1 Interdisciplinary Center on Smell and Taste , Department of Otorhinolaryngology, TU Dresden , Dresden, Germany .
2 Department of Neuroradiology, TU Dresden , Dresden, Germany .
J Neurotrauma. 2018 Nov 15;35(22):2632-2640. doi: 10.1089/neu.2017.5393. Epub 2018 Jul 23.
Olfactory loss and traumatic brain injury (TBI) both lead to anatomical brain alterations in humans. Little research has been done on the structural brain changes for TBI patients with olfactory loss. Using voxel-based morphometry, the gray matter (GM) density was examined for 22 TBI patients with hyposmia, 24 TBI patients with anosmia, and 22 age-matched controls. Olfactory bulb (OB) volumes were measured by manual segmentation of acquired T2-weighted coronal slices using a standardized protocol. Brain lesions in the olfactory-relevant areas also were examined for TBI patients. Results showed that patients with anosmia have more frequent lesions in the OB, orbitofrontal cortex (OFC), and the temporal lobe pole, compared with patients with hyposmia. GM density in the primary olfactory area was decreased in both groups of patients. In addition, compared with controls, patients with anosmia showed GM density reduction in several secondary olfactory eloquent regions, including the gyrus rectus, medial OFC, anterior cingulate cortex, insula, and cerebellum. However, patients with hyposmia showed a lesser degree of GM reduction, compared with healthy controls. Smaller OB volumes were found for patients with olfactory loss, compared with controls. TBI patients with anosmia had the smallest OB volumes, which were caused by the lesions for OB. In addition, post-TBI duration was negatively correlated with GM density in the secondary olfactory areas in patients with hyposmia, but was positively correlated with GM density in the frontal and temporal gyrus in patients with anosmia. The GM density and OB volume reduction among TBI patients with olfactory loss was largely dependent on the location and severity of brain lesions in olfactory-relevant regions. Longer post-TBI duration had an impact on brain GM density changes, which indicate a decreased olfactory function in patients with hyposmia and possible compensatory mechanisms in patients with anosmia.
嗅觉丧失和创伤性脑损伤(TBI)都会导致人类大脑解剖结构的改变。对于嗅觉丧失的 TBI 患者,关于其大脑结构变化的研究较少。本研究使用基于体素的形态测量学方法,对 22 名嗅觉减退的 TBI 患者、24 名嗅觉丧失的 TBI 患者和 22 名年龄匹配的对照组进行了灰质(GM)密度检查。使用标准化方案通过手动分割获得的 T2 加权冠状切片来测量嗅球(OB)体积。还检查了与嗅觉相关区域的 TBI 患者的脑损伤情况。结果表明,与嗅觉减退的患者相比,嗅觉丧失的患者在 OB、眶额皮质(OFC)和颞极更频繁地出现病变。两组患者的初级嗅觉区 GM 密度均降低。此外,与对照组相比,嗅觉丧失的患者在几个次级嗅觉相关区域的 GM 密度降低,包括直回、内侧 OFC、前扣带皮层、脑岛和小脑。然而,与健康对照组相比,嗅觉减退的患者 GM 减少程度较小。与对照组相比,嗅觉丧失的患者 OB 体积较小。嗅觉丧失的 TBI 患者的 OB 体积较小,这是由 OB 的病变引起的。此外,在嗅觉减退的患者中,TBI 后的时间与次级嗅觉区域的 GM 密度呈负相关,而在嗅觉丧失的患者中,TBI 后的时间与额颞叶回的 GM 密度呈正相关。嗅觉丧失的 TBI 患者的 GM 密度和 OB 体积减少在很大程度上取决于与嗅觉相关区域的脑损伤位置和严重程度。TBI 后时间的延长对脑 GM 密度变化有影响,这表明嗅觉减退的患者嗅觉功能下降,嗅觉丧失的患者可能存在代偿机制。