基于体素的形态学测量的创伤后应激障碍患者脑结构变化研究

目的探讨交通事故致创伤后应激障碍(PTSD)患者的脑结构形态学改变。方法选择46例经历交通事故后自2021年1月至2022年6月就诊于广东省第二人民医院心理精神科的PTSD患者(PTSD组)以及同期招募的49例性别、年龄相匹配的正常健康者(对照组)为研究对象。所有受试者均行全脑MRI 3D-T1WI结构像扫描, 并应用基于体素的形态学测量(VBM)方法分析2组受试者间脑区灰质体积的差异, 并对PTSD组较对照组有差异的脑区灰质体积与其临床用创伤后应激障碍诊断量表(CAPS)、创伤后应激障碍自评量表(PCL-C)及汉密尔顿抑郁量表(HAMD)评分进行相关性分析。结果与对照组相比, PTSD组左侧海马、左侧中央后回及右侧额上回灰质体积明显缩小, 差异均有统计学意义(P<0.001, GRF校正), 未发现较对照组灰质体积增加的脑区。PTSD组患者的左侧中央后回灰质体积与其CAPS评分呈负相关关系(r=-0.443, P=0.002), 其余有差异的脑区灰质体积与CAPS、PCL-C及HAMD评分间均无相关性(P>0.05)。结论交通事故致PTSD患者存在左侧海马、左侧中央后回及...     

重症监护病房患者配偶创伤后应激障碍海马体积的研究

目的:探索重症监护病房(ICU)患者配偶中患创伤后应激障碍(PTSD)者双侧海马体积变化。方法:采用3.0 T磁共振检查(MRI)对20例ICU患者之配偶中患有PTSD者(PTSD组)及20例未患有PTSD者(对照组)进行全脑3D T1扫描;使用FreeSurfer获取并分析双侧海马体积变化,同时分析PTSD组双侧海马体积与PTSD诊断量表(CAPS)得分的相关性。结果:与对照组比较,PTSD组的双侧海马体积均显著缩小,差异具有统计学意义(P均0.01),但左侧海马体积减小比例大于右侧(左侧15%,右侧11%)。同时PTSD组的左右侧海马均与CAPS得分呈负相关(P均0.05)。结论:ICU患者配偶中患有PTSD者其海马体积存在缩小并存在偏侧性,需要给予及时有效的关心和干预。     

创伤后应激障碍的记忆损害与脑结构磁共振研究

目的 探讨创伤后应激障碍(post-traumatic stress disorder,PTSD)患者的记忆功能损害以及结构性核磁共振的变化.方法 收集符合美国精神障碍诊断与统计手册第四版诊断标准的16例PTSD患者、17例首发抑郁症患者和28名正常对照.采用临床应用的PTSD诊断量表(Clinician Administered PTSD Scale,CAPS)、汉密尔顿焦虑量表、汉密尔顿抑郁量表评定临床症状;韦氏记忆量表评定记忆功能;以磁共振静态三维结构进行影像学检查.结果 PTSD组理解记忆、延迟理解记忆、视觉再生、延迟视觉再生得分均明显低于对照组和抑郁症组(P均小于0.05).PTSD组视觉再生、延迟视觉再生记忆成绩与CAPS得分呈负相关(r=-0.66,P<0.05;r=-0.53,P均小于0.05),但与情绪症状评分均无相关性(P均大于0.05).PTSD组和抑郁症组的额叶、颞叶灰质体积均明显小于对照组(未校正的P<0.001);而PTSD组颞叶灰质体积小于抑郁症组(未校正的P<0.001).结论 PTSD的记忆损害与创伤症状而非抑郁症状明显相关,而其脑结构损害也与抑郁症有所不同,提示PTSD的记忆损害可能独立于抑郁症状之外.     

基于体素的MRI形态学测量对遗忘型轻度认知障碍和轻度阿尔茨海默病脑灰质萎缩的研究

目的：利用磁共振3DT1WI成像研究遗忘型轻度认知障碍（aMCI）、轻度阿尔茨海默病（AD）患者相对于正常老年人灰质体积改变的特点。方法：采用3．0T磁共振,对33例aMCI患者（aMCI组）、32例轻度AD患者（轻度AD组）及31名正常老年人（对照组）进行3DT1WI扫描,利用基于SPM5的DARTEL工具箱对扫描获得的结构图像进行预处理,再对aMCI组、轻度AD组和对照组的全脑灰质体积进行基于体素的统计学比较。结果：与对照组比较,aMCI组左侧海马、海马旁回、舌回、颞上回,双侧岛叶和颞中回等结构的灰质体积萎缩,其差异有显著统计学意义（P〈0．01,FDR corrected,K〉50体素）。轻度AD组的双侧海马、海马旁回及杏仁核、双侧丘脑、双侧颞顶叶皮质等结构灰质体积萎缩,额叶和枕叶皮质也出现灰质萎缩,其差异也有统计学意义（P〈0．05,FDR corrected,K≥50体素）。结论：基于体素的MRI形态学测量能够客观揭示AD早期阶段的脑灰质萎缩改变,对左侧海马萎缩的识别有助于AD的早期诊断。     

