Nolano Maria, Provitera Vincenzo, Estraneo Anna, Selim Mona M, Caporaso Giuseppe, Stancanelli Annamaria, Saltalamacchia Anna Maria, Lanzillo Bernardo, Santoro Lucio
Neurology Department S. Maugeri Foundation, Medical Center of TeleseTerme (BN), Via Bagni Vecchi, 1 - 82037 Telese Terme (BN), Italy.
Brain. 2008 Jul;131(Pt 7):1903-11. doi: 10.1093/brain/awn102. Epub 2008 May 31.
Sensory disturbances are part of the clinical picture of Parkinson's disease. Abnormalities in sensory processing, through a basal ganglia involvement, are thought to be responsible for the sensory dysfunction since sensory nerve conduction velocity (NCV) is usually normal. However, NCV does not examine small fibres or terminal endings of large sensory fibres, whereas skin biopsy is more suitable for these purposes. To evaluate peripheral sensory nerves in Parkinson's disease, we studied cutaneous free and encapsulated sensory nerve endings in 18 patients and 30 healthy controls using 3-mm punch biopsies from glabrous and hairy skin. Ten patients had additional skin biopsies from the contralateral side. Further evaluation included NCV and Quantitative Sensory Testing. Parkinson's disease patients showed a significant increase in tactile and thermal thresholds (P < 0.01), a significant reduction in mechanical pain perception (P < 0.01) and significant loss of epidermal nerve fibres (ENFs) and Meissner corpuscles (MCs) (P < 0.01). In patients with bilateral biopsies, loss of pain perception and ENFs was higher on the more affected side (P < 0.01). We found evidence suggesting attempts at counteracting degenerative processes as increased branching, sprouting of nerves and enlargement of the vascular bed. Morphological and functional findings did not correlate with age or disease duration. Disease severity correlated with loss of MCs and reduction in cold perception and pain perception. We demonstrated a peripheral deafferentation in Parkinson's disease that could play a major role in the pathogenesis of the sensory dysfunction.
感觉障碍是帕金森病临床表现的一部分。由于感觉神经传导速度（NCV）通常正常，因此通过基底神经节受累导致的感觉处理异常被认为是感觉功能障碍的原因。然而，NCV无法检测小纤维或大感觉纤维的终末，而皮肤活检更适合这些目的。为了评估帕金森病患者的外周感觉神经，我们使用来自无毛和有毛皮肤的3毫米钻孔活检，研究了18例患者和30名健康对照者的皮肤游离和被囊感觉神经末梢。10例患者对侧进行了额外的皮肤活检。进一步评估包括NCV和定量感觉测试。帕金森病患者的触觉和热阈值显著升高（P < 0.01），机械性疼痛感知显著降低（P < 0.01），表皮神经纤维（ENF）和Meissner小体（MC）显著丢失（P < 0.01）。在进行双侧活检的患者中，疼痛感知和ENF的丢失在受影响更严重的一侧更高（P < 0.01）。我们发现有证据表明存在对抗退行性过程的尝试，如神经分支增加、神经芽生和血管床扩大。形态学和功能学发现与年龄或病程无关。疾病严重程度与MC的丢失以及冷觉和痛觉的降低相关。我们证明帕金森病存在外周传入神经阻滞，这可能在感觉功能障碍的发病机制中起主要作用。
