Pezeshkpour G H, Dalakas M C
Neuromuscular Pathology Division, Armed Forces Institute of Pathology, Washington, DC.
Arch Neurol. 1988 May;45(5):505-8. doi: 10.1001/archneur.1988.00520290033010.
In a retrospective study, we reviewed sections from the spinal cords from eight patients, aged 36 to 61 years, who had had poliomyelitis and who died of nonneurologic diseases nine months to 44 years (mean, 20.7 years) after the acute poliomyelitis infection. Five patients had stable postpoliomyelitis deficits without new symptoms, and three patients had new slowly progressive muscle weakness defined as postpoliomyelitis progressive muscular atrophy (PPMA). Representative spinal cord sections matched the patients' clinical involvement in both groups. Control tissues from ten patients with amyotrophic lateral sclerosis and five with spinocerebellar degeneration were examined simultaneously. The spinal cord segments from all patients who had had poliomyelitis showed loss or atrophy of motor neurons, severe reactive gliosis (disproportional to the neuronal loss), and a surprising mild to moderate perivascular and interparenchymal inflammation. There was no difference in these pathologic changes between the patients with stable postpoliomyelitis deficits and those with PPMA. Additional findings were axonal spheroids (dystrophic axons) and occasional chromatolytic neurons in the spinal cord of patients with PPMA. Corticospinal tracts were spared.
在一项回顾性研究中，我们检查了8例患者脊髓切片，这些患者年龄在36至61岁之间，曾患小儿麻痹症，并在急性感染小儿麻痹症后9个月至44年（平均20.7年）死于非神经系统疾病。5例患者患有稳定的小儿麻痹后遗症缺陷且无新症状，3例患者出现新的缓慢进展性肌无力，定义为小儿麻痹后遗症进行性肌肉萎缩（PPMA）。两组患者的代表性脊髓切片均与临床受累情况相符。同时检查了10例肌萎缩侧索硬化症患者和5例脊髓小脑变性患者的对照组织。所有曾患小儿麻痹症患者的脊髓节段均显示运动神经元丧失或萎缩、严重的反应性胶质增生（与神经元丧失不成比例）以及令人惊讶的轻度至中度血管周围和实质间炎症。稳定的小儿麻痹后遗症缺陷患者和PPMA患者之间的这些病理变化没有差异。其他发现包括PPMA患者脊髓中的轴突球体（营养不良性轴突）和偶尔的染色质溶解神经元。皮质脊髓束未受累。
