Biomedical subjects
Publications and source records attributed to L B Dahlin.
The basic pathophysiology of an acute and chronic nerve compression lesion is complex. Compression of a peripheral nerve induces marked changes in intraneural microcirculation and nerve fiber structure, impairment of axonal transport, and alterations in vascular permeability, with edema formation and deterioration of nerve function. The peripheral nerves of subjects with underlying neuropathies are more susceptible to compression injury.
To study the effects of drying on regeneration, crush lesions were made on the sciatic nerve of 38 rats and the injured area was then air-dried for various periods of time (0-60 min). The regeneration distance of sensory nerve fibres was measured by the pinch reflex test three or six days later. Regeneration was significantly impaired by drying the nerve for 30 or 60 min, but shorter periods (10 min) also seemed to affect axonal outgrowth. Regeneration distances were increased in nerves that were subjected to drying and then allowed to recover for a week (conditioning interval) before the nerve was crushed. The results show that drying of a peripheral nerve is detrimental to nerve regeneration, and we suggest that nerves should not be exposed to air for more than a few minutes during operation without irrigation.
Gore-Tex (expanded Polytetrafluoroethylene, E-PTFE) was used to replace the distal pulleys on the proximal phalanges of 20 rabbits. Morphology and function of the reconstructed pulleys were evaluated at 12-20 weeks. The breaking strength of the E-PTFE pulley equalled that of a normal pulley. Range of motion, tendon excursion, and force of flexion were no different from those of normal pulleys. No adhesions between flexor tendons and synovial tendon sheaths or the E-PTFE pulleys could be detected. No adverse tissue reactions were seen. Fibroblast-like cells from the surrounding tissues had grown into the membrane. In other experiments, where the pulleys had been either removed or detached, local fibrosis and adhesions were seen, and the deep flexor tendons had ruptured. The results of the present study indicate that E-PTFE can be used as a biosynthetic replacement for damaged pulleys.
The ulnar nerve of a 21-year old man was repaired at the wrist by a silicone chamber technique 10 days after a traumatic transection. A 3 mm gap was left between the nerve ends inside the chamber. At follow-up three years later, motor and sensory recovery was excellent. At exploration at that time a macroscopically normal nerve was found in the tube.
To investigate the importance of nutritive environment in the healing of reconstructed ligaments, the morphology of sutured free patellar ligaments in synovial fluid of the contralateral knee joint, without re-establishment of microcirculation, was studied in rabbits. After two weeks (n = 6) and one (n = 6) and three (n = 5) months, the sutured ligament was removed from the joint and fibroblasts were seen growing into the suture gap. The ligaments were enveloped in a capsule of fibroblasts, which was more developed in those ligaments that were studied three months after operation. The collagen of the piece of ligament was disorganised at all time points, and tensile strength (n = 6) was low compared with non-sutured patellar ligament. Some ligaments disappeared or were partly attached to the synovial membrane and revascularised. The findings indicate that diffusion of nutrients may be important for the survival and healing of reconstructed ligaments, as the ligaments can heal in synovial fluid without re-establishment of the microcirculation.
The microanatomy of the neuron and the peripheral nerve, which is a composite tissue, should be considered when discussing the pathophysiology of nerve compression injuries. Acute and chronic compression of peripheral nerve can induce changes in intraneural microcirculation and nerve fiber structure, increase vascular permeability with subsequent edema formation, and impair anterograde and retrograde axonal transport, which all contribute to the clinical symptoms and deterioration of nerve function. Morphologic and functional changes in the nerve cell bodies can be observed after compression which may be due to inhibition of axonal transport. The latter findings might be a theoretical explanation for double crush syndromes. Diabetes mellitus may confer on the peripheral nerve an increased susceptibility to compression injuries. Clinical stages of compression syndromes, such as carpal tunnel syndrome, may be related to specific pathophysiologic events occurring in the nerve.
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In all types of peripheral nerve injury, it is important to realize that the lesion affects one extended cell, the neurone, which extends from the central nervous system down to the target tissue in the extremity. Compression of a peripheral nerve can disturb the intraneural transport (axonal transport) of a large variety of substances. This may be followed by morphological and biochemical changes in the nerve cell body. These central changes may effect the axon as a whole and confer on the nerve an increased susceptibility to trauma. Studies concerning the reaction of neurones to compression, relevant when discussing the double crush syndrome, are reviewed.
The hind leg of adult rats was exposed to vibrations (82 Hz; amplitude peak-to-peak 0.21 mm) for 4 hours during 5 consecutive days. Light and electron microscopic examination of the plantar and sciatic nerves were done immediately after the exposure period or after a 2- or 4-week recovery period. Light microscopic examination did not reveal any distinct signs of injury. However, ultrastructurally unmyelinated fibers in the plantar nerves showed distinct changes, with deranged axoplasmic structure and/or accumulation of smooth endoplasmatic reticulum. These changes were to a large extent reversible in 2 weeks and appeared normalized after a 4-week recovery period. No ultrastructural changes could be observed in the sciatic nerve. However, when the sciatic nerve was crushed after 5 days of vibration exposure, axonal outgrowth was increased 23% as compared with controls. These findings confirm that vibration induces nerve fiber damage, in this experimental model expressed as a "conditioning effect" contributing to increased regeneration potential of the corresponding neurones.
