Biomedical subjects
Publications and source records attributed to S E Mackinnon.
The terminal branch of the anterior interosseous nerve is described anatomically and demonstrated histologically. Injury to this nerve can be the source of persistent, dull aching volar wrist pain. Suitability for partial volar wrist denervation is determined by functional testing before and after a diagnostic nerve block. Experience with twelve patients with this problem is presented.
One hundred forty-five consecutive three-phase radionuclide bone scans were reviewed. One hundred two of these were performed to evaluate pain in the hand. Of these, 23 patients clinically had reflex sympathetic dystrophy (RSD). The hand scans were performed by the three-phase technique. Phase I is a radionuclide angiogram. Phase II is the blood pool or tissue phase. Phase III consists of delayed images obtained 3 to 4 hours after radionuclide injection. Detailed analysis of the 145 three-phase radionuclide bone scans of the hand demonstrated that the diffuse increased tracer uptake in the delayed image (phase III) is diagnostic for RSD, with a sensitivity of 96% and a specificity of 98%. The two early phases (radionuclide angiogram and blood pool) were positive in only 45% and 52% of the RSD patients, respectively. The strictly interpreted delayed radionuclide image is extremely sensitive in the diagnosis of RSD and will facilitate the early diagnosis and subsequent treatment of this syndrome.
Traumatic injuries to the distal forearm present a challenging problem for soft tissue coverage. There is a need for a local flap to provide a vascularized soft tissue bed. This article demonstrates the anatomic basis that enables the pronator quadratus muscle potentially to fulfill these needs.
Clinical and experimental observations are reported which suggest that a classic neuroma does not form when a transected nerve is implanted into muscle.
This study reports a rat model of chronic nerve compression. The sciatic nerves of adult male Sprague Dawley rats were bonded with 1-cm lengths of tubing with varying internal diameters. Histological and electrical studies as well as studies to assess the blood-nerve barrier function were carried out at one through six months. With marked compression of the sciatic nerve, profound electrical changes were noted as early as one month, and histological findings were those of degeneration and regeneration. In the rats with minimal compression, nerve conduction studies remained normal. The earliest findings were alterations in the blood-nerve barrier, followed by histological changes in the large myelinated fibers at the periphery of the fascicles and changes about the nodes of Ranvier. This model appears to be a valid one with which to study other aspects of both the pathophysiology and treatment of chronic nerve compression.
In an attempt to establish specific scintigraphic criteria for the reflex sympathetic dystrophy syndrome (RSD) as defined by a group of specialized hand surgeons, 145 consecutive patients, 23 of whom had clinical RSD, underwent three phase radionuclide bone scanning (TPBS). Specific patterns for positive radionuclide angiogram, blood pool, and delayed images were established. The delayed images were sensitive (96%), specific (97%), and had a valuable negative predictive value (99%). We concluded that TPBS could provide an objective marker for RSD, and it could also be used to exclude RSD in patients who had less specific signs and symptoms.
An in vivo immunological assay was used to determine quantitatively the nerve allograft response in a rat model. The nerve allograft was then pretreated with a number of pretreatment methods that have been used clinically and experimentally. Using the same immunological assay to determine quantitatively the nerve allograft response, we found that lyophilization and high doses of irradiation could modify the nerve allograft in such a way as to make it less immunogenetic to the host animal. The other methods of pretreatment did not alter the antigenicity of the allograft.
Regeneration across lyophilized and irradiated peripheral nerve allografts was assessed using electrical and histological parameters. Regeneration did occur across these pretreated nerve allografts and was intermediate between that regeneration which occurred across a fresh, untreated nerve allograft and that which occurred across the control autograft.
Chymopapain injected into the intervertebral disc space (chemonucleolysis) has been used clinically in patients with disc disease with success. Neurosurgical complications secondary to the procedure have, however, been reported. In this study, the authors have investigated the possible neurotoxic effect of chymopapain on the peripheral nerve in rat and primate models. While the extrafascicular injection caused no nerve fiber damage, the intrafascicular injection caused dose-related nerve fiber damage in both species.
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A splint was designed that effectively protected a nonhuman primate extremity following an injury or experimental procedure. The splint was fabricated from a thermoplastic material. Fabrication was simple, rapid, inexpensive, and versatile.
