Bodman Myron A., Dreyer Mark A., Varacallo Matthew A.
Kent State University CPM
Intercoastal Medical Group
Peripheral neuropathy encompasses a broad range of clinical pathologies potentially presenting with peripheral nervous system dysfunction. Patients with peripheral neuropathy often present with varying degrees of numbness, tingling, aching, burning sensation, weakness of limbs, hyperalgesia, allodynia, and pain. This pain has been characterized as superficial, deep-seated, or severe, unremitting pain with exacerbation at night. While metabolic disorders represent the predominant etiology of extremity pain caused by an underlying peripheral neuropathy clinical pathology, broad clinical consideration is given to many clinical conditions. Although there are many possible causes of peripheral neuropathy, the most prevalent subtype, diabetic peripheral neuropathy (DPN), can lead to significant complications ranging from paresthesia to loss of limb and life. Early assessment of symptoms of peripheral polyneuropathy helps avoid neuropathic foot ulcers to combat potential morbidity and mortality resulting from the pathophysiologic poor wound healing potential, which can lead to limb compromise, local to systemic infection, septicemia, and even death. DPN is primarily diagnosed clinically through history and neurological assessment of small fiber sensation with temperature changes or pinpricks, large fiber sensation with vibrations, and ulceration risk with pressure testing using a 10 g monofilament. Neurology consultation and specialized testing, including nerve conduction studies and intraepidermal nerve fiber density testing, are only indicated for patients with atypical clinical features (eg, rapid symptom onset, severe neuromotor impairment, and asymmetrically abnormal sensation). The exact cause of DPN is not known. Proposed theories include metabolic, neurovascular, and autoimmune pathways have been proposed. Mechanical compression (eg, carpal tunnel), genetics, and social and lifestyle factors such as chronic alcohol consumption and smoking have all been implicated. Perpetually high blood serum glucose leads to insulin resistance, promoting oxidative stress, inflammation, and cell damage. First, the distal sensory and autonomic nerve fibers are damaged; the damage continues with proximal progression, leading to a gradual loss of protective sensation in the skin and foot joints. DPN management consists of several strategies, including preventative measures (eg, patient education, proper foot care, correct shoe wear, and annual foot exam), glucose control, dietary modifications, weight loss, and pain control. Half of the diabetic peripheral neuropathies may be asymmetric. If not recognized and preventative foot care is not implemented, patients have an increased risk of injury due to their insensate feet.
周围神经病变涵盖了一系列可能表现为周围神经系统功能障碍的临床病理情况。周围神经病变患者常出现不同程度的麻木、刺痛、酸痛、烧灼感、肢体无力、痛觉过敏、感觉异常和疼痛。这种疼痛的特点为浅表性、深部性或严重的、夜间加剧的持续性疼痛。虽然代谢紊乱是由潜在的周围神经病变临床病理引起的肢体疼痛的主要病因,但也会广泛考虑许多临床情况。尽管周围神经病变有许多可能的病因,但最常见的亚型——糖尿病性周围神经病变(DPN),可导致从感觉异常到肢体丧失和危及生命等严重并发症。早期评估周围多发性神经病变的症状有助于避免神经性足部溃疡,以对抗因病理生理上伤口愈合能力差而导致的潜在发病率和死亡率,这可能会导致肢体功能受损、局部至全身感染、败血症,甚至死亡。DPN主要通过临床病史以及对小纤维感觉(通过温度变化或针刺)、大纤维感觉(通过振动)和使用10克单丝进行压力测试评估溃疡风险的神经学评估来诊断。只有具有非典型临床特征(如症状快速发作、严重神经运动障碍和感觉异常不对称)的患者才需要进行神经科会诊和专门检查,包括神经传导研究和表皮内神经纤维密度测试。DPN的确切病因尚不清楚。已提出的理论包括代谢、神经血管和自身免疫途径。机械压迫(如腕管综合征)、遗传因素以及社会和生活方式因素,如长期酗酒和吸烟,都与之有关。持续高血糖会导致胰岛素抵抗,促进氧化应激、炎症和细胞损伤。首先,远端感觉神经纤维和自主神经纤维受损;损伤随着向近端发展而持续,导致皮肤和足部关节的保护性感觉逐渐丧失。DPN的管理包括多种策略,包括预防措施(如患者教育、正确的足部护理、合适的鞋类穿着和年度足部检查)、血糖控制、饮食调整、体重减轻和疼痛控制。一半的糖尿病性周围神经病变可能是不对称的。如果未被识别且未实施预防性足部护理,患者因足部感觉减退而受伤的风险会增加。