Unilateral angioedema of the tongue is a rare adverse reaction to angiotensin-converting enzyme inhibitors. Early recognition may prevent unnecessary surgical intervention and complications.

Spinal cord injury (SCI) is a complex syndrome that has profound effects on patient well-being, including the development of medically-resistant chronic pain. The mechanisms underlying SCI pain have been the subject of thorough investigation but still remain poorly understood. While the majority of the research has focused on changes occurring within and surrounding the site of injury in the spinal cord, there is now a consensus that alterations within the peripheral nervous system, namely sensitization of nociceptors, contribute to the development and maintenance of chronic SCI pain. Here we demonstrate that thoracic spinal contusion injury results in the emergence of autotomy and spasticity, both indicators of spontaneous pain, in areas below the level of the injury within 24 hr of SCI. These behaviors were associated with hindpaw edema and elevated cutaneous calcitonin gene-related peptide (CGRP) concentration. Electrophysiological recordings using an ex vivo skin/nerve/DRG/spinal cord preparation demonstrated that SCI increased mechanical and thermal sensitivity, as well as the incidence of spontaneous activity (SA) and afterdischarge (AD), in below-level C-fiber nociceptors 24 hr following injury. Interestingly, the distribution of nociceptors that exhibit SA and AD are not identical, and the development of SA was observed more frequently in nociceptors with low thermal thresholds, while AD was found more frequently in nociceptors with high thermal thresholds. These results demonstrate that SCI causes rapid-onset of peripheral inflammation-like processes that sensitize nociceptors, which may contribute to the early emergence and persistence of chronic SCI pain.