目的:通过表面形态学(SBM)测量带状疱疹(HZ)和带状疱疹后遗神经痛(PHN)患者大脑皮层厚度的变化,并进一步评估其与临床评分的相关性。
方法:29位HZ患者,包括30名PHN患者和30名匹配良好的健康对照(HC)。收集所有受试者的磁共振成像(MRI)数据,然后通过SBM进行分析。HZ之间皮质厚度的变化,PHN和HC组通过ANOVA分析并与临床评分相关。
结果:双侧初级视觉皮层(V1,V2)和右侧初级视觉皮层(V3)的厚度,左体感皮层(L3A),PHN组右前扣带回和内侧前额叶皮质(RS32)增加,以及左岛和额叶皮层(LFOP4)的厚度,左运动皮层(L3B),与HC组相比,HZ和PHN组的右颞上视觉皮层(RSTV)降低。HZ和PHN患者的RS32,LFOP4和(L3B)的厚度测量与疾病持续时间相关。在HZ和PHN患者中,汉密尔顿焦虑量表(HAMA)与汉密尔顿抑郁量表(HAMD)评分呈显著正相关。
结论:与感觉相关的区域皮质厚度的变化,电机,PHN患者的认知/情绪变化会影响大脑的神经可塑性过程,这可能是HZ转化为PHN的原因,并为PHN患者疼痛持续的神经病理学机制提供了可能的解释。
OBJECTIVE: To measure the changes in cerebral cortical thickness in patients with herpes zoster (HZ) and postherpetic neuralgia (PHN) by surface-based morphometry (
SBM) and further estimate its correlation with clinical scores.
METHODS: Twenty-nine HZ patients, 30 PHN patients and 30 well-matched healthy controls (HCs) were included. Magnetic resonance imaging (MRI) data from all subjects were collected and then analyzed by
SBM. The changes in cortical thickness among the HZ, PHN and HC groups were analyzed by ANOVA and correlated with clinical scores.
RESULTS: The thickness of the bilateral primary visual cortex (V1, V2) and right primary visual cortex (V3), left somatosensory cortex (L3A), right anterior cingulate gyrus and medial prefrontal cortex (RS32) increased in PHN group, and the thickness the left insular and frontal opercular cortex (LFOP4), left motor cortex (L3B), and right superior temporal visual cortex (RSTV) were decreased in the HZ and PHN groups compared to the HC group. The thickness measurements of RS32, LFOP4, and (L3B) in HZ and PHN patients were correlated with the duration of disease. In HZ and PHN patients, the Hamilton Anxiety Scale (HAMA) and Hamilton Depression Scale (HAMD) scores were significantly positively correlated.
CONCLUSIONS: Changes in cortical thickness in the areas related to sensory, motor, and cognitive/emotional changes in patients with PHN affect the neuroplasticity process of the brain, which may be the reason for the transformation of HZ into PHN and provide a possible explanation for the neuropathological mechanism of pain persistence in PHN patients.