最近一项研究发现嗅觉受损或可与重症肌无力相关。嗅觉和味觉改变是阿尔兹海默病和帕金森病的早期表现，但现在，来自宾夕法尼亚大学的研究显示嗅觉受损和重症肌无力存在一定的相关性。该研究结果发表在最新一期 PLOS ONE杂志上。
宾夕法尼亚大学嗅觉和味觉研究中心主任、高级研究员Richard Doty博士介绍说：“该项研究首次阐述了重症肌无力与嗅觉系统显著的功能障碍相关，与阿尔兹海默病和帕金森病伴发嗅觉障碍的情况相似。研究结果强力证明了重症肌无力不仅仅只是单纯的外周神经系统性疾病，而且可能与大脑也密切相关。”
普遍观念认为重症肌无力仅仅是外周神经系统疾病这，部分原因是由于在该病患者大脑中没有发现明显的病理改变.虽有行为学和生理学证据支持重症肌无力伴有中枢神经系统改变,但由于结果不具有重复性而未予重视.例如,有研究发现重症肌无力相关性语言记忆障碍,但也有研究并不支持.此外,科学家们持续报道重症肌无力相关性中枢神经功能障碍,比如视觉、听觉损害.另外，重症肌无力患者脑电图检查也有异常改变，其脑脊液中还可检测出重症肌无力相关抗体。
为了进一步探索中枢神经系统在重症肌无力中的作用，Richard Doty博士和他的同事们进行了嗅觉试验，该实验曾被用于评估嗅觉与其它一些神经变性性疾病 的潜在联系。Richard Doty博士说：“我们的嗅觉与很多大脑功能都有着直接的联系，嗅觉可作为其它复杂大脑神经环路一个良好模型系统。对嗅觉的认识与否，将会拓宽对大脑功能以及起源自大脑的疾病的理解。
在Richard Doty博士进行的研究中，纳入了27名重症肌无力患者，27例性别和年龄正常人群匹配对照者，11名多发性肌炎患者。 所有研究对象均进行嗅觉识别检测(UPSIT)和图形识别检测试验。研究人员发现重症肌无力患者的嗅觉识别检测评分明显低于同性别年龄对照组和多发性肌炎患者。重症肌无力患者中，只有15%患者在进行该实验之前已知存在嗅觉问题。
Doty博士说：“重症肌无力患者与正常对照组比，存在显著的嗅觉功能障碍，这一点不能被任何其它生理或者认知功能差异所解释。尽管目前我们还在探寻重症肌无力患者伴嗅觉障碍的生理学基础，但有一点需要强调的是：该项研究中发现的嗅觉障碍与其它中枢神经系统疾病伴发嗅觉障碍程度相似，包括阿尔茨海默病和帕金森病。“
根据以上研究结果，作者认为有必要进行更大规模试验探寻重症肌无力的中枢神经系统病变基础，如有可能，嗅觉检测将有助于该病的识别和进展监测。他们还建议临床医师应该与重症肌无力患者讨论嗅觉障碍情况，警醒患者避免一些环境灾害例如食物烧糊、天然气泄漏、火灾等，甚至包括由于感官减退导致的潜在营养问题。（生物谷Bioon.com）
doi: 10.1371/journal.pone.0045544
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Profound olfactory dysfunction in myasthenia gravis
Leon-Sarmiento FE, Bayona EA, Bayona-Prieto J, Osman A, Doty RL.
In this study we demonstrate that myasthenia gravis, an autoimmune disease strongly identified with deficient acetylcholine receptor transmission at the post-synaptic neuromuscular junction, is accompanied by a profound loss of olfactory function. Twenty-seven MG patients, 27 matched healthy controls, and 11 patients with polymiositis, a disease with peripheral neuromuscular symptoms analogous to myasthenia gravis with no known central nervous system involvement, were tested. All were administered the University of Pennsylvania Smell Identification Test (UPSIT) and the Picture Identification Test (PIT), a test analogous in content and form to the UPSIT designed to control for non-olfactory cognitive confounds. The UPSIT scores of the myasthenia gravis patients were markedly lower than those of the age- and sex-matched normal controls [respective means (SDs)?=?20.15 (6.40) & 35.67 (4.95); p<0.0001], as well as those of the polymiositis patients who scored slightly below the normal range [33.30 (1.42); p<0.0001]. The latter finding, along with direct monitoring of the inhalation of the patients during testing, implies that the MG-related olfactory deficit is unlikely due to difficulties sniffing, per se. All PIT scores were within or near the normal range, although subtle deficits were apparent in both the MG and PM patients, conceivably reflecting influences of mild cognitive impairment. No relationships between performance on the UPSIT and thymectomy, time since diagnosis, type of treatment regimen, or the presence or absence of serum anti-nicotinic or muscarinic antibodies were apparent. Our findings suggest that MG influences olfactory function to the same degree as observed in a number of neurodegenerative diseases in which central nervous system cholinergic dysfunction has been documented.
