Post-operative emergence of acute brachial neuritis following posterior cervical laminectomy with fusion: A case report and review of the literature.

INTRODUCTION: Idiopathic brachial plexus neuritis or neuralgic amyotrophy is a rare neurological condition whose true etiology currently remains unknown. Epidemiologically, the incidence of this condition is exceptionally rare with only 1.6 cases for every 100,000 people (Turner and Parsonage, 1987). Symptoms present an initial acute and sudden pain to the shoulder girdle and upper arm which is followed by a sense of profound weakness and numbness to the upper arm (Parsonage and Turner, 1948). Localized neuropathy within the arm-pit region may also be presented. The pain often exacerbates upon movement of the shoulder. Due to the anatomic location affected and the nature of the clinical symptoms presented, accurate diagnosis of brachial plexus neuritis poses a challenging diagnostic task for physicians due to remarkably similar symptoms expressed by differential diagnoses. PRESENTATION OF CASE: Here, we report the case of a 55-year-old woman who underwent surgery entailing cervical laminectomy with instrumented fusion. She presented with postoperative symptoms of severe pain in the left arm with significant weakness within 24 h after surgery. A diagnosis of brachial plexus neuritis was made based on the symptoms presented and upon review of imaging scans. DISCUSSION: After a six-month follow-up visit, the patient recovered from the brachial neuritis but has residual numbness in the hand. The presentation of this case serves to transmit three fundamental purposes. First, this case serves to establish an intriguing possible association of the post-surgical period of cervical laminectomy with acute brachial neuritis and signifies the importance post-operative linkage with brachial neuritis in general. Second, this case also highlights the importance of close clinical monitoring of patients with unique symptoms within the postoperative follow-up period to ensure successful improvement and accurate diagnosis. CONCLUSION: As an underdiagnosed and relatively obscure condition, this case serves as an imperative reference for physicians to illuminate differential diagnosis of similar symptomatic conditions and also to promote knowledge of brachial plexus neuritis which can lead to an early and precise diagnosis.

Intracranial and spinal metastases from eccrine mucinous carcinoma: case report.

BACKGROUND AND IMPORTANCE: Mucinous eccrine carcinoma (MEC) is a rare but distinct type of sweat gland tumor. MECs tend to recur locally, and their spread to distant organs is very uncommon. This article describes the first case of MEC metastasizing to the brain and the spine. CLINICAL PRESENTATION: A 45-year-old female presented with a 2-year history of a scalp mass in the occipital area with lymph node spread. She underwent excision of the mass and neck lymph node dissection. Pathology confirmed the diagnosis of MEC. Postoperatively, she received radiation to the involved areas. Four years later the patient presented with left hemiparesis and underwent craniotomy for gross total resection of the metastasis. This recurred after 2.5 years and she underwent another craniotomy for gross total resection followed by whole brain radiation. In addition, the patient had metastases to T11 vertebral body and the left C6 to 7 neural foramen. Moreover, the patient developed leptomeningeal disease in the spine. The metastases to the spine were treated with radiation therapy. The patient died 1.5 years later. CONCLUSION: Even though it is rare for MEC to spread to distant organs, physicians should be aware of the risk of metastatic invasion of the brain and spine and be vigilant about surveillance of these sites. MEC metastases to the brain should be treated aggressively with surgical resection followed by stereotactic radiosurgery to the tumor bed. Spine metastases should be treated with a combination of surgery and image-guided radiation therapy, depending on the degree of cord compression from epidural metastatic disease.

Transplantation of human bone marrow-derived stromal cells into the contused spinal cord of nude rats.