Non-myelinated C-fibre responses during sympathetic trunk stimulation were studied in rabbit common peroneal nerve 2 weeks after the nerve had been subjected to compression at 400 mmHg for 30 min. Our previous studies have demonstrated that during sympathetic trunk stimulation the compound action potential of uninjured somatic C-fibres is characterized by a reduced amplitude and an increased latency. In the present study, nerve compression changed the C-fibre response to sympathetic stimulation. Three out of eight nerves reacted to nerve compression by increased C-fibre compound action potential amplitude in response to sympathetic stimulation. In three other rabbits with compressed nerves the C-fibre action potential amplitude was unchanged, and in the remaining two rabbits the action potential amplitude was decreased during sympathetic stimulation. The action potential latency increased in all tested compressed C-fibres. The phenomenon of increased C-fibre amplitude during sympathetic activation has not been observed in uninjured nerves. As in uninjured nerves, noradrenaline infusion produced an increased C-fibre action potential amplitude and latency in six animals. Sympathetic stimulation did not affect the A-fibre response. These results indicate that sympathetic activity influences the conduction properties in C-fibres of somatic origin and that the response can be changed after a nerve injury. The findings may be of importance for the understanding of pain aggravation in different types of nerve injuries during increased sympathetic activity.
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Compound action potentials of both myelinated (A) and non-myelinated (C) fibres in the common peroneal nerve of rabbits were studied during and after acute, graded compression of the nerve at 200 or 400 mmHg applied for 2 h or during ischaemia created by nitrogen inhalation or aortic occlusion. Compression of the nerve at 200 mmHg blocked the AI component (large myelinated fibres) after about 23 min, while compression at 400 mmHg shortened this time to 11 min. The A2 component (thinner myelinated fibres) had a lower conduction velocity and a higher resistance to compression. There was just a slight decrease in conduction velocity of the non-myelinated fibres when the nerves were compressed at 200 mmHg for 2 h. However, compression at 400 mmHg for 2 h induced a marked deterioration of amplitude and conduction velocity of the C-fibres. There was an incomplete restitution of function of A- and C-fibres during 2 h of recovery. The thinner myelinated fibres were more susceptible to deprivation of oxygen than the thicker ones, while non-myelinated fibres differed in response according to method of ischaemia induction. It is concluded that non-myelinated fibres are very resistant to compression and a very high pressure (greater than 400 mmHg) is needed to affect these fibres.
Preformed, autologous mesothelial chambers were utilized to study axonal growth following selective predegeneration of the distal nerve stump and/or preconditioning of the proximal nerve stump. The left and/or right sciatic nerve of rats was exposed and transected in the thigh. Two weeks after transection, the left proximal nerve stump was cross-anastomosed with the right distal nerve stump by using a mesothelial chamber leaving a 15-mm gap between the two nerve stumps. Previous studies have shown that axonal overgrowth normally does not occur over this gap distance to the distal stump. Three months after cross-anastomosing, regeneration across the 15-mm gap was evaluated by muscle action potential recordings and light microscopical examination. In experiments in which a distal nerve stump was selectively degenerated and the proximal segment was freshly cut, axons had bridged the 15-mm gap in six of seven rats. When a proximal preconditioned nerve stump was matched with a freshly cut distal stump, axonal overgrowth occurred in only 4 of 10 experiments. In experiments including a proximal preconditioned nerve stump and a distal predegenerated stump, axons bridged the gap in 6 of 8 experiments. We concluded that a priming lesion, including manipulation with proximal and/or distal stump, enhances axonal growth in mesothelial chambers.
Hind legs of adult rats were exposed to vibrations (81 Hz; amplitude 0.50 mm peak to peak) for 4 h during two consecutive days. The sciatic, tibial and plantar nerves were isolated and processed for immunohistochemical demonstration of IGF-I (insulin-like growth factor I; somatomedin C) immunoreactivity at different time intervals after the vibration exposure. In sham-exposed rats the axons in peripheral nerves showed no or faint IGF-I immunoreactivity while most Schwann cells were negative. Exposure of the hind legs to vibrations induced increased IGF-I immunoreactivity in the Schwann cells, demonstrable at the end of the exposure period and reaching maximal intensity 2-3 days after vibration exposure. Several distended axons similarly showed increased staining. The IGF-I immunoreactivity decreased after 7-10 days to almost the level in the control nerves. The most extensive changes were observed in the plantar nerves. The tibial nerves similarly expressed strongly increased IGF-I immunoreactivity in their Schwann cells. The sciatic nerve showed, however, only slightly to moderately increased staining. Cells in the epineurium of the plantar and, to a limited extent, of the tibial nerves expressed concomitantly increased IGF-I immunoreactivity. We conclude that the transiently increased IGF-I immunoreactivity in peripheral nerves reflects reactive changes caused by vibrations and most prominently expressed by the Schwann cells.
