Neuropathic pain and SCI: Identification and treatment strategies in the 21st century.

Pain is a common complication in patients following spinal cord injury (SCI), with studies citing up to 80% of patients reporting some form of pain. Neuropathic pain (NP) makes up a substantial percentage of all pain symptoms in patients with SCI and is often complex. Given the high prevalence of NP in patients with SCI, proper identification and treatment is imperative. Indeed, identification of pain subtypes is a vital step toward determining appropriate treatment. A variety of pharmacological and non-pharmacological treatments can be undertaken including antiepileptics, tricyclic antidepressants, opioids, transcranial direct current stimulation, and invasive surgical procedures. Despite all the available treatment options and advances in the field of SCI medicine, providing adequate treatment of NP after SCI continues to be challenging. It is therefore extremely important for clinicians to have a strong foundation in the identification of SCI NP, as well as an understanding of appropriate treatment options. Here, we highlight the definitions and classification tools available for NP identification, and discuss current treatment options. We hope that this will not only provide a better understanding of NP for physicians in various subspecialties, but that it will also help guide future research on this subject.

Absence of bone morphogenetic protein-2 in human breast milk after spinal surgery.

BACKGROUND CONTEXT: Bone morphogenetic protein-2 (BMP-2) has been used extensively in recent years to enhance the process of spinal fusion. However, numerous side effects have been reported. This raises concerns regarding the safety of using this material in human beings. There are no published reports, that we are aware of, that demonstrate detectable levels of BMP-2 in human milk. PURPOSE: The purpose of this study was to determine the presence/absence of recombinant human bone morphogenetic protein-2 (rhBMP-2) in milk samples taken from a patient who underwent spinal surgery using rhBMP-2 shortly after delivering a child. STUDY DESIGN/SETTING: The study design comprises a case report dealing with analyzing milk from a patient who underwent spinal surgery using rhBMP-2 shortly after delivering a child. METHODS: We report the analysis of milk samples from a patient who underwent spinal surgery using rhBMP-2 shortly after delivering a child to determine the presence/absence of rhBMP-2. The milk samples were taken before and after the spinal surgery. Enzyme-linked immunosorbent assays were performed repeatedly to the samples. RESULTS: The standard curve for the assay had an r(2) value of 0.9853 indicating an acceptable degree of statistical reliability. The dose range for the standard curve was 62.5 to 2,000 pg/mL. None of the samples had an optical density greater than that of the lowest standard. CONCLUSIONS: No rhBMP-2 was detected in human milk in this single case report. Although this result seemed promising, it did not eliminate the concern regarding the potential risk of rhBMP-2 on child development. We still need further studies including more cases to verify this conclusion.

Sustained spinal cord compression: part I: time-dependent effect on long-term pathophysiology.

BACKGROUND: The objective of this study is to determine whether there is a relationship between the duration of sustained spinal cord compression and the extent of spinal cord injury and the capacity for functional recovery after decompression. METHODS: Sixteen dogs underwent sustained spinal cord compression for thirty or 180 minutes. The cords were compressed with use of a loading device with a hydraulic piston. A pressure transducer was attached to the surface of the piston, which transmitted real-time spinal cord interface pressures to a data-acquisition system. Somatosensory evoked potentials were monitored during a sixty-minute recovery period as well as at twenty-eight days after the injury. Functional motor recovery was judged throughout a twenty-six-day period after the injury with use of a battery of motor tasks. The volume of the lesion and damage to the tissue were assessed with both magnetic resonance imaging and histological analysis. RESULTS: Sustained spinal cord compression was associated with a gradual decline in interface pressure. Despite this, there was continuous decline in the amplitude of the somatosensory evoked potentials, which did not return until the cord was decompressed. Within one hour after the decompression, the dogs in the thirty-minute-compression group had recovery of somatosensory evoked potentials, but no animal had such recovery in the 180-minute group. Recovery of the somatosensory evoked potentials in the thirty-minute group was sustained over the twenty-eight days after the injury. Motor tests demonstrated rapid recovery of hindlimb motor function in the thirty-minute group, but there was considerable impairment in the 180-minute group. Within two weeks after the injury, balance, cadence, stair-climbing, and the ability to walk up an inclined plane were significantly better in the thirty-minute group than in the 180-minute group. The longer duration of compression produced lesions of significantly greater volume, which corresponded to the long-term functional outcome. CONCLUSIONS: The relatively rapid viscoelastic relaxation of the spinal cord during the early phase of sustained cord compression suggests that there are mechanisms of secondary injury that are linked to tissue displacement. Longer periods of displacement allow propagation of the secondary injury process, resulting in a lack of recovery of somatosensory evoked potentials, limited functional recovery, and more extensive tissue damage.

Sustained spinal cord compression: part II: effect of methylprednisolone on regional blood flow and recovery of somatosensory evoked potentials.

