Introduction. Shoulder pain is one of the most common etiologies of chronic pain representing roughly 16% of all presenting patients (1). The branches of the subscapular nerve have been suggested as contributing to the sensory innervation of the shoulder and may have clinical value as a therapeutic target for nerve block, ablation, and stimulation. Methods. Six formalin embalmed willed body donors were used, reflecting twelve shoulders for study. Careful dissection was performed to identify the upper and lower subscapular nerves and respective branches as they approached the shoulder joint. After placing the cadaver in anatomical position, measurements were taken from two landmarks: 1) just proximal to the immediate branch from the upper subscapular nerve (USN); and 2) the medial aspect of the coracoid process (CP). The distance from the medial aspect of the CP directly to USN just proximal to its first branch was taken using a digital caliper in millimeters (table I). Results. The USN sends articular branches that directly innervate the anterior glenohumeral joint (GHJ). The average distance from the medial aspect of the CP to the USN just prior to its branches was 3.76 cm +/- 0.62 cm. The average distance from the medial aspect of the CP to an intersecting perpendicular line drawn directly superior from the USN just proximal to its first branch was 0.94 cm +/- 0.03 cm. Conclusions. Our findings of the USN and LSN add to prior quantitative neuroanatomical relationships of these nerves and potential targets for therapeutic intervention.

P001 - Sepsis impairs the capillary response within hypoxic capillaries and decreases erythrocyte oxygen-dependent ATP efflux

Spinal cord stimulators (SCSs) produce electrical signals to suppress perception of chronic neuropathic pain, but they can have complications. We present a case of thoracic wall dysesthesia associated with spinal cord stimulator use due to leakage current from electrode degeneration. Case: A 51 y/o female presented with new left sided chest pain with usage of her SCS. Patient had history of multiple back surgeries and failed back surgery syndrome. Ten year previously, she had a SCS implanted with 2 Medtronic Pisce percutaneous-style 4 contact electrodes at the T8-T9 spinal levels for low back and left leg pain. She had excellent pain relief until 14 months after initial implantation, when the SCS was revised due to increasing voltage demands. Electrodes were replaced with a Specify 4x2 paddle electrode at T8-T9. After 7 years she abruptly started to experience left sided chest wall pain consistently during SCS activation despite multiple attempts at reprogramming. Imaging displayed perfect midline and dorsal electrode alignment with no migration from previous studies. There were, however, signs of discontinuity in some contacts. After multidisciplinary discussions between pain medicine, neurosurgery, neuroradiology, we hypothesized that leakage current could be causing the thoracic dysesthesias, and the patient was offered another revision with a new paddle electrode. During surgery the left electrode appeared to have a defect in the insulation. A Specify 8x2 paddle electrode was then placed. Excellent relief of the patient’s neuropathic pain was achieved, with complete resolution of the thoracic dysesthesias during stimulation. New SCS related dysesthesia in a previously well-functioning system is not commonly reported in the absence of lead migration. This case demonstrates the possibility of aberrant electrical current paths that can develop over time, particularly as electrodes age and fray. Electrode revision should be considered, particularly if impedance values in the existing electrode are abnormal.

Diabetic peripheral neuropathy is a common complication of diabetes due to suboptimal glycemic control that is marked by pain, paresthesia and sensory loss. Paradoxically, there have been reports of acute painful neuropathy caused by rapid glycemic control following the initiation of insulin therapy. The term, insulin neuritis, has been used to describe this unexpected phenomenon that appears to be related to the initiation of insulin therapy. A 29 year-old male presented to our academic pain center with bilateral feet pain with burning, numbness and tingling in the sole, lateral, medial and dorsum of bilateral feet with some allodynia that started 6 weeks after new diagnoses of insulin dependent DM and rapid glucose control. His HbA1c reduced from 18 to 11 rapidly during his treatment. EMG revealed severe sensorimotor peripheral polyneuropathy. His condition caused a severe decrease in ADL's but his main complaint was unable to sleep at nights. The patient was treated with gabapentin, lyrica, various opioids, NSAIDS , elavil without any relief. He then underwent bilateral LSB with 10cc of 1:1 mixture of 0.5% bupivacaine and 2% lidocaine. He had 50% pain relief for 10 days during which he reported improved ADL's and significant sleep improvement. He just underwent second LSB which was 10 days after the first one. He had further improved pain relief following the second injection. He will continue to have LSB's until he has no benefit from them. Insulin induced A-V shunting followed by endoneural ischemia in addition to acute neural vascular insufficiency and metabolic disequilibrium following dramatic control of diabetes are thought to be the mechanism involved in insulin neuritis. Per some reports, pain gradually dissipates within a year of onset. LSB can be considered as a treatment if other therapies fail. (Song, J Neurol, 2009), (Leow, PostgradMed, 2005).