OBJECT: Human bone marrow stromal cells (hMSCs) constitute a potential source of pluripotent stem cells. In the present study, hMSCs were transplanted into an area of spinal cord contusion in nude rats to determine their survival, differentiation, potential for neuroprotection, and influence on axonal growth and functional recovery. METHODS: Twenty-nine animals received 6 x 10(5) hMSCs in 6 microl medium 1 week after a contusion, while 14 control animals received an injection of 6 microl medium alone. Basso-Beattie-Bresnahan (BBB) tests were performed weekly. The spinal cords were collected at 6 weeks posttransplantation for histological analysis and assessment of tissue injury. RESULTS: Immunostaining with anti-human mitochondria antibody and pretransplantation labeling with green fluorescent protein demonstrated that the grafted hMSCs survived and were capable of achieving a flattened appearance in the grafted area; however, none of the transplanted cells stained positively for human-specific neuronal, anti-neurofilament H or glial fibrillary acidic protein within the sites of engraftment. While neuronal or astrocytic differentiation was not seen, cells lining blood vessels in the vicinity of the transplant stained positively for anti-human endothelium CD105 antibody. Staining for anti-neurofilament H antibody demonstrated abundant axonlike structures around the transplanted area in the hMSC group. Tissue sparing analysis showed that animals with grafted hMSCs had a smaller area of contusion cyst compared with controls, but there was no significant difference between the two groups in BBB scores. CONCLUSIONS: The grafted hMSCs survived for > or = 6 weeks posttransplantation, although they did not differentiate into neural or glial cells. Cells with human endothelial characteristics were observed. Spinal cord-injured rats grafted with hMSCs had smaller contusion cavities, which did not have a significant influence on functional recovery.

Modification of Wright's technique for placement of bilateral crossing C2 translaminar screws: technical note.

BACKGROUND CONTEXT: Several relatively new screw techniques have been described that rigidly capture the posterior elements of C2. The previously described procedures of axis fixation are technically demanding and place the vertebral artery at some risk. A novel and less technically demanding technique of obtaining C-2 translaminar screws has been recently described. Although the risk of vertebral artery injury has been essentially eliminated, the authors recognize that neurologic injury from breakthrough of the inner cortex of the lamina by the drill or screw is still a possibility. PURPOSE: Describe and illustrate a modified C2 translaminar technique and review the results of patients who have undergone the surgery. The current modification of the C2 translaminar screw technique was designed to reduce the risk of inadvertent screw placement within the spinal canal. STUDY DESIGN/SETTING: A techniques paper combined with a retrospective clinical review of patients undergoing the surgery. PATIENT SAMPLE: Patients undergoing posterior instrumented fusion surgery of the cervical spine, which incorporates C2 posterior elements using the translaminar technique. OUTCOME MEASURES: Radiographic analysis of the fusion construct incorporating the C2 translaminar screws. METHODS: We have modified the previously described technique of C-2 translaminar screw placement with the addition of "exit" cortical windows to assure bicortical, intralaminar screw placement. RESULTS: The results of the first six patients with an average follow-up of 12 months demonstrated this method to be safe and effective in fixating the axis. CONCLUSIONS: We have made a simple modification of Wright's elegant technique with the addition of "exit" windows at the facet-laminar junctions. This gives us the assurance that the C2 screw has not entered the spinal canal by directly visualizing the tip of the screw exiting the outer cortices of the lamina before leaving the operating room.

Open-door expansile cervical laminoplasty.

Open-door expansile laminoplasty is a practical surgical technique for the treatment of cervical myelopathy secondary to cervical spinal stenosis. Laminoplasty procedures were first described in the late 1970s and have undergone numerous modifications. The current article reviews the indications, techniques, and outcome data for cervical laminoplasty. Complications of laminoplasty and comparison to laminectomy outcomes are also discussed.

Surgical treatment of thoracic outlet syndrome: a randomized trial comparing two operations.

