of the block lesion was the result of direct pressure in axon becoming bared or being left with only a which 'ischaemia, due to compression of the thin coat of myelin. There was no, or very little, intra-neural blood vessels, plays little ifany part'. Schwann cell activity. The nerve fibres appeared Nerve fibre changes constituting a subclinical normal below the site of compression, though form of entrapment neuropathy have since beading of the axons and myelin was observed been reported at entrapment sites in human in some specimens. Conduction through the median and ulnar nerves (Neary and Eames, affected segment was blocked for periods of up 1975; Neary et al., 1975). Because of the par- to 19 days, and was then followed by rapid and ticular importance and special significance of the complete recovery. Return of conductivity recently published investigations and views of appeared to be associated with the remyelination those advocating mechanical deformation as of previously bared segments. However, histo- the cause of compression lesions, these are fully logical changes outlasted the return of conduct- discussed in the epilogue at the conclusion of ivity, and Denny-Brown and Brenner were this paper. uncertain whether they were ever fully corrected. The histological changes in nerves subjected Protected by copyright. They concluded that 'compression ofmammalian to chronic progressive constriction by tubing nerve without angulation must be effective have been investigated by Weisl and Osborne through the related ischaemia'. In arriving at (1964) and Aguayo et al. (1971). The latter this conclusion emphasis was placed on Grund- reported findings that are in agreement with fest's (1936) report that isolated frog nerve the observations of Ochoa and Marotte referred enclosed in oxygenated oil in a pressure chamber to earlier, with the additional note that the could tolerate pressures of 14,000 lb per sq. superficial fibres were the most severely affected, inch before becoming inexcitable. an observation later confirmed by Spinner and More recently, attention has been redirected Spencer (1974). Aguayo and his associates were to the structural changes associated with the uncertain about the genesis of the lesion, experimental conduction block caused by nerve believing that both ischaemia and mechanical compression. Fullerton (1963) studied the effects deformation could be responsible. The account of cuff compression in human subjects and by Weisl and Osborne includes the significant concluded that, while the disturbances offunction comment that 'the first effect of gentle nerve http://jnnp.bmj.com/ were due to ischaemia, the structural changes in compression is partial obstruction of the vasa nerve fibres were more likely the consequence of nervorum leading to hyperaemia and oedema'. direct pressure. Subsequently, Fullerton and They observed that the constricted nerve became Gilliatt (1967a, b) used the spontaneously occur- swollen proximally and distally and demon- ring entrapment lesions in the median, ulnar, strated that these moderately hyperaemic swel- and plantar nerves of the guinea-pig to study lings were due, not to obstruction to axonal the histological changes in the nerve fibres at the flow, but to the accumulation of tissue fluid on September 28, 2021 by guest. site of compression. Using the same model between the axons. The constricted section of Ochoa and Marotte (1973) and Marotte (1974) the nerve was oedematous and the axons extended these studies to reveal more histo- narrowed. This narrowing was attributed to logical detail but the essential features of the pressure transmitted by the fluid from the structural changes were confirmed. They con- constriction device. cluded that the findings pointed to a mechanical The behaviour of the intraneural vessels in rather than an ischaemic cause for the fibre nerves subjected to cuff compression has been damage. Nerves in the baboon have also been investigated by Lundborg (1970). He demon- acutely compressed by pneumatic tourniquet strated that the intrafunicular capillaries are (Fowler et al., 1972; Ochoa et al., 1972; Gilliatt more resistant to ischaemia than those in the J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.39.7.615 on 1 July 1976. Downloaded from Nerve compression 617 epineurium, epineurial oedema appearing before 3. The clumsiness of thenar movements in the any leakage occurred from the endoneurial morning which gradually improves during the day. vessels. These findings were in agreement with 4. Swelling of the hand and digits in the morning those reported by Olsson (1966). With continuing which is relieved by exercise. 5. The immediate relief from pain which follows ischaemia the intrafunicular capillaries com- decompression of the carpal tunnel. menced to leak with the development of an 6. The failure of long-standing motor and sensory intrafunicular oedema, which, it was stated, defects to improve after decompression. could be expected to not only raise
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