Complex Regional Pain Syndrome (CRPS) is a painful, often debilitating condition characterized by severe spontaneous or evoked pain (such as allodynia) accompanied in various phases by vasomotor, sudomotor, motor, and trophic changes. Usually precipitated by extremity injury, surgery, or immobilization, this chronic pain syndrome can be highly refractory to both conservative medical management and invasive pain therapies. We present a case of a 37 year old man that developed CRPS type-1 of the lower extremities after a bunionectomy of the left first toe in 1998. Over the next 12 years this patient underwent a multitude of treatments including sympathetic nerve blocks, spinal cord stimulator implantation, and intrathecal pump therapy with ziconatide without significant pain improvement. He concurrently developed massive spreading lymphedema of his lower extremities probably attributable to chronic opioid therapy and CRPS. After significant planning and discussion, the patient gave consent to receive anesthetic dose ketamine therapy in the ICU under the direction of a critical care anesthesiologist with guidance from chronic pain specialists. He then received direct lymphedema therapy, psychiatric, psychological management, and surgical management for related co-morbid conditions. We describe the multidisciplinary team approach prior, during, and after ketamine coma, including the resources, close communication, and cooperation required between medical disciplines. With this coordinated effort, the patient achieved dramatic resolution of lymphedema and significant improvement in pain, functioning, and use of analgesic medications. Anesthetic ketamine therapy for refractory CRPS has been previously described but has not become a universally available therapy in the United States. This case exemplifies the utility of ketamine in the treatment of CRPS as well as the important roles played by subspecialty trained physicians working closely together to offer complex therapies to effectively help restore pain independence in the lives of carefully selected patients.

Sacroiliitis and sacroiliac (SI) joint dysfunction accounts for approximately 15% to 30% of cases of chronic low back pain. Sacroiliac pain has been treated with varying responses with physical therapy, intra-atricular injections, lateral-branch radiofrequency denervation and surgical fusion. Hypertonic dextrose is thought to have chemoneuromodulatory and possibly neurolytic potential. We report the results of a consecutive series of 15 patients with Sacroiliac pain who underwent fluoroscopic guided SI joint injections with 16.6 % Dextrose. Subjects consisted of 8 men and 7 women, 37 to 84 years old. All patients underwent diagnostic SI joint injections with local anesthetic before denervation. Changes in visual analog pain scores (VAS), pain diagrams, physical examination including tenderness over the joint, overlying myofascial trigger points, SI joint pain provocation tests, and range of motion of the lumbar spine were assessed pre- and postdenervation. The criteria for successful denervation were at least a 50% decrease in VAS for a period of at least 6 months; 80% of patients (12 of 15) met these criteria. 2 patients had < 50 % response and one patient's pain worsened. Average VAS pain score decreased from 6.4 +/- 0.7 to 1.2 +/- 0.5 (p < 0.0001). The average duration of pain relief was 8.8+/- 1.1 months in responders. Good responders had significantly reduced pain on the day of the procedure, whereas the poor responders did not demonstrate the same dramatic pain reduction on the day of their procedure, possibly indicating poor technical results or incorrect diagnosis. There were no complications. This study suggests that SI joint denervation with hypertonic dextrose could provide effective and durable pain relief in selected patients with sacroiliac pain.