阿尔茨海默病谱系患者的海马亚区体积损害特征

目的探讨主观认知障碍(subjective cognitive decline,SCD)、遗忘型轻度认知障碍(amnestic mild cognitive impairment,a MCI)及阿尔茨海默病(Alzheimer’s disease,AD)患者海马亚区体积的萎缩模式及与记忆功能障碍的关联。方法收集2016年6月-2019年5月至南京大学医学院附属鼓楼医院神经内科门诊就诊的151例患者。根据认知测试结果和受试者有无记忆下降主诉,分认知正常组43例,SCD组37例,a MCI组35例和AD组36例。Free Surfer 6. 0图像分析软件计算海马12个亚区体积,偏相关分析海马亚区与记忆功能的相关性。结果随着疾病进展,双侧海马总体积、双侧分子层、左侧海马齿状回、左侧CA4亚区体积显著下降(P均<0. 05)。SCD组内海马亚区体积与记忆功能无显著相关(P> 0. 05),a MCI组内左侧海马尾体积与AVLT-再认评分显著正相关(P<0. 05); AD组内双侧下托、前下托,左侧海马裂、旁下托、分子层、齿状回、CA4、海马杏仁核过渡区、右侧海马伞体积与AVLVT-延时回忆评分相关(P均<0. 05)。结论 SCD患者已经出现海马总体积和部分海马亚区体积萎缩。AD谱系患者的双侧分子层、左侧海马齿状回、左侧CA4亚区体积呈显著下降模式,海马亚区体积与记忆功能相关。     

矿难后急性重性创伤后应激障碍症状激发和创伤有关短期记忆提取的功能性磁共振成像研究

目的 探讨急性重性创伤后应激障碍(post traumatic stress disorder,PTSD)患者的脑功能及执行记忆功能时的脑反应.方法 采用功能磁共振成像技术,对经历矿难的10例急性重性PTSD患者(PTSD组)和7例非PTSD对照(非PTSD组)执行症状激发任务,并首次采用1项创伤有关的短期记忆提取任务进行记忆功能的测定.结果 症状激发试验中,PTSD组负性图片相比中性图片,左侧后扣带回、双侧尾状核和右侧丘脑等脑区激活增强,右侧扣带回和双侧额中回激活下降;PTSD组相比非PTSD组,右侧前扣带回、左侧额下回、双侧额中回及双侧颞中回等脑区激活下降,左侧海马旁回激活增高.短期记忆提取任务中,PTSD组负性图片相比中性图片,右侧后扣带回和双侧海马存在明显激活;PTSD组相比非PTSD组,右侧额下回、右侧额中回、左侧枕中回等脑区激活下降.记忆提取任务相比症状激发任务,PTSD组右侧海马旁回激活下降.结论 急性重性PTSD患者在急性期已存在部分脑区激活的下降以及记忆功能的减退.     

早期创伤后应激障碍的执行功能与额叶损害

目的探讨创伤后应激障碍(Post-traumatic stress disorder,PTSD)患者的执行功能损害特点以及结构性核磁共振的变化。方法收集12例病程小于1年的首发PTSD患者为PTSD组,16名健康志愿者为对照组。PTSD组应用艾司西酞普兰治疗3个月,治疗前后均使用临床应用的PTSD诊断量表(Clinician AdministeredPTSD Scale,CAPS)评估临床症状,威斯康星卡片分类测验(Wisconsin Card Sorting Test,WCST)评定PTSD组执行功能,对照组WCST只评估一次。采用基于体素的形态学分析技术比较PTSD组治疗前后及对照组的脑结构形态。结果 PTSD组治疗前、治疗后总应答数(Ra)、错误应答数(Re)及持续性错误数(Rpe)评分均差于对照组,差异有统计学意义(均P0.05);治疗前Ra、Cc、Re及Rpe评分均差于治疗后,差异有统计学意义(均P0.05)。PTSD组治疗前和治疗后CAPS得分均与执行功能(Ra、Cc、Re、Rp及Rpe)无统计学相关性(P0.05)。PTSD组治疗前额叶部分脑区灰质体积小于对照组[P0.01(uncorrected)],治疗后PTSD患者额叶部分脑区灰质体积较治疗前恢复[P0.01(uncorrected)],但仍小于对照组[P0.01(uncorrected)]。结论 PTSD患者存在明显执行功能障碍,临床症状恢复后,执行功能障碍依然存在。大脑额叶部分脑区灰质体积治疗后不能完全恢复,可能为其认知功能损害的病理基础。     