OBJECT: Various surgical approaches have been proposed for the treatment of thoracic outlet syndrome (TOS). The authors of this study focused on the differences in outcome after supraclavicular neuroplasty of brachial plexus (SNBP [no rib resection]) and transaxillary first rib resection (TFRR) in patients in whom the dominant clinical problem was pain. METHODS: Fifty-five patients were randomized to undergo TFRR or SNBP. Patients with an anomalous cervical rib, intrinsic weakness, and primarily vascular findings were excluded from the study. Preoperatively, the following findings were typically observed: provocation of symptoms by certain postures (the so-called spear-throwing position as well as downward tugging of the shoulder) and marked tenderness in the supraclavicular fossa. The intergroup severity of the symptoms was comparable. Eight patients were lost to follow up. There were 24 TFRRs (in two cases the procedure was bilateral) and 25 SNBPs. The mean follow-up interval was 37 months. In both groups pain decreased significantly after surgery. By all measures the TFRR operation conferred superior results. Patients reported significantly less pain (39 +/- 7 compared with 61 +/- 7; score range 0-100 on a visual analog scale), greater percentage of pain relief (52 +/- 8% compared with 30 +/- 7%), and less pain (3.7 +/- 0.4 compared with 5.1 +/- 0.5) on an affective scale (all p < 0.05) in the TFRR and SNBP groups, respectively). In the TFRR group, 75% of patients reported good or excellent outcomes compared with 48% in the SNBP group (p < 0.05). CONCLUSIONS: Transaxillary first rib resection provided better relief of symptoms than SNBP. The major compressive element in patients with TOS-associated pain appeared to be the first rib.

Nerve injury induces a tonic bilateral mu-opioid receptor-mediated inhibitory effect on mechanical allodynia in mice.

BACKGROUND: Mice lacking the mu-opioid receptor gene have been used to characterize the role of mu-opioid receptors in nociception and the analgesic actions of opioid agonists. In this study, the authors determined the role of mu-opioid receptors in neuropathic pain behaviors and the effectiveness of mu- and kappa-opioid receptor agonists on this behavior in mice. METHODS: The authors studied the behavioral responses of mu-opioid receptor knockout and wild-type mice to thermal and mechanical stimuli before and after neuropathic pain induced by unilateral ligation and section of the L5 spinal nerve. Response to mechanical stimuli was evaluated by determining the frequency of hind paw withdrawal to repetitive stimulation using a series of von Frey monofilaments. Thermal hyperalgesia was assessed by determining the paw withdrawal latencies to radiant heat and frequency of hind paw withdrawal to cooling stimuli. The effects of systemic morphine, the kappa-opioid agonist U50488H, and naloxone on responses to mechanical and thermal stimuli were also studied in spinal nerve-injured mice. RESULTS: After spinal nerve injury, wild-type mice developed increased responsiveness to mechanical, heat, and cooling stimuli ipsilateral to nerve injury. mu-Opioid receptor knockout mice not only had more prominent mechanical allodynia in the nerve-injured paw, but also expressed contralateral allodynia to mechanical stimuli. Hyperalgesia to thermal stimuli was similar between mu-opioid knockout and wild-type animals. Morphine decreased mechanical allodynia dose dependently (3-30 mg/kg subcutaneous) in wild-type mice--an effect that was attenuated in the heterozygous mice and absent in the homozygous mu-opioid knockout mice. The kappa-opioid agonist U50488H (3-10 mg/kg subcutaneous) attenuated mechanical allodynia in wild-type, heterozygous, and homozygous mu-opioid mice. Naloxone in wild-type mice resulted in enhanced ipsilateral and contralateral allodynia to mechanical stimuli that resembled the pain behavior observed in mu-opioid receptor knockout mice. CONCLUSIONS: The authors' observations indicate that (1) unilateral nerve injury induces a bilateral tonic activation of endogenous mu-opioid receptor-mediated inhibition that attenuates mechanical allodynia but not thermal hyperalgesia, (2) both mu- and kappa-opioid agonists attenuate neuropathic pain in mice, and (3) the antihyperalgesic actions of morphine are mediated primarily via mu-opioid receptors.

Severity and duration of hyperalgesia in rat varies with type of nerve lesion.

