Oaklander Anne Louise, Cohen Steven P, Raju Shubha V Y
Neuropathic Pain Study Group, Department of Anesthesiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
Pain. 2002 Mar;96(1-2):9-12. doi: 10.1016/s0304-3959(01)00400-6.
Some patients develop chronic itch from neurological injuries, and shingles may be a common cause. Neuropathic itch can lead to self-injury from scratching desensate skin. A 39-year-old woman experienced severe postherpetic itch, but no postherpetic neuralgia, after ophthalmic zoster. Within 1 year, she had painlessly scratched through her frontal skull into her brain. Sensory testing and skin biopsies were performed on itchy and normal scalp to generate preliminary hypotheses about mechanisms of neuropathic itch. Quantitation of epidermal neurites in PGP9.5-immunolabeled skin biopsies demonstrated loss of 96% of epidermal innervation in the itchy area. Quantitative sensory testing indicated severe damage to most sensory modalities except itch. These data indicate that in this patient, severe postherpetic itch was associated with loss of peripheral sensory neurons. Possible mechanisms include electrical hyperactivity of hypo-afferented central itch-specific neurons, selective preservation of peripheral itch-fibers from neighboring unaffected dermatomes, and/or imbalance between excitation and inhibition of second-order sensory neurons.
一些患者因神经损伤而出现慢性瘙痒，带状疱疹可能是常见原因。神经性瘙痒会导致因搔抓感觉减退的皮肤而造成自我伤害。一名39岁女性在患眼部带状疱疹后出现严重的疱疹后瘙痒，但无疱疹后神经痛。在1年内，她无痛地搔抓至穿透额骨进入脑部。对瘙痒头皮和正常头皮进行了感觉测试及皮肤活检，以对神经性瘙痒的机制提出初步假设。对PGP9.5免疫标记的皮肤活检标本中的表皮神经纤维进行定量分析，结果显示瘙痒区域的表皮神经支配丧失了96%。定量感觉测试表明，除瘙痒外，大多数感觉模式均受到严重损害。这些数据表明，在该患者中，严重的疱疹后瘙痒与外周感觉神经元的丧失有关。可能的机制包括传入减少的中枢瘙痒特异性神经元的电活动亢进、来自相邻未受影响皮节的外周瘙痒纤维的选择性保留，和/或二级感觉神经元兴奋与抑制之间的失衡。
