Central neuropathic pain / Dores neuropáticas centrais

ABSTRACT BACKGROUND AND OBJECTIVES: Central pain, classified as neuropathic, is defined as a painful syndrome caused by injury to central nervous system structures. This is one of the most complexes, intriguing and difficult to treat syndromes. This study aimed at promoting a narrative review including the concept of central pain, its intercurrent symptoms which are important for the diagnosis, and different available treatments, indications, results and complications. CONTENTS: Relevant articles available in Medline, Scielo, Cochrane Library and Pubmed databases in the last 10 years were selected by means of keywords: chronic neuropathic pain, central neuropathic pain, central pain. CONCLUSION: Central painful syndrome is diagnosed by means of neurological clinical evaluation. It is often refractory to clinical and neuromodulatory treatment, its management should be multimodal and allow for rehabilitation.

RESUMO JUSTIFICATIVA E OBJETIVOS: A dor central, classificada como neuropática, é definida como uma síndrome dolorosa que decorre da lesão de estruturas no sistema nervoso central. Trata-se de uma das síndromes dolorosas mais complexas, intrigantes e de difícil tratamento. O objetivo deste estudo foi promover uma revisão narrativa que inclui desde o conceito de dor central, seus sintomas intercorrentes importantes no diagnóstico; e diversos tratamentos disponíveis, indicações, resultados e complicações. CONTEÚDO: Foi realizada uma seleção de artigos relevantes disponíveis nas plataformas Medline, Scielo, Biblioteca Cochrane e Pubmed nos últimos 10 anos, por meio dos descritores: dor crônica neuropática, dor neuropática central, dor central. CONCLUSÃO: A síndrome dolorosa central tem seu diagnóstico realizado por meio do exame clínico neurológico. É frequentemente refratária ao tratamento clínico e neuromodulatório e, portanto, deve ser multimodal e permitir a reabilitação.

Neuronal Hyperexcitability Mediates Below-Level Central Neuropathic Pain after Spinal Cord Injury in Rats / 한국실험동물학회지

Spinal cord injury often leads to central neuropathic pain syndromes, such as allodynic and hyperalgesic behaviors. Electrophysiologically, spinal dorsal horn neurons show enhanced activity to non-noxious and noxious stimuli as well as increased spontaneous activity following spinal cord injury, which often called hyperexcitability or central sensitization. Under hyperexcitable states, spinal neurons lose their ability of discrimination and encoding somatosensory information followed by abnormal somatosensory recognition to non-noxious and noxious stimuli. In the present review, we summarize a variety of pathophysiological mechanisms of neuronal hyperexcitability for treating or preventing central neuropathic pain syndrome following spinal cord injury.

Long-term Follow-up of Cutaneous Hypersensitivity in Rats with a Spinal Cord Contusion

Sometimes, spinal cord injury (SCI) results in various chronic neuropathic pain syndromes that occur diffusely below the level of the injury. It has been reported that behavioral signs of neuropathic pain are expressed in the animal models of contusive SCI. However, the observation period is relatively short considering the natural course of pain in human SCI patients. Therefore, this study was undertaken to examine the time course of mechanical and cold allodynia in the hindpaw after a spinal cord contusion in rats for a long period of time (30 weeks). The hindpaw withdrawal threshold to mechanical stimulation was applied to the plantar surface of the hindpaw, and the withdrawal frequency to the application of acetone was measured before and after a spinal contusion. The spinal cord contusion was produced by dropping a 10 g weight from a 6.25 and 12.5 mm height using a NYU impactor. After the injury, rats showed a decreased withdrawal threshold to von Frey stimulation, indicating the development of mechanical allodynia which persisted for 30 weeks. The withdrawal threshold between the two experimental groups was similar. The response frequencies to acetone increased after the SCI, but they were developed slowly. Cold allodynia persisted for 30 weeks in 12.5 mm group. The sham animals did not show any significant behavioral changes. These results provide behavioral evidence to indicate that the below-level pain was well developed and maintained in the contusion model for a long time, suggesting a model suitable for pain research, especially in the late stage of SCI or for long term effects of analgesic intervention.

Clinical Features of Central Neuropathic Pain after Contusive Spinal Cord Injury in Rats

OBJECTIVE: To investigate the characteristics of the central neuropathic pain (CNP) after contusive spinal cord injury in rats. METHOD: Twenty Sprague-Dawley rats (300+/-50 g, male) undergone the free-drop contusion injury from the drop-height of 2.5 cm at T10 cord (n=20) and ten rats undergone sham operation (n=10) were subjected to the neurobehavioral analyses by the Basso Beattie Bresnahan (BBB) locomotor rating scales, Touch test(TM) sensory evaluator (TTSE, North Coast Medical Inc., Canada) and Plantar test(R)(Ugo Basile, Italy) after contusion at the 1(st), 3(rd), 5(th), 7(th), 14(th), 21(st) and 28(th) day. RESULTS: The scores of BBB scales were the lowest at the 1st day and then slowly increased to spontaneous recovery state, but they were significantly lower than those of control group (p<0.05). The thresholds of mechanical allodynia were significantly increased just after cord contusion, but progressed to decline, and significantly decreased after the 21(st) day (p<0.05). The latencies of thermal hyperalgesia were delayed just after cord contusion, but significantly shorter than those of the control group after the 7(th) day (p<0.05). CONCLUSION: These results would be helpful for the study of the CNP after contusive spinal cord injury in rats.