Benson M D, Cohen A S, Brandt K D, Cathcart E S
Lancet. 1975 Jan 4;1(7897):10-2. doi: 10.1016/s0140-6736(75)92373-9.
Of eighty-seven patients with nonhereditary systemic amyloidosis, ten had evidence of peripheral neuropathy. There was median-nerve neuropathy due to infiltration of the flexor retinaculum with amyloid in six patients. Two patients had diffuse sensorimotor neuropathy and two patients had sensory loss without evidence of motor impairment--three of these cases had amyloid deposition demonstrated by nerve biopsy. Neurological manifestations in all ten patients preceded other evidence of amyloidosis by 6 months-4 years (mean, 1 to 5 years). Neuropathy occurred in six of thirty-eight patients with primary amyloidosis and four of fourteen with amyloidosis associated with malignant B-cell dyscraias; and all patients with neuropathy had either a serum-M-component or Bence-Jones proteinuria. In contrast, neuropathy was not noted in any of the fifty-six patients in this series who had no evidence of a monoclonal gammopathy (thirty-five with secondary and twenty-one with primary amyloidosis).
在87例非遗传性系统性淀粉样变性患者中，10例有周围神经病变的证据。6例患者因屈肌支持带被淀粉样物质浸润而出现正中神经病变。2例患者有弥漫性感觉运动神经病变，2例患者有感觉丧失但无运动障碍证据——其中3例经神经活检证实有淀粉样物质沉积。所有10例患者的神经学表现均先于淀粉样变性的其他证据6个月至4年（平均1至5年）。38例原发性淀粉样变性患者中有6例出现神经病变，14例与恶性B细胞异常有关的淀粉样变性患者中有4例出现神经病变；所有有神经病变的患者均有血清M成分或本-周蛋白尿。相比之下，本系列中56例无单克隆丙种球蛋白病证据的患者（35例继发性淀粉样变性和21例原发性淀粉样变性）均未发现神经病变。
