Gropman Andrea L, Anderson Afrouz
Department of Neurology, Children's National Medical Center, Washington, DC 20010, USA.
Department of Research, Focus Foundation, Crofton, MD 21035, USA.
J Transl Genet Genom. 2020;4:429-445. doi: 10.20517/jtgg.2020.09. Epub 2020 Nov 13.
Many inborn errors of metabolism and genetic disorders affect the brain. The brain biochemistry may differ from that in the periphery and is not accessible by simple blood and urine sampling. Therefore, neuroimaging has proven to be a valuable tool to not only evaluate the brain structure, but also biochemistry, blood flow and function. Neuroimaging in patients with inborn errors of metabolism can include additional sequences in addition to T1 and T2-weighted imaging because in early stages, there may be no significant findings on the routine sequnces due to the lack of sensitivity or the evolution of abnormalities lags behind the ability of the imaging to detect it. In addition, findings on T1 and T2-weighted imaging of several inborn errors of metabolism may be non-specific and be seen in other non-genetic conditions. Therefore, additional neuroimaging modalities that have been employed including diffusion tensor imaging (DTI), magnetic resonance spectroscopy, functional MRI (fMRI), functional near infrared spectroscopy (fNIRS), or positron emission tomography (PET) imaging may further inform underlying changes in myelination, biochemistry, and functional connectivity. The use of Magnetic Resonance Spectroscopy in certain disorders may add a level of specificity depending upon the metabolite levels that are abnormal, as well as provide information about the process of brain injury (i.e., white matter, gray matter, energy deficiency, toxic buildup or depletion of key metabolites). It is even more challenging to understand how genetic or metabolic disorders contribute to short and/or long term changes in cognition which represent the downstream effects of IEMs. In order to image "cognition" or the downstream effects of a metabolic disorder on domains of brain function, more advanced techniques are required to analyze underlying fiber tracts or alternatively, methods such as fMRI enable generation of brain activation maps after both task based and resting state conditions. DTI can be used to look at changes in white matter tracks. Each imaging modality can explore an important aspect of the anatomy, physiology or biochemisty of the central nervous system. Their properties, pros and cons are discussed in this article. These imaging modalities will be discussed in the context of several inborn errors of metabolism including Galactosemia, Phenylketonruia, Maple syrup urine disease, Methylmalonic acidemia, Niemann-Pick Disease, type C1, Krabbe Disease, Ornithine transcarbamylase deficiency, Sjogren Larsson syndrome, Pelizeaus-Merzbacher disease, Pyruvate dehydrogenase deficiency, Nonketotic Hyperglycinemia and Fabry disease. Space constraints do not allow mention of all the disorders in which one of these modalities has been investigated, or where it would add value to diagnosis or disease progression.
许多先天性代谢缺陷和遗传疾病会影响大脑。大脑的生物化学过程可能与外周不同,无法通过简单的血液和尿液采样来了解。因此,神经影像学已被证明是一种有价值的工具,不仅可以评估大脑结构,还可以评估生物化学、血流和功能。对于患有先天性代谢缺陷的患者,神经影像学检查除了T1加权成像和T2加权成像外,还可包括其他序列,因为在疾病早期,由于缺乏敏感性或异常变化的发展滞后于成像检测能力,常规序列可能没有明显发现。此外,几种先天性代谢缺陷在T1加权成像和T2加权成像上的表现可能不具有特异性,也可见于其他非遗传疾病。因此,已采用的其他神经影像学检查方法,包括扩散张量成像(DTI)、磁共振波谱、功能磁共振成像(fMRI)、功能近红外光谱(fNIRS)或正电子发射断层扫描(PET)成像,可能会进一步揭示髓鞘形成、生物化学和功能连接方面的潜在变化。在某些疾病中使用磁共振波谱可能会根据异常的代谢物水平增加一定程度的特异性,并提供有关脑损伤过程的信息(即白质、灰质、能量缺乏、关键代谢物的毒性积累或消耗)。理解遗传或代谢疾病如何导致认知的短期和/或长期变化更具挑战性,而认知变化代表了先天性代谢缺陷的下游效应。为了成像“认知”或代谢紊乱对脑功能领域的下游效应,需要更先进的技术来分析潜在的纤维束,或者,诸如功能磁共振成像等方法能够在基于任务和静息状态条件下生成脑激活图。扩散张量成像可用于观察白质束的变化。每种成像方式都可以探索中枢神经系统解剖学、生理学或生物化学的一个重要方面。本文将讨论它们的特性、优缺点。这些成像方式将在几种先天性代谢缺陷的背景下进行讨论,包括半乳糖血症、苯丙酮尿症、枫糖尿症、甲基丙二酸血症、尼曼-匹克病C1型、克拉伯病、鸟氨酸转氨甲酰酶缺乏症、舍格伦-拉尔松综合征、佩利措伊斯-梅茨巴赫病、丙酮酸脱氢酶缺乏症、非酮症高甘氨酸血症和法布里病。篇幅所限,无法提及所有已对其中一种成像方式进行研究的疾病,或者该成像方式对诊断或疾病进展有价值的所有疾病。