Amount Of Nerve Damage Research Articles

Lack of correlation between spinal microgliosis and long-term development of tactile hypersensitivity in two different sciatic nerve crush injury.

Microglia activation following peripheral nerve injury has been shown to contribute to central sensitization of the spinal cord for the development of neuropathic pain. In a recent study, we reported that the amount of nerve damage does not necessarily correlate with chronic pain development. Here we compared the response of spinal microglia, using immunohistochemistry as a surrogate of microglial activation, in mice with two different types of crush injury of the sciatic nerve. We confirmed that incomplete crush of the sciatic nerve (partial crush injury, PCI) resulted in tactile hypersensitivity after the recovery of sensory function (15 days after surgery), whereas the hypersensitivity was not observed after the complete crush (full crush injury, FCI). We observed that immunoreactivity for Iba-1, a microglial marker, was greater in the ipsilateral dorsal horn of lumbar (L4) spinal cord of mice 2 days after FCI compared to PCI, positively correlating with the intensity of crush injury. Ipsilateral Iba-1 reactivity was comparable between injuries at 7 days with a significant increase compared to the contralateral side. By day 15 after injury, ipsilateral Iba-1 immunoreactivity was much reduced compared to day 7 and was not different between the groups. Our results suggest that the magnitude of the early microgliosis is dependent on injury severity, but does not necessarily correlate with the long-term development of chronic pain-like hypersensitivity after peripheral nerve injury.

Histologic and Electrophysiologic Changes Following Subepineurial Hematoma Induction in Rat Sciatic Nerve

The sciatic nerves of 34 rats were used to study the effects of intraneural, extrafascicular hematoma, exclusive of any other trauma. Electrodiagnostic, histologic, and electron microscopic techniques were used. The amount of nerve fiber damage was assessed using computerized planimetry. The effects of hematoma evacuation were also investigated. Changes consistent with partial denervation, such as prolongation of insertion activity and distal latency, and the presence of positive waves and fibrillations, were present in the blood-injected but not in the control groups. Degenerative nerve fiber changes localized to the area of hematoma were present in the blood-injected group and were significantly higher than those in the control group. Although there was a difference in the amount of nerve damage between the blood-injected and the hematoma-evacuated group (less damage), this difference was not statistically significant. These findings suggest that intraneural extrafascicular hematoma produces electrophysiologic and histologic evidence of axonal degeneration affecting nerve fibers in the vicinity of the hematoma. Early evacuation of the intraneural hematoma appears to slightly reduce the deleterious effects of the lesion.