OBJECTIVE: To learn how lesions with differing capacity for nerve regeneration affect the severity and duration of hyperalgesia in an animal model of neuropathic pain. METHODS: Three groups of rats were studied: 1). L5 nerve root crush (favorable for regeneration); 2). L5 root ligation and section; and 3). sham-operated group. An experimenter who did not know the rats' groups tested the animals for hyperalgesia to mechanical and cold stimuli. RESULTS: Measures of adverseness of mechanical and cooling stimuli for the crush group and ligation/cut groups were significantly higher than for the sham-operated group (P < 0.001 for both) for the first 30 days after lesioning. By 40 days, the crush group recovered from mechanical hyperalgesia, whereas the ligation/cut group continued to have significant hyperalgesia. At this time, both lesion groups displayed hyperalgesia to the cooling stimulus (P < 0.001), but the hyperalgesia in the ligation/cut group was significantly greater (P < 0.01). No recovery from cooling hyperalgesia was evident during the 54-day period of observation. Histological studies of the sciatic nerve indicated higher numbers of regenerating fibers in the crush group compared with the ligation/cut group. CONCLUSION: This study demonstrates that axotomy, regardless of how it is induced, produces hyperalgesia to both mechanical and cold stimuli. However, the lesion that favors regeneration is associated with earlier signs of recovery from mechanical hyperalgesia and less severe signs of cooling hyperalgesia. The data support the hypothesis that inputs from the injured afferents play an ongoing role in neuropathic pain from nerve injury. Nerve ligation induces more severe and more sustained behavioral signs of pain than nerve crush.

Naloxone increases pain induced by topical capsaicin in healthy human volunteers.

Opioid receptors occur in locations of strategic importance within the central nervous system for modulation of pain. Is pain reduced by ongoing inhibition mediated by activation of these receptors? Experiments to date in which the opioid-receptor antagonist, naloxone, is administered during a painful event have yielded unclear results. Topically applied capsaicin can be used to induce tonic pain of moderate to severe intensity without tissue injury and is an ideal stimulus for studying acute pain modulation. We therefore conducted a placebo-controlled double-blind crossover study to investigate the effects of naloxone on capsaicin-induced pain (five men, four women, aged 29 +/- 5 years). Capsaicin (10%) was applied topically and subjects rated pain every 2 min. The subjects were told that any drug given to them could increase, decrease, or not change their pain sensation. Pain plateaued after 20 min. At 26 min subjects received either naloxone or placebo in double-blind fashion. At 56 min subjects received the alternative (placebo or naloxone). In a second session the order of presentation was reversed. The naloxone induced a significant increase in pain compared both to baseline (P < 0.01) and placebo (P < 0.01). The peak effect, reached at 12-20 min after naloxone delivery, was 59% greater than placebo. This experiment suggests that acute pain is actively suppressed by endogenous opioid-receptor activation.

Mechanical hyperalgesia after an L5 ventral rhizotomy or an L5 ganglionectomy in the rat.

An L5 spinal nerve ligation (SNL) in the rat leads to behavioral signs of mechanical hyperalgesia. Our recent finding that an L5 dorsal root rhizotomy did not alter the mechanical hyperalgesia following an L5 SNL suggests that signals originating from the proximal stump of the injured nerve are not essential. We postulate that Wallerian degeneration of L5 nerve fibers leads to altered properties of adjacent intact nociceptive afferents. To investigate the role of degeneration in sensory versus motor fibers, five injury models were examined concurrently in a blinded fashion. An L5 ganglionectomy produced a selective lesion of sensory fibers. An L5 ventral root rhizotomy produced a selective lesion of motor fibers. The three control lesions included: (1) SNL with L5 dorsal root rhizotomy; (2) L5 dorsal root rhizotomy; and (3) exposure of the L5 roots without transection (sham). Paw withdrawal thresholds to mechanical stimuli were measured at three sites in the rat hindpaw corresponding to the L3, L4, and L5 dermatomes. Both the ganglionectomy and the ventral rhizotomy produced a significant, lasting (>or=20 d) decrease of mechanical withdrawal thresholds that was comparable to that produced by the SNL lesion. The L5 dorsal rhizotomy, by itself, produced a short lasting (