Minimally invasive lateral lumbar interbody fusion with direct psoas visualization.

BACKGROUND: Minimally invasive lateral approaches to the lumbar spine have been adopted to allow access to the intervertebral disc space while avoiding the complications associated with anterior or posterior approaches. This report describes a minimally invasive technique for lateral lumbar interbody fusion LLIF that allows direct intraoperative visualization of the psoas and surrounding neurovasculature (DV-LIF). METHODS: The technique utilizes a radiolucent tubular retractor and a secondary psoas retractor that allows a muscle-sparing approach while offering excellent visualization of the operative site. The unique advantage of this procedure is that the psoas muscle and surrounding nerves can be directly visualized intraoperatively to supplement neuromonitoring. We retrospectively reviewed complication rates in 34 patients treated with DV-LLIF (n = 19) or standard lateral lumbar interbody fusion (S-LLIF, n = 15). RESULTS: There were 29 complications (median: 1 per patient) with DV-LLIF and 20 (median: 1 per patient) complications with S-LLIF. Postoperative sensory deficits were reported in eight (42%) and seven (47%) patients, respectively. Thigh pain or numbness was reported in eight (42%) and five (33%) patients, respectively. The percentage of the overall complications directly attributable to the procedure was 69% with DV-LLIF and 83% with S-LLIF. One severe complication (back pain) was reported in one DV-LLIF patient and four severe complications (severe bleeding, respiratory failure, deep venous thrombosis and gastrointestinal prophylaxis, and nicked renal vein and aborted procedure) were reported in two S-LLIF patients. CONCLUSIONS: Preliminary evidence suggests that minimally invasive lateral interbody fusion with direct psoas visualization may reduce the risk for severe procedural complications.

Development of fatty atrophy after neurologic and rotator cuff injuries in an animal model of rotator cuff pathology.

BACKGROUND: Detachment of a tendon from its osseous insertion, as can be the case with severe rotator cuff injuries, leads to atrophy of and increased fat in the corresponding muscle. We sought to validate a rotator cuff injury model in the rabbit and to test the hypothesis that tenotomy of a rotator cuff tendon would consistently create muscle atrophy and fatty degeneration analogous to the changes that occur after injury to a nerve innervating the same muscle. METHODS: New Zealand white rabbits were divided into three groups: (1) partial rotator cuff tear without retraction of the muscle, (2) complete rotator cuff tear with retraction of the muscle, and (3) nerve transection of the subscapular nerve. Animals were killed at two or six weeks after injury, and the muscles were analyzed for weight, cross-sectional area, myosin fiber-type composition, and fat content. In addition, the subscapular nerve was harvested at two weeks and evaluated for neuronal injury. RESULTS: At six weeks after injury, the rabbit muscles in the complete tenotomy and nerve transection groups had significant decreases in wet mass and increases in fat content relative to the control groups. Fat accumulation had a similar spatial pattern at six weeks in both the nerve transection and complete tenotomy groups. Such changes were not seen in the partial tenotomy group. No change was found in muscle myosin fiber-type composition. At two weeks after injury, subscapular nerves in the complete tenotomy group showed gross evidence of neuronal injury. CONCLUSIONS: This study establishes the rabbit subscapularis muscle as a valid model to study the muscular changes associated with rotator cuff tears. Our data suggest that the muscular changes associated with complete tenotomy are comparable with those seen with denervation of the muscle and suggest that chronic rotator cuff tears may induce a neurologic injury.

Local down-regulation of myelin-associated glycoprotein permits axonal sprouting with chronic nerve compression injury.

Chronic nerve compression (CNC) injuries induce a robust Schwann cell proliferation in a distinct spatial and temporal pattern, which is accompanied by an increase in the number of small un-myelinated axons in the area of the injury. These findings suggest that this local proliferation of Schwann cells may induce local axonal sprouting. Here, we use quantitative electron microscopic techniques to define the nature of this sprouting response, and explore whether the local sprouting is in response to down-regulation of expression of myelin-associated glycoprotein (MAG) by proliferating Schwann cells. Axonal sprouting was observed without evidence of Wallerian degeneration in the outer region of CNC-injured nerves with a noticeable increase in Remak bundles within this region of injury. Immunolabeling of teased nerve fibers and Western blot analysis of nerves from CNC-injured animals revealed a local down-regulation of MAG protein within the zone of injury. Moreover, local delivery of purified MAG protein intraneurally at the time of CNC model creation abrogates the axonal sprouting response. These data demonstrate that CNC injury triggers axonal sprouting and suggests that a local down-regulation of MAG within the peripheral nerve secondary to CNC injury is the critical signal for the sprouting response.

Chronic nerve compression induces local demyelination and remyelination in a rat model of carpal tunnel syndrome.

In a previous study, we demonstrated that chronic compression of rat sciatic nerve, a model of compressive neuropathies, triggered dramatic Schwann cell proliferation and concurrent apoptosis. Importantly, this Schwann cell response occurred before there are signs of overt axonal pathology, raising the question of whether there are alterations in axonal myelination in the areas of the nerve in which Schwann cell apoptosis and proliferation occur. Here, we use nerve teasing techniques and unbiased stereology to assess myelination in nerves after 1 and 8 months of compression. Evaluations of myelin thickness and axonal diameter (AD) using design-based, unbiased stereology revealed alterations in myelin structure that indicate remyelination, specifically a dramatic decrease in the average internodal length (IL) and an increase in the proportion of axons with thin myelin sheaths. The mean IL was reduced after 1 month of chronic nerve injury with no further decrease in IL at 8 months. There was limited change in average axonal diameter at both 1 and 8 months. Measures of myelin thickness revealed not only a greater than 6-fold increase in the number of axons with very thin (<5 microm thickness) myelin sheaths, but also a proportional decrease in the number of axons with the thick myelin sheaths characteristic of normal nerve. These results confirm that an early consequence of chronic nerve compression (CNC) is local demyelination and remyelination, which may be the primary cause of alterations in nerve function during the early period post-compression.

Effect of electroacupuncture on pressor reflex during gastric distension.

The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and alpha-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 +/- 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1-2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5-6) over the median nerve for 30 min significantly decreased the pressor response from 33 +/- 6 to 18 +/- 4 mmHg (n = 7, P < 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36-37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped (n = 6, P < 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37-39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously (n = 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA (n = 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.