IntroductionThe role of pain as a warning system necessitates a rapid transmission of information from the periphery for the execution of appropriate motor responses. The nociceptive withdrawal reflex (NWR) is a physiological response to protect the limb from a painful stimulus and is often considered an objective measure of spinal nociceptive excitability. The NWR is commonly defined by its latency in the presumed Aδ-fiber range consistent with the canonical view that “fast pain” is signaled by Aδ nociceptors. We recently demonstrated that human skin is equipped with ultrafast (Aβ range) nociceptors. Here, we investigated the short-latency component of the reflex and explored the relationship between reflex latency and pain perception.MethodsWe revisited our earlier work on NWR measurements in which, following convention, only reflex responses in the presumed Aδ range were considered. In our current analysis, we expanded the time window to search for shorter latency responses and compared those with pain ratings.ResultsIn both cohorts, we found an abundance of recordings with short-latency reflex responses. In nearly 90% of successful recordings, only single reflex responses (not dual) were seen which allowed us to compare pain ratings based on reflex latencies. We found that shorter latency reflexes were just as painful as those in the conventional latency range.ConclusionWe found a preponderance of short-latency painful reflex responses. Based on this finding, we suggest that short-latency responses must be considered in future studies. Whether these are signaled by the ultrafast nociceptors remains to be determined.

Objectives To assess the prevalence of residual trans-lesion connectivity in persons with chronic clinically complete spinal cord injury (discompleteness) by neurophysiological methods. Participants A total of 23 adults with chronic sensorimotor complete spinal cord injury, identified through regional registries the regional spinal cord registry of Östergötland, Sweden. Methods Diagnosis of clinically complete spinal cord injury was verified by standardized neurological examination. Then, a neurophysiological examination was performed, comprising electroneurography, electromyography, sympathetic skin response and evoked potentials (sensory, laser and motor). Based on this assessment, a composite outcome measure, indicating either strong, possible or no evidence of discomplete spinal cord injury, was formed. Results Strong neurophysiological evidence of discomplete spinal cord injury was found in 17% (4/23) of participants. If also accepting “possible evidence”, the discomplete group comprised 39% (9/23). The remaining 61% showed no neurophysiological evidence of discompleteness. However, if also counting reports of subjective sensation elicited during neurophysiological testing in the absence of objective findings, 52% (12/23) showed indication of discomplete spinal cord injury. CONCLUSION Evidence of discomplete spinal cord injury can be demonstrated using standard neurophysiological techniques in a substantial subset of individuals with clinically complete spinal cord injury. This study adds to the evidence base indicating the potential of various modes of cross-lesional sensorimotor functional restoration in some cases of chronic clinically complete spinal cord injury. LAY ABSTRACT Spinal cord injuries are usually classed as complete or incomplete. A complete injury implies that no residual function exists below the neurological level of injury. This status is determined by standardized neurological examination and is thought to correlate with spinal cord function in each individual with spinal cord injuries. However, studies have indicated that, in some people with complete spinal cord injury, there may be residual function that is not detected by such testing. The aim of the current study was to examine whether residual function, which is not detected by such testing, exists, and, if so, how common it is among people with complete spinal cord injuries (based on clinical testing) in a chronic stage (>2 years since injury). A battery of neurophysiological tests was used. Signs of “subclinical” residual function were found in 17–39% of 23 participants. This finding may lead to improvements in rehabilitative outcomes for people with complete spinal cord injury.

In Sweden, a large family with a point mutation in the nerve growth factor-beta gene has previously been identified. The carriers of this mutation have reduced small-fiber density and selective deficits in deep pain and temperature modalities. The clinical findings in this population are described as hereditary sensory and autonomic neuropathy type V. The purpose of the current study was to investigate the prevalence of carpal tunnel syndrome in hereditary sensory and autonomic neuropathy type V based on clinical examinations and electrophysiological measurements. Further, the cross-sectional area of the median nerve at the carpal tunnel inlet was measured with ultrasonography. Out of 52 known individuals heterozygous for the nerve growth factor-beta mutation in Sweden, 23 participated in the current study (12 males, 11 females; mean age, 55 years; range, 25 to 86 years). All participants answered a health questionnaire and underwent clinical examination followed by median nerve conduction study in a case-control design, and measurement of the nerve cross-sectional area with ultrasonography. The diagnosis of carpal tunnel syndrome was made based on consensus criteria using patient history and nerve conduction study. The prevalence of carpal tunnel syndrome in the hereditary sensory and autonomic neuropathy group was 35% (95% CI 19-55%) or 52% (95% CI 37-74%) depending on whether those individuals who had classic symptoms of carpal tunnel syndrome but negative nerve conduction studies were included or not. Those who had a high likelihood of carpal tunnel syndrome based on classic/probable patient history with positive nerve conduction study had a significantly larger median nerve cross-sectional area than those who had an unlikely patient history with negative nerve conduction study. The prevalence of carpal tunnel syndrome was 10 to 25 times higher in individuals heterozygous for the nerve growth factor-beta mutation than the general Swedish population. Further studies are needed to better understand the underlying pathophysiological mechanisms.