The possible neurotoxic effects of five commonly used steroid agents were examined. Using histologic studies and studies of the microneural circulation, it was found the steroids can indeed cause neurotoxicity. The injection site was critical in effecting injury. Only intrafascicular injection caused damage. The damage produced varied with the agent used. Dexamethasone (Decadron) caused minimal damage, while hydrocortisone (Solu-Cortef) and triamcinolone hexacetonide (Aristospan) caused widespread axonal and myelin degeneration. Disturbance in the blood-nerve barrier correlated with the changes noted on light and electron microscopy, but is thought to be coincidentally and not causally related. In conclusion, it was shown that the intrafascicular injection of commonly used steroid agents had a direct toxic effect on peripheral nerve-fibers and caused a disruption of the blood-nerve barrier. Use of the more toxic agents in the vicinity of peripheral nerves should probably be avoided.
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Nerve compression or musculoskeletal diagnoses require consideration of both the repetitive movements and static postures that may be contributing to the problem. Certain postures and positions assumed at home, at work, and during sleep will have three major influences: (1) directly increasing pressure on nerves at entrapment sites; (2) placing muscles in shortened positions so that adaptive muscle shortening may then secondarily compress nerves; and (3) placing some muscles in elongated and weakened positions, resulting in other muscles being over-used, thus creating the cycle of muscle imbalance. Successful management of the patient with upper extremity pain, paresthesia, and numbness should begin with initial identification of all sites that are contributing to the presenting symptoms. Treatment must then be directed toward the sources of nerve compression and musculoskeletal dysfunction. Upper quadrant symptomatology can be alleviated with an appropriate therapy program, even in the patient with chronic symptoms, but only with patient education, compliance with an exercise program, and behavioral modification at home, work, and during sleep.
BACKGROUND AND OBJECTIVES: Regional nerve blocks are often used for the treatment of postoperative pain in children. Ammonium sulfate is a non-narcotic anesthetic agent, which has been reported to provide pain relief lasting days to weeks, with few reported side effects in adult studies. Prior to considering clinical use in children, the neurotoxicity of ammonium sulfate in 4-day and 3-week old rats was assessed and compared with that of bupivacaine. METHODS: Each rat received a posterior tibial nerve intrafascicular injection (0.01 mL in 4-day-old and 0.02 mL in 3-week-old rats) using either 10% ammonium sulfate (n = 24 per age group), 0.5% bupivacaine (n = 18 per age group), 0.9% saline (n = 18 per age group), or 5% phenol (n = 18 per age group). A functional assessment by serial walking track analysis and a morphologic assessment by neurohistology were made. RESULTS: No abnormalities in serial walking track analysis and no structural nerve damage were detected after ammonium sulfate, bupivacaine, or saline injection. Bupivacaine caused mild focal changes in both age groups, which recovered by 8 weeks. CONCLUSIONS: Intrafascicular injection of ammonium sulfate was as safe as bupivacaine in this animal model. Further animal studies must be made before human trials are initiated.
While compression neuropathy is a common clinical problem, the opportunity to study human nerve material is rare. A histological assessment of the superficial radial nerve of four human cases with entrapment syndrome is reported. Changes in the perineurium and the endoneurial microvessels as well as the presence of Renaut bodies were the earliest histological abnormalities noted. Connective tissue changes included epineurial and perineurial fibrosis. Nerve fibre pathology varied from fascicle to fascicle. The myelinated and unmyelinated fibre populations responded differently to this compression. In the myelinated fibre population, marked thinning of the myelin was noted. In the unmyelinated fibre population, a shift in the fibre histogram due to a new population of very small fibres was observed suggesting degeneration with subsequent regeneration of this fibre population.
The restoration of effective and meaningful axonal function following peripheral nerve injury continues to be a considerable clinical challenge. The use of conduits to bridge the gap between severed ends is a contemporary experimental maneuver that isolates the microenvironment of regenerating axons. Entubulation has allowed analysis and manipulation of putative influences upon nerve regeneration. A review is provided of the research efforts that have explored the neurobiological and mechanical factors that guide nerve regeneration within conduits. Levels of specificity, from tissue specific growth to end-organ specific growth, are outlined within the framework of the theories of Neurotropism, Contact Guidance and Neurotrophism. Included are investigations utilizing different conduit materials and the few clinical applications of these conduits. A number of chamber manipulations, extra-cellular matrix substrates and growth factors and their molecular receptors have been implicated in enhanced regeneration specificity. This information has been extended to the conduit model. The interposition of healthy nerve segments into conduits is proposed as a means of extending the length of successful nerve regeneration.
Reports of nerve compression syndromes have been increasing in frequency. The authors discuss evaluation, management, and surgical repair of these multifactorial disorders.