Verdugo R J, Ochoa J L
Department of Neurology, Faculty of Medicine, University of Chile.
J Neurol Neurosurg Psychiatry. 1998 Aug;65(2):196-203. doi: 10.1136/jnnp.65.2.196.
To gain understanding of the mechanism and meaning of improvement of hypoaesthesia after a diagnostic intervention, and of the nature of the population that displays such a sign.
Patients with chronic "neuropathic" pain underwent rigorous clinical and laboratory investigations, including placebo controlled local anaesthetic block. Patients displaying profound regional cutaneous hypoaesthesia and pain entered the study through either of two criteria: (a) reversal of hypoaesthesia after diagnostic block, (b) nerve injury as the cause of hypoaesthesia and pain. The semeiology displayed by these patients together with the behaviour of their sensory phenomena in response to blocks were compared. Three groups were expected: (1) patients with "neuropathic" pain with profound hypoaesthesia reversed by block, but without neuropathy; (2) patients whose hypoaesthesia did not reverse and who had neuropathy as the cause of their sensory dysfunction; and (3) patients whose hypoaesthesia reversed, and had neuropathy.
Two groups emerged: (1) patients with profound hypoaesthesia reversed by block, but without neuropathy (27 patients), and (2) patients whose hypoaesthesia did not reverse and who had a neuropathy (13 patients). No patient with neuropathy was found whose cutaneous hypoaesthesia improved with block. The first group displayed the sensory-motor characteristics of psychogenic pseudoneuropathy. The semeiology of the second group was in keeping with organic neuropathy and displayed no pseudoneurological features. Spontaneous pain was relieved by placebo in 66.6% of the patients in groupl and 53.8% in group 2.
Such reversal of hypoaesthesia is due to a placebo effect, acting on a psychogenic symptom because: (a) 27 of 27 patients in which the sign occurred had absence of nerve disease behind the "neuropathic" symptoms, (b) In 26 of 27 patients the area of hypoaesthesia was non-anatomical, (c) 16 of 27 patients had other sensory-motor signs that could not be explained as a result of organic pathology (give way weakness and punctual denial of hypoaesthesia), and (d) the phenomenon was not found in patients with organic neuropathy.
了解诊断性干预后感觉减退改善的机制及意义，以及出现该体征的人群的特征。
患有慢性“神经性”疼痛的患者接受了严格的临床和实验室检查，包括安慰剂对照的局部麻醉阻滞。表现出严重局部皮肤感觉减退和疼痛的患者通过以下两个标准之一进入研究：（a）诊断性阻滞后感觉减退逆转；（b）神经损伤是感觉减退和疼痛的原因。比较这些患者表现出的症状学以及其感觉现象对阻滞的反应。预期分为三组：（1）患有“神经性”疼痛且严重感觉减退经阻滞逆转但无神经病变的患者；（2）感觉减退未逆转且神经病变是其感觉功能障碍原因的患者；（3）感觉减退逆转且有神经病变的患者。
出现了两组：（1）严重感觉减退经阻滞逆转但无神经病变的患者（27例），（2）感觉减退未逆转且有神经病变的患者（13例）。未发现神经病变患者的皮肤感觉减退经阻滞改善。第一组表现出精神性假性神经病变的感觉运动特征。第二组的症状学符合器质性神经病变，未表现出假性神经学特征。安慰剂使第1组66.6%的患者和第2组53.8%的患者的自发性疼痛得到缓解。
这种感觉减退的逆转是由于安慰剂效应作用于精神性症状，原因如下：（a）出现该体征的27例患者中，27例“神经性”症状背后无神经疾病；（b）27例患者中有26例感觉减退区域不符合解剖学；（c）27例患者中有16例有其他感觉运动体征，无法用器质性病变解释（让步性虚弱和点状感觉减退否认）；（d）器质性神经病变患者未出现该现象。