The hind limbs of anaesthetized rats were exposed to vibration trauma (81 Hz; amplitude peak to peak 0.50 mm) for 4 hours during 2 consecutive days. The animals were examined in groups of 4 immediately after the last exposure, and after 1, 2, 3, 5, 7, 10, 14 and 28 days. The Achilles tendons and the tendons of the anterior tibialis muscles were sampled and processed to demonstrate IGF-I immunoreactivity. In the normal Achilles tendon and in the tendon of the anterior tibial muscle, slight IGF-I immunoreactivity was seen in many of the long slender fibroblasts between the collagen bundles. A strong increase in the IGF-I immunoreactivity appeared in the anterior tibialis muscle tendon 3 days after the last vibration exposure. In addition, the tendon fibroblasts became hypertrophic. A similar but less striking increase in IGF-I immunoreactivity appeared in the Achilles tendon. The peak intensity and frequency of stained cells were achieved after 7 days for both tendons. The intensity then levelled off, and was normalized after 28 days. It is concluded that acute exposure to vibrations induces reactive changes in fibroblasts in tendons, which may reflect a change to a more active synthesising state, as a response to the vibration trauma. The transiently altered expression of IGF-I immunoreactivity forms a link in a chain of events regulating the functional activity level of fibroblasts in response to a trauma.
Gore-tex chambers were used to bridge a 6 mm gap between the proximal and distal nerve stumps of a rat sciatic nerve. The wall structure of these chambers is characterized by "nodes" interconnected by smaller fibrils. Chambers with internodal distances of 5, 10 and 30 microns were used. Some 30 microns chambers were coated from the outside with Gore-tex (0.2 micron internodal distance) and others were coated from the inside. Regeneration after 12 weeks, as evidenced by muscle action potential recordings and light microscopy, was successful regardless of what type of chamber had been used. The organization of the nerve structure varied among different chamber types. A well organized coaxial nerve structure with myelinated axons was observed if inner-coated chambers were used. In chambers that were not coated or in outer-coated chambers tissue completely filled the chambers, and myelinated axons were arranged in mini-fascicles surrounded by loose connective tissue.
The effect of treatment with an aldose reductase inhibitor on the susceptibility of peripheral nerves to compression was studied in rats made diabetic by the injection of streptozotocin (50 mg.kg-1). The response to nerve compression was determined in untreated diabetic rats after 22 days of diabetes and compared with the response in two similar groups of diabetic rats which had been treated with the aldose reductase inhibitor 'Statil' (ICI 128436; 25 mg.kg-1.day-1 orally) either from the induction of diabetes or for 7 days prior to nerve compression. Two groups of non-diabetic rats were treated with 'Statil' for either 22 days or 7 days to act as controls. Inhibition of fast axonally transported proteins was induced by local compression of the sciatic nerves 4 h after application of 3H-leucine to the motor neurone cell bodies in the spinal cord. The inhibition of fast axonal transport was quantified by calculation of a transport block ratio. Compression at 30 mmHg for 3 h induced a significantly greater (p less than 0.05) inhibition of axonal transport at the site of compression in nerves of untreated diabetic rats (transport block ratio 0.96 +/- 0.24, n = 8) than in nerves of control rats treated with the aldose reductase inhibitor for either the shorter time of 7 days (0.71 +/- 0.17, n = 10) or the longer time of 22 days (0.69 +/- 0.08, n = 5).(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of experimental nerve fiber compression on the morphology of nerve cell bodies were studied. Rabbit cervical vagus nerves were crushed or subjected to compression at 0 (sham compression), 30, 200, or 400 mm Hg for 2 h. Morphometric measurements and light microscopical evaluation of the nerve cell bodies in the nodose ganglion were carried out 7 days after the injury on the injured and control sides. Crush and compression at 30, 200, or 400 mm Hg induced a slight decrease in total cell profile area compared with the control side, but it was not related to degree of injury. There was a marked decrease in the ratio between nuclear and total cell profile area (nuclear volume density) after compression at 200 and 400 mm Hg, as well as after crush, and to a lesser extent after compression at 30 mm Hg. Compression at 30, 200, or 400 mm Hg as well as crush of the vagus nerve induced migration of the nucleus to the periphery and dispersion of Nissl substance in the cytoplasm of the nerve cell bodies. Sham compression induced no obvious changes in total cell profile area, nuclear volume density, or migration of nucleus. There was a somewhat increased percentage of cells showing dispersion of Nissl substance in sham-compressed animals than in controls. The results show that nerve fiber compression induced pronounced reactive changes in nerve cell bodies, even at low pressures, corresponding to those found in human carpal tunnel syndrome. Such pressures are known to induce reversible inhibition of fast axonal transport as well as inhibition of retrograde axonal transport. The nerve cell body changes in the nodose ganglion may thus be a reaction to disturbances in axonal transport.