Aydin Nazan, Ramazanoglu Leyla, Onen Mehmet Resid, Yilmaz Ilhan, Aydin Mehmet Dumlu, Altinkaynak Konca, Calik Muhammet, Kanat Ayhan
Department of Psychiatry, Mazhar Osman Mental Health Disease Hospital, Bakirkoy, Istanbul, Turkey.
Clinic of Neurology, Health Science University, FSM Research and Training Hospital, Istanbul, Turkey.
World Neurosurg. 2017 Nov;107:400-408. doi: 10.1016/j.wneu.2017.07.180. Epub 2017 Aug 8.
Hypothyroidism is defined as an underactive thyroid gland and one of the reasons for inadequate stimulation of thyroid is dysfunction of the hormone regulating brain centers. Olfaction disorders have been considered as a problem in hypothyroidism. It has been hypothesized that olfaction disorders reduce olfactory stimulation and diminished olfactory stimulus may trigger hypothyroidism. In this study, an examination was made of the thyroid hormone levels, histologic features of thyroid glands, and vagal nerve network degradation in an experimental animal model of olfactory bulbectomy (OBX).
A total of 25 rats were divided into control (n = 5), SHAM (n = 5), and OBX (n = 15) groups and were followed up for 8 weeks. Thyroid hormone levels were measured before (1 time), during the experiment (1 time/month) and the animals were decapitated. The olfactory bulbs, dorsal motor nucleus of the vagal nerves, and thyroid gland sections were stained with hematoxylin-eosin and tunnel dye to determine OBX-related damage. Specimens were analyzed stereologically to evaluate neuron density of the vagal nucleus and hormone-filled total follicle volume (TFV) per cubic centimeter, and these were statistically compared with thyroid hormone levels.
The mean degenerated neuron density of the vagal nucleus was 21 ± 8/mm. TFV and triiodothyronine (T)-thyroxine (T) levels were measured as TFV, (312 ± 91) × 10μm/cm; T, 105 μg/dl; T, 1.89 μg/dl in control (group I). Mean degenerated neuron density, 56 ± 12/mm; TFV, (284 ± 69) × 10μm/cm; T, 103 μg/dl; T, 1.85 μg/dl in SHAM (group II). Mean degenerated neuron density, 235 ± 64/mm; TFV, (193 ± 34) × 10μm/cm; T, 86 μg/dl; T, 1.37 μg/dl in the OBX group (group III). The TFV were significantly diminished because of apoptotic degradation in olfactory bulbs and thyroid gland with decreased T- T levels with increased thyroid-stimulating hormone levels in OBX-applied animals of subarachnoid hemorrhage (P < 0.005).
The results suggested that diminished hormone secretion as a result of thyroid gland degradation results in both olfaction loss and vagal complex degeneration in OBX animals, contrary to the common belief that anosmia results from hypothyroidism.
甲状腺功能减退症定义为甲状腺功能低下,甲状腺刺激不足的原因之一是调节激素的脑中枢功能障碍。嗅觉障碍一直被认为是甲状腺功能减退症中的一个问题。据推测,嗅觉障碍会减少嗅觉刺激,而嗅觉刺激减弱可能会引发甲状腺功能减退症。在本研究中,对嗅球切除(OBX)实验动物模型的甲状腺激素水平、甲状腺组织学特征及迷走神经网络退化情况进行了检查。
将25只大鼠分为对照组(n = 5)、假手术组(n = 5)和OBX组(n = 15),并随访8周。在实验前(1次)、实验期间(每月1次)测量甲状腺激素水平,之后将动物断头。用苏木精-伊红和隧道染料对嗅球、迷走神经背运动核及甲状腺切片进行染色,以确定与OBX相关的损伤。对标本进行体视学分析,以评估迷走神经核的神经元密度及每立方厘米充满激素的总滤泡体积(TFV),并将这些结果与甲状腺激素水平进行统计学比较。
迷走神经核的平均退化神经元密度为21±8/mm。对照组(I组)的TFV及三碘甲状腺原氨酸(T)-甲状腺素(T)水平分别为TFV,(312±91)×10μm/cm;T,105μg/dl;T,1.89μg/dl。假手术组(II组)的平均退化神经元密度为56±12/mm;TFV,(284±69)×10μm/cm;T,103μg/dl;T,1.85μg/dl。OBX组(III组)的平均退化神经元密度为235±64/mm;TFV,(193±34)×10μm/cm;T,86μg/dl;T,1.37μg/dl。在蛛网膜下腔出血的OBX应用动物中,由于嗅球和甲状腺的凋亡性退化,TFV显著降低,T-T水平降低,促甲状腺激素水平升高(P < 0.005)。
结果表明,与嗅觉减退由甲状腺功能减退症引起的普遍观点相反,OBX动物中甲状腺退化导致的激素分泌减少会导致嗅觉丧失和迷走神经复合体退化。