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Biomedical subjects

Susan E Mackinnon

Publications and source records attributed to Susan E Mackinnon.

80 records · Page 5Linked to original sources
PubMed2002

Axonal regeneration after cold preservation of nerve allografts and immunosuppression with tacrolimus in mice.

OBJECT: The purpose of this study was to combine the immunosuppressive and neuroregenerative effects of tacrolimus (FK506) with cold preservation of peripheral nerve allografts to maximize axonal regeneration across short peripheral nerve gaps. METHODS: Ninety-six male C3H mice were randomized to six groups, which were composed of animals with isografts (Group 1, positive control), allografts (Group 2, negative control), allografts treated with subtherapeutic doses of FK506 without and with cold preservation (Groups 3 and 4), and allografts treated with therapeutic doses of FK506 without and with cold preservation (Groups 5 and 6). Results were determined using walking-track data and histomorphometric measurements. Three weeks postoperatively, animals treated with therapeutic doses of FK506 after receiving cold-preserved allografts demonstrated accelerated functional recovery relative to all other groups. In addition, histomorphometric parameters in these animals (1,257 +/- 847 total axons, 6.7 +/- 3.3% nerve tissue, 11.8 +/- 6.5% neural debris, 8,844 +/- 4,325 fibers/mm2 nerve density, and 2.53 +/- 0.25 microm fiber width) were the same as or better than in all other groups. The parameters of percent nerve tissue (p < 0.016), nerve density (p < 0.038), and percent neural debris (p < 0.01) were statistically significantly better than those in all other groups, including Group 1 (isograft, positive control). CONCLUSIONS: The combination of FK506 treatment with cold preservation of nerve allografts resulted in functional and histomorphometric recovery superior to that with either modality alone.

Animals↗
PubMed1988

Myelinated afferents signal the hyperalgesia associated with nerve injury.

Pain to light touching of the skin is a hallmark sign of causalgia. The purpose of this study was to determine whether myelinated or unmyelinated afferent fibers signal this hyperalgesia. Sensory testing was performed in 17 patients with long-standing hyperalgesia after nerve injury. The patients underwent a differential ischemic block of nerve function of the involved area. At a time when touch sensation in adjacent normal skin was eliminated, but when sensibility to warming and cooling stimuli was unaffected, the hyperalgesia to mechanical stimuli was abolished in 15 of the subjects. In 2 of these 15 patients, a differential local anesthetic block of the injured nerve was performed proximal to the site of injury. When temperature sensibility was absent, but when touch sensation was intact, hyperalgesia was present. In a third study, latency measurements in response to 400 micron stepped displacement stimuli were made in two patients who had hyperalgesia on the foot. The mean latency for detection of pain in the hyperalgesic region was 414 +/- 18 msec, compared to 458 +/- 16 msec for the detection of touch to the same stimuli applied to the opposite normal foot. These 3 lines of evidence indicate that myelinated primary afferents, perhaps A beta fibers, signal the hyperalgesic pain in causalgia. These fibers may be sensitized A beta nociceptors or low-threshold mechanoreceptors.

Adult↗
PubMedDate not supplied

Functional recovery after facial and sciatic nerve crush injury in the rat.

OBJECTIVES: To systematically record rat facial nerve recovery following crush injury to the main trunk with respect to ocular and vibrissial function and to compare the rates of facial and sciatic nerve recovery from crush injury in the same animals. This serves as a means of validating the functional parameters of facial nerve recovery against the well-known measure of hind limb function, the Sciatic Function Index. METHODS: The main trunk of the facial nerve and the proximal segment of the sciatic nerve were exposed in all animals. Both nerves were subjected to standardized crush injury and subsequent daily functional testing. After a plateau of functional recovery was achieved, the animals were killed, and the distances between the sites of injury and the end musculature were measured, which allowed determination and comparison of recovery rates in both systems. RESULTS: All crush injuries resulted in loss of electrical conductivity, as proven by intraoperative proximal nerve stimulation. Recovery of ocular and vibrissial motor function occurred starting at postoperative day (POD) 9 and continuing through POD 20. Hind limb function returned later (POD 14-34); however, when corrected for distance, the sciatic recovery rate (2.26 mm/d) appeared to match that of the facial nerve (1.5-2.4 mm/d). CONCLUSIONS: Recovery after facial nerve crush injury follows a predictable time course, and the rate of recovery is consistent with that of sciatic nerve injury. Return of the blink reflex, loss of vibrissial fibrillations, and return of vibrissial sweeping function appear to be internally consistent functional measures of facial recovery. These quantitative measures will be useful for future facial nerve manipulation studies.

Animals↗
PubMedDate not supplied

Evaluation of nerve injury and nerve compression in the upper quadrant.

Evaluation of the patient with nerve compression and/or nerve injury should include a complete motor and sensory evaluation to establish the level and degree of injury and/or compression. No one test has been accepted as the standard procedure for the evaluation of sensibility. The various sensory tests available for patient assessment will yield different information regarding the integrity of the quickly and slowly adapting sensory receptors. Tests such as provocative maneuvers and sensory thresholds (cutaneous and vibration) will be more sensitive in the evaluation of patients with nerve compression, and other discriminatory measures will yield better functional information in patients with nerve injury.

Humans↗
PubMedDate not supplied

Surgical options for facial reanimation.

Facial palsy has devastating functional and psychosocial sequelae for patients, thus its treatment requires thorough understanding of state-of-the-art modalities that can optimize facial reanimation. Treatment depends on the mechanism and timing of injury, patient goals, overall health, and motivation. Because of its significant impact on patient's quality of life, both acute and long-standing deficits should be addressed. Often requiring multi-disciplinary efforts, an institution well-equipped in dealing with facial reanimation offers patients the most consistent results.

Algorithms↗