Neurology Department, Istanbul University-Cerrahpaşa, Cerrahpaşa Faculty of Medicine, Istanbul, Fatih 34098, Turkey.
Internal Medicine Department, Istanbul University-Cerrahpaşa, Cerrahpaşa Faculty of Medicine, Istanbul, Fatih 34098, Turkey.
Pain Med. 2023 Oct 3;24(10):1161-1168. doi: 10.1093/pm/pnad077.
The nociceptive flexion reflex (NFR) is a polysynaptic and multisegmental spinal reflex that develops in response to a noxious stimulus and is characterized by the withdrawal of the affected body part. The NFR possesses two excitatory components: early RII and late RIII. Late RIII is derived from high-threshold cutaneous afferent A-delta fibers, which are prone to injury early in the course of diabetes mellitus (DM) and may lead to neuropathic pain. We investigated NFR in patients with DM with different types of polyneuropathies to analyze the role of NFR in small fiber neuropathy (SFN).
We included 37 patients with DM and 20 healthy participants of similar age and sex. We performed the Composite Autonomic Neuropathy Scale-31, modified Toronto Neuropathy Scale, and routine nerve conduction studies. We grouped the patients into large fiber neuropathy (LFN), SFN, and no overt neurological symptom/sign groups. In all participants, NFR was recorded on anterior tibial (AT) and biceps femoris (BF) muscles after train stimuli on the sole of the foot, and NFR-RIII findings were compared.
We identified 11 patients with LFN, 15 with SFN, and 11 with no overt neurological symptoms or signs. The RIII response on the AT was absent in 22 (60%) patients with DM and 8 (40%) healthy participants. The RIII response on the BF was absent in 31 (73.8%) patients and 7 (35%) healthy participants (P = .001). In DM, the latency of RIII was prolonged, and the magnitude was reduced. Abnormal findings were seen in all subgroups; however, they were more prominent in patients with LFN compared to other groups.
The NFR-RIII was abnormal in patients with DM even before the emergence of the neuropathic symptoms. The pattern of involvement before neuropathic symptoms was possibly related to an earlier loss of A-delta fibers.
伤害性屈肌反射（NFR）是一种多突触和多节段的脊髓反射，对伤害性刺激作出反应，其特征是受影响的身体部位的退缩。NFR 具有两个兴奋性成分：早期 RII 和晚期 RIII。晚期 RIII 源自高阈值皮肤传入 Aδ纤维，这些纤维在糖尿病（DM）的早期阶段容易受到损伤，可能导致神经病理性疼痛。我们研究了不同类型多发性神经病的 DM 患者的 NFR，以分析 NFR 在小纤维神经病（SFN）中的作用。
我们纳入了 37 名 DM 患者和 20 名年龄和性别相似的健康参与者。我们进行了复合自主神经病变量表-31、改良多伦多神经病量表和常规神经传导研究。我们将患者分为大纤维神经病（LFN）、SFN 和无明显神经症状/体征组。在所有参与者中，在足底进行训练刺激后，在前胫骨（AT）和肱二头肌（BF）肌肉上记录 NFR，比较 NFR-RIII 的发现。
我们发现 11 名患者患有 LFN，15 名患者患有 SFN，11 名患者无明显神经症状或体征。22 名（60%）DM 患者和 8 名（40%）健康参与者的 AT 上的 RIII 反应消失。31 名（73.8%）患者和 7 名（35%）健康参与者的 BF 上的 RIII 反应消失（P = .001）。在 DM 中，RIII 的潜伏期延长，幅度减小。所有亚组均可见异常发现，但在 LFN 患者中更为明显。
即使在出现神经病变症状之前，DM 患者的 NFR-RIII 也异常。在出现神经病变症状之前的受累模式可能与 Aδ 纤维的早期丧失有关。