BACKGROUND: The efficacy of methylprednisolone in the treatment of traumatic spinal cord injury is controversial. We examined the effect of methylprednisolone on regional spinal cord blood flow and attempted to determine whether recovery of electrophysiological function is dependent on reperfusion, either during sustained spinal cord compression or after decompression. METHODS: The effects of methylprednisolone therapy on recovery of somatosensory evoked potentials and on spinal cord blood flow were examined in a canine model of dynamic spinal cord compression. Methylprednisolone (30 mg/kg intravenous loading dose followed by 5.4 mg/kg/hr intravenous infusion) or saline solution was administered to thirty-six beagles (eighteen in each group) five minutes after cessation of dynamic spinal cord compression and loss of all somatosensory evoked potentials. After ninety minutes of sustained compression, the spinal cords were decompressed. Somatosensory evoked potentials and spinal cord blood flow were evaluated throughout the period of sustained compression and for three hours after decompression. RESULTS: Seven dogs treated with methylprednisolone and none treated with saline solution recovered measurable somatosensory evoked potentials during sustained compression. After decompression, three more dogs treated with methylprednisolone and seven dogs treated with saline solution recovered somatosensory evoked potentials. Four dogs treated with methylprednisolone lost their previously measurable somatosensory evoked potentials. In the methylprednisolone group, spinal cord blood flow was significantly higher (p < 0.05) in the dogs that had recovered somatosensory evoked potentials than it was in the dogs that had not. Reperfusion blood flow was significantly higher (p < 0.05) in the saline-solution group than it was in the methylprednisolone group. Spinal cord blood flow in the saline-solution group returned to baseline levels within five minutes after decompression. It did not return to baseline levels in the dogs treated with methylprednisolone. CONCLUSIONS: The methylprednisolone administered in this study did not provide a large or significant lasting benefit with regard to neurological preservation or restoration. Methylprednisolone may reduce regional spinal cord blood flow through mechanisms affecting normal autoregulatory blood-flow function.

Cerebral spinal fluid pressure: effects of body position and lumbar subarachnoid drainage in a canine model.

STUDY DESIGN: This study used in vivo an model of subarachnoid cerebrospinal fluid pressure measurement. OBJECTIVES: To examine the relation between subarachnoid cerebrospinal fluid pressure in the cervical and lumbar spine and varying body positions, and to test the hypothesis that increasing body inclination and lumbar subarachnoid drainage decreases cervical cerebrospinal fluid pressures. SUMMARY OF BACKGROUND DATA: Cerebrospinal fluid leaks are a recognized complication of anterior or posterior cervical surgery. Conflicting opinion exists regarding the benefits of postoperative patient positioning and lumbar subarachnoid drainage. METHODS: Subarachnoid cerebrospinal fluid pressure of 7 beagles was monitored via two angiocatheters attached to pressure transducers inserted into the subarachnoid space through laminectomies at C3 and L4. Pressure measurements were taken when body position was inclined to 30 degrees, 60 degrees, and 90 degrees. A lumbar durotomy was performed to simulate the effects of lumbar subarachnoid drainage. The body was repositioned to 90 degrees, and pressure was measured. RESULTS: As inclination increased from 0 degrees to 90 degrees, the mean cervical cerebrospinal fluid pressure significantly decreased. The mean lumbar subarachnoid pressure significantly increased as inclination increased from 0 degrees to 90 degrees. Lumbar durotomy plus repositioning to 90 degrees resulted in a significant reduction in cervical cerebrospinal fluid subarachnoid pressure, with pressures dropping by 46%. Lumbar cerebrospinal fluid subarachnoid pressure dropped to zero after lumbar durotomy plus repositioning to 90 degrees. CONCLUSIONS: Cerebrospinal fluid pressures in the subarachnoid space of both the cervical and lumbar spines are affected by changes in body position. Both patient positioning and lumbar drainage may be important in reducing cervical cerebrospinal fluid pressure, and may reduce the occurrence of cerebrospinal fluid leaks after primary dural repair in the neck.

Current developments in spinal cord injury research.

BACKGROUND CONTEXT: Recent advances in neuroscience have opened the door for hope toward prevention and cure of the devastating effects of spinal cord injury (SCI). PURPOSE: To highlight the current understanding of traumatic SCI mechanisms, provide information regarding state-of-the-art care for the acute spinal cord-injured patient, and explore future treatments aimed at neural preservation and reconstruction. STUDY DESIGN/SETTING: A selective overview of the literature pertaining to the neuropathophysiology of traumatic SCI is provided with an emphasis on pharmacotherapies and posttraumatic experimental strategies aimed at improved neuropreservation and late neuroregenerative repair. METHODS: One hundred fifty-four peer-reviewed basic science and clinical articles pertaining to SCI were reviewed. Articles cited were chosen based on the relative merits and contribution to the current understanding of SCI neuropathophysiology, neuroregeneration, and clinical SCI treatment patterns. RESULTS: A better understanding of the pathophysiology and early treatment for the spinal cord-injured patient has led to a continued decrease in mortality, decreased acute hospitalization and complication rates, and more rapid rehabilitation and re-entry into society. Progressive neural injury results from a combination of secondary injury mechanisms, including ischemia, biochemical alterations, apoptosis, excitotoxicity, calpain proteases, neurotransmitter accumulation, lipid peroxidation/free radical injury, and inflammatory responses. Experimental studies suggest that the final posttraumatic neurologic deficit is not only a result of the initial impaction forces but rather a combination of these forces and secondary time-dependent events that follow shortly after the initial impact. CONCLUSIONS: Experimental studies continue to provide a better understanding of the complex interaction of pathophysiologic events after traumatic SCI. Future approaches will involve strategies aimed at blocking the multiple mechanisms of progressive central nervous system injury and promoting neuroregeneration.