Yamashita Mariko, Yamamoto Toru, Nakamura Michikazu
Department of Neurology, Osaka Saiseikai Nakatsu Hospital, 2-10-39 Shibata, Kita-ku, Osaka 530-0012, Japan.
No To Shinkei. 2003 Dec;55(12):1033-9.
We examined the peroneus brevis (PB) muscles obtained with the sural nerves from 12 consecutively biopsied patients who were clinically and electrophysiologically ascertained to have peripheral neuropathies. Histopathological examinations revealed fiber type grouping in all of the 12 PB muscles and group atrophy associated with hypertrophic fibers in 6. These neuropathic changes were ascribable to denervation and reinnervation, being compatible with the neuropathies. Further, internal nuclei were noted in all PB muscles, and fiber splittings in 10. These myopathic changes tended to be more pronounced in the PB muscles having severe neuropathic changes and regarded as the alteration secondary to the preceding neuropathic changes. Degenerated muscle fibers, consisting of phagocytosis, basophilia and whorled fibers, were sparsely found in 8 PB muscles, while rare necrotic fibers were seen in 2. Type 1 fiber predominance was present in 7 PB muscles, in 4 of which the ratio of type 1 fiber was more than 67%. Overall, the neuropathic changes were milder in the PB muscles of CIDP patients and more marked in those showing definite axonal degeneration in the sural nerve. The severity of the neuropathic changes in the PB muscles, however, did not necessarily correlate with the strength of the leg muscles, prognoses of the diseases or the results of the nerve conduction study in the peroneal nerve. The PB muscle is liable to be affected by trauma or aging, which may modify the histopathological features of the biopsied PB muscle and therefore make the relationship between the clinical findings and the alteration of this muscle seems obscured. The available data of PB muscle have been sparse, particularly in the normal individuals, and we should be cautious in interpretation of the results of PB muscle biopsy.
我们检查了12例经临床和电生理确诊为周围神经病的连续活检患者的腓骨短肌(PB)及腓肠神经。组织病理学检查显示,12例PB肌均有纤维类型群组化,6例伴有肥大纤维的群组萎缩。这些神经病变改变归因于失神经支配和再支配,与周围神经病相符。此外,所有PB肌均可见内部细胞核,10例有纤维分裂。这些肌病性改变在神经病变严重的PB肌中往往更明显,被认为是先前神经病变继发的改变。8例PB肌中散在发现由吞噬作用、嗜碱性和漩涡状纤维组成的变性肌纤维,2例可见罕见的坏死纤维。7例PB肌中1型纤维占优势,其中4例1型纤维比例超过67%。总体而言,慢性炎性脱髓鞘性多发性神经病(CIDP)患者的PB肌神经病变改变较轻,而腓肠神经有明确轴索变性的患者则更明显。然而,PB肌神经病变改变的严重程度不一定与腿部肌肉力量、疾病预后或腓总神经神经传导研究结果相关。PB肌易受创伤或衰老影响,这可能会改变活检PB肌的组织病理学特征,从而使临床发现与该肌肉改变之间的关系似乎变得模糊。关于PB肌的现有数据很少,尤其是在正常个体中,我们在解释PB肌活检结果时应谨慎。