Management of nerve compression lesions.
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UNLABELLED: Compression neuropathy can occur simultaneously at dual points on a nerve, but the details of such lesions are still unknown. An experimental study was performed in order to investigate the vulnerability of the peripheral nerve in the "double crush" situation. Materials and Methods The sciatic nerves of 46 adult dogs were used. Compression was applied by special devices, and the compression force was 15 g (27.6 mmHg). The animals were divided into three groups. Group 1: One device was applied to the sciatic nerve 3 cm distal to the sciatic tuberculum. Group 2: Two devices were applied simultaneously with a 2 cm interval. Group 3: Two devices were applied at the same sites as in Group 2, but the second was applied three weeks after the first. These three groups were followed electrophysiologically up to eight or ten weeks postoperatively, at which time histological studies were undertaken. Results Electrophysiological studies: In Group I, complete conduction block was never induced. Mean motor nerve conduction velocity (M.N.C.V.) was 39% of the preoperative value at three weeks and increased slightly at six weeks. In Group 2, complete conduction block was induced in 50% at six weeks. Mean M.N.C.V. was 34% of the preoperative value at three weeks, and there was no significant change after this time. In Group 3, complete conduction block was induced in 50% at five weeks after the second operation. Mean M.N.C.V. was reduced to 14% of the preoperative value at three weeks after the second operation. HISTOLOGY: In Group 1, the number of large myelinated fibers was reduced at the site of compression and in the distal segment. Mean values for the diameter of the fibers distal to the compression site were shifted to the left when compared with the controls. In Groups 2 and 3, severer changes were noticed, especially in the segment distal to the site of the second compression. Conclusion Subclinical neuropathy was induced by a compression force of 15 g, and it was considered to be axonostenosis . The nerve had been compressed in the proximal region, became vulnerable to an additional compression trauma in the distal region. Even complete conduction block could be induced under such circumstances, and it was considered to be as axonocachexia . Impairment of axonal flow should be considered as a causes of the vulnerability.(ABSTRACT TRUNCATED AT 400 WORDS)
Neurolysis has been a widely accepted treatment for entrapment neuropathy and other nerve injuries in continuity. The purpose of this experimental study is to clarify the effects of neurolysis on the recovery from subacute compression neuropathy. The sciatic nerves of 49 mongrel dogs were used. In order to make the model of subacute compression neuropathy, the apparatus designed by Horiuchi to compress the nerve with constant force was applied to each nerve for three weeks. The pressure of compression was 55 mmHg when the thickness of the nerve was 2 mm. According to the degree of injury of the motor nerve in the peroneal funiculus of the sciatic nerve, 18 nerves were classified as first-degree injury ( Sunderland ) and 31 as second-degree injury. After removing the compressing apparatus, either external neurolysis (E.N.) or internal neurolysis (I.N.) was performed on these neuropathies under magnification. After the operation, each nerve was electrophysiologically followed up to 24 weeks; at one-week interval in the early stage and at four-week interval in the late stage. The macroscopic and histological observations were made on the fifth, eighth and 24th week. Electrophysiological findings: In the first-degree injuries, conduction block at the compressed site had already disappeared at the first week and motor nerve conduction velocity (M.N.C.V.) recovered rapidly with no apparent difference among the removal group (removal of apparatus only) and the neurolysis groups. In the second-degree injuries, evoked muscle action potential in the anterior tibial muscle appeared at the sixth week, about one week earlier in the I.N. group than in the removal group. M.N.C.V. of the removal group recovered gradually without exception, but that of the neurolysis groups inconstantly in the early stage. In the late stage, M.N.C.V. of all groups reached about 60 m/sec gradually and exponentially and never exceeded the average value (75.3 m/sec) of normal M.N.C.V. Macroscopic findings: The swelling of the portion adjacent to the compressed site ( pseudoneuroma ), which had been observed until the eighth week, disappeared at the 24th week. A scar around the nerve existed even at 24 weeks post-operatively, but it became loose and appeared like a mesoneurium and its vessels communicated with epineurial nerve vessels.(ABSTRACT TRUNCATED AT 400 WORDS)
Nerve conduction studies using nerve action potential (NAP), sensory nerve action potential (SNAP), evoked muscle action potential (M-response), retrograde conduction in the motor axon (F-response), and cortical and subcortical somatosensory evoked potential (SEP) are useful tools for evaluation of the peripheral nervous system. SEP recording has the advantages of being applicable to severely damaged nerves because of its amplification mechanism and of disclosing proximal root lesions that would not be disclosed by other methods. When SEP recording is used in an operating theater, the amplification mechanism is suppressed by the effect of the anesthetic. Nevertheless, it is valuable for evaluating proximal root lesions in conjunction with NAP recording and M-response. Strong M-response of the serratus anterior and paraspinal muscles is a most encouraging finding if nerve repair is performed more than seven days after brachial plexus injury. SEP recording can clarify the functional continuity of the spinal root to the spinal cord. Thus the presence of SEPs becomes an important positive finding and implies the potential of nerve repair even when an M-response is not provoked by a situation such as prolonged conduction block.
An inflatable silicone rubber balloon implanted in the orbit has been used to simulate an expanding orbital tumour. The changes produced in the compressed cat optic nerve have been investigated by light and electron microscopy. Within the first week extensive demyelination occurred; some fibres degenerated completely and there was marked proliferation of astrocytic processes. Some partially and completely demyelinated axons were seen throughout the period studied but after 5 weeks many axons had become remyelinated. Remyelinated fibres were seen in all longer-term animals despite the continued presence of the orbital mass. The significance of these observations is discussed in the light of the physiology of conduction in demyelinated and remyelinated central axons.
