Noda K, Katayama S, Watanabe C, Yamamura Y, Nakamura S
Third Department of Internal Medicine, Hiroshima University, Japan.
J Neurol Sci. 1997 Oct 3;151(1):89-91. doi: 10.1016/s0022-510x(97)00101-9.
The physiological functions of the medullary arcuate nucleus are supposed to be involved in autonomic cardioventilatory regulation, but neuropathological studies on neurodegenerative diseases have rarely reported about the arcuate nucleus. We quantitatively examined the neuronal density of the arcuate nucleus in patients with multiple system atrophy (MSA, n = 3), Parkinson's disease (PD, n = 3), amyotrophic lateral sclerosis (ALS, n = 2), and control subjects (n = 6), and statistically compared the findings in each group. Although the neuronal densities in PD and ALS patients were not different from that in the controls, MSA patients showed a marked depletion of neurons in the arcuate nucleus. The neuronal density (/mm2, mean +/- SEM) in the arcuate nucleus was 9.27 +/- 10.4 in MSA, and was significantly decreased (P < 0.05; Wilcoxon test), compared with that in control subjects (87.1 +/- 12.2). These results suggest that the lesioned arcuate nucleus is related to the pathogenesis of dysatonomia in MSA.
延髓弓状核的生理功能被认为参与自主心血管呼吸调节,但关于神经退行性疾病的神经病理学研究很少报道弓状核的情况。我们对多系统萎缩患者(MSA,n = 3)、帕金森病患者(PD,n = 3)、肌萎缩侧索硬化患者(ALS,n = 2)和对照受试者(n = 6)的弓状核神经元密度进行了定量检测,并对每组结果进行了统计学比较。虽然PD和ALS患者的神经元密度与对照组无差异,但MSA患者的弓状核神经元明显减少。MSA患者弓状核的神经元密度(/mm²,平均值±标准误)为9.27±10.4,与对照受试者(87.1±12.2)相比显著降低(P < 0.05;Wilcoxon检验)。这些结果表明,受损的弓状核与MSA中自主神经功能障碍的发病机制有关。