Unusual complications associated with local microcrystalline corticosteroid injections were observed in four patients with diverse rheumatic disorders. Adverse reactions included (1) bilateral digital flexor tendon rupture following carpal tunnel injection for idiopathic median nerve compression syndrome; (2) bowstring deformity of a finger after local corticosteroid treatment of psoriatic digital flexor tendonitis; (3) carpal tunnel infection following dorsal arthrocentesis of a wrist in a patient with rheumatoid arthritis; and (4) pronounced flushing of the face, neck, and chest after intrasynovial corticosteroid injection in a patient with psoriasis and arthritis. This article considers some physiologic actions of corticosteroids possibly responsible for development of these untoward effects.
The buccolabial branches of guniea pig facial nerves were crushed to produce axonotmesis, Wallerian degeneration, and demyelination. The lesions were followed from 1 to 8 weeks by transmission electron microscopy, electrophysiological tests, and cytochemical staining methods for Na+ channels. The first week demonstrated the classic degenerative neural changes. At 2 weeks the axoplasmic side of the demyelinated axolemma demonstrated diffuse staining for Na+ channels at a distance of 1 micrometer. At 4 weeks multiple condensed areas of dense staining were noted along the demyelinated axolemma. These staining areas resemble in character and length a normal node of Ranvier and denote new Na+ channels. The internodal distance is shorter than for the normal facial nerve. At 6 weeks a thin layer of myelin covered the nerve fibers. At 8 weeks half of the nerves were normal sized and the myelin sheath was normal in width. Following nerve crushing, electrical activity is present for 24-48 hours in the axonotmetic distal stump. Then the axon becomes unresponsive to electrical stimulation. There is gradual resumption of electrical activity between 5 and 14 days. Normal conduction resumes by 8 weeks. This study provides ultrastructural and cytochemical evidence for nerve fiber reorganization, axolemmal plasticity and sodium channel production and redistribution following Wallerian degeneration and demyelination in axonotmesis. Resumption of electrical neural excitability is achieved by an increase in the density of sodium channels and reduction in the internodal distance as a means for impedence matching. Reduction of the cross sectional diameter of the regenerating axon facilitates electrical conduction.
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A total of 93 cases of nerve lesions in the limbs in children is reported. After blunt trauma (n = 53), there was most often damage to the ulnar nerve (n = 28), especially in the area of the elbow joint, followed by the radial nerve (n = 14) and the median nerve (n = 11). Causes were primary pressure and scar compression following fractures of the elbow and forearm, where ventral re-siting and/or neurolysis were necessary in serious denervation processes. Among the cutting injuries (n = 40), the lesions in the area of the underside of the wrist severing the ulnar and median nerves, more rarely the radial nerve, are particularly mentioned. They have a good prognosis following microsurgery. Independent of their localisation, the following have a poor prognosis: all crushing injuries, multiple injuries, multilation lesions and non-visible stretching and tearing in the area of the plexus.
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Characteristic degeneration of the nerves in shoulder joints was recognized in 26 of 35 capsules (74.3%) from 20 cadavers. No left or right or gender differences were found. Histologic features of the nerves were (1) thickening of the perineurium, (2) myxoid degeneration in the endoneurium, and (3) hyaline globular structures with a whorled, oligocellular appearance regarded as Renaut bodies. The results of histochemical and electron microscopic studies showed prominent degenerated collagen fibers in the globular areas. These features resembled those found in the fusiform swelling in the axillary nerve branch to the teres minor muscle, believed to be caused by chronic nerve compression. Sixty percent of the degenerated nerves occurred in the anteroinferior and posteroinferior portions of the capsule, an area that is considered to be innervated by the axillary nerve. No correlation between age and severity of these degenerative nerve changes was noted. Compression of the axillary nerve and inferior joint capsule caused by repetitive shoulder movement such as forward flexion, abduction, and external rotation of the humerus might result in this form of nerve degeneration found histologically over a lifetime without necessarily causing clinical symptoms.
Symptoms due to nerve entrapment syndromes are a frequent reason for attendance at GP, rheumatology and orthopaedic clinics. This article outlines the presenting symptoms and signs of some of the more common syndromes and gives guidelines on the clinical diagnosis and subsequent management.
The operative treatment of six cases of paresis of the fibular nerve caused by external compression in five patients are reported. From the intraoperative findings and the postoperative results, decompression of the fibular nerve with simultaneous neurolysis can be recommended as the optimal method for cases, which have been treated conservatively without success.
The most common cause of wrist pain, due to neurological disorder is carpal tunnel syndrome. In aging patients with atrophy of the hand muscles it is to be differentiated from s.c. myelopathic hand, caused by denervation of anterior horn cells in conditions such as cervical spondylosis. The referred pain affiliated with palpable bands and trigger points in the muscles has to be also considered as origin of pain.
An isolated accessory nerve lesion was diagnosed in three patients. At clinical investigation of patients with this lesion, paresis of the trapezius muscle is found. This finding can be substantiated by electromyography. An accessory nerve lesion is usually caused by trauma (including surgical trauma) or space-occupying lesions such as tumour or abscess. There are also idiopathic forms. The prognosis is poor. Treatment may include electrostimulation, administration of NSAIDs, nerve transplantation and muscle transposition.