艾司西酞普兰改善创伤后应激障碍症状及脑结构的磁共振研究

目的 探讨艾司西酞普兰对创伤后应激障碍(PTSD)核心症状、伴发症状及脑结构的影响.方法 收集符合美国精神障碍诊断与统计手册第四版诊断标准的12例PTSD患者,单独应用艾司西酞普兰治疗3个月.采用临床应用的PTSD诊断量表(CAPS)、汉密尔顿抑郁量表(HAMD)、汉密尔顿焦虑量表(HAMA)、威斯康星分类卡片(WCST)、韦氏记忆量表(WMS)对PTSD患者治疗前后进行评估.治疗前后,所有患者进行核磁共振扫描.采用基于体素的形态学分析(VBM)技术,用统计参数 图5(SPM5)软件包分析治疗前后脑灰质体积的差异.结果 PTSD患者经艾司西酞普兰治疗后CAPS、HAMD、HAMA、WCST、WMS评分均较治疗前明显下降(P＜0.05).磁共振结果显示,经艾司西酞普兰治疗后PTSD患者额叶、颞叶等部分脑区灰质体积明显恢复.结论 艾司西酞普兰能有效改善PTSD患者的核心症状,以及伴发的抑郁、焦虑及认知功能损害症状；并明显促进脑灰质体积的恢复.     

强迫障碍患者脑灰质体积改变及其与认知功能和临床症状的相关性

目的比较强迫障碍患者脑灰质体积与健康对照的差异,并分析患者脑灰质体积有改变脑区与认知功能和临床症状的关系。方法选取首发强迫障碍患者36例和年龄、性别、受教育程度相匹配的健康对照35名,进行头部磁共振扫描,采用基于体素的形态学分析测量受试者大脑灰质体积,患者组使用神经认知成套测验和耶鲁—布朗强迫症状量表(Yale-Brown obsessive-compulsive scale,Y-BOCS)评估认知功能和强迫症状。结果与对照组相比,患者组脑灰质体积增加的脑区有额顶叶(左侧中央后回、左侧中央前回)(t=4.299,P0.0005,体素100)、颞叶—边缘系统(左侧梭状回、左侧颞上回、左侧颞中回、左侧海马旁回)(t=4.841,P 0.0005,体素100);脑灰质体积减少的脑区为双侧前扣带回(t=-4.181,P0.0005,体素100)。患者组中,颞叶—边缘系统的灰质体积与社会认知评分正相关(r=0.347,P=0.038),前扣带回的灰质体积与强迫思维评分正相关(r=0.416,P=0.012)。结论强迫障碍患者在额顶叶、颞叶—边缘系统、双侧前扣带回等广泛的脑区存在灰质体积改变,其中颞叶—边缘系统灰质体积与社会认知、前扣带回灰质体积与强迫思维存在关联。     

创伤后应激障碍患者脑结构的磁共振研究

目的探讨创伤后应激障碍（PTSD）患者是否存在大脑结构形态学的改变。方法对12例因火灾事故而致PTSD患者（PTSD组）、12名年龄、性别和创伤暴露均与PTSD组相匹配的正常人（对照组）进行MRI扫描，获取脑结构的T1加权像和3维图像，进行基于像素的形态测量学分析，比较两组灰质、白质密度的异同。结果在控制了年龄和性别的影响后，PTSD组与对照组灰质密度比较的差值，在左侧海马（Talairaeh坐标：x=-26mm，y=-13Inln，z=-17mm，t=5．05）、左侧前扣带回（X=-2mm，y=40mm，z=17mm，t=5．06）和双侧岛叶（右侧岛叶x=34mm，y=4mm，z=6mm，t=4．64；左侧岛叶x=-34mm，y=4mm，z=6mm，t=4．44）的差异有统计学意义（P〈0．001）；两组在其他脑区灰质或白质密度的差异无统计学意义。结论创伤后应激障碍患者的海马、前扣带回和岛叶都有灰质密度的减少，提示这些脑区的结构存在病理性改变。     

Decreased gray matter volume in the left hippocampus and bilateral calcarine cortex in coal mine flood disaster survivors with recent onset PTSD

Although limbic structure changes have been found in chronic and recent onset post-traumatic stress disorder (PTSD) patients, there are few studies about brain structure changes in recent onset PTSD patients after a single extreme and prolonged trauma. In the current study, 20 coal mine flood disaster survivors underwent magnetic resonance imaging (MRI). Voxel-based morphometry (VBM) and region of interest (ROI) techniques were used to detect the gray matter and white matter volume changes in 10 survivors with recent onset PTSD and 10 survivors without PTSD. The correlation between the Clinician-Administered PTSD Scale (CAPS) and gray matter density in the ROI was also studied. Compared with survivors without PTSD, survivors with PTSD had significantly decreased gray matter volume and density in left anterior hippocampus, left parahippocampal gyrus, and bilateral calcarine cortex. The CAPS score correlated negatively with the gray matter density in bilateral calcarine cortex and left hippocampus in coal mine disaster survivors. Our study suggests that the gray matter volume and density of limbic structure decreased in recent onset PTSD patients who were exposed to extreme trauma. PTSD symptom severity was associated with gray matter density in calcarine cortex and hippocampus.     

Changes in brain anatomy during the course of posttraumatic stress disorder

The goal of this study was to determine whether posttraumatic stress disorder (PTSD) was associated with an increase in time-related decline in macrostructural brain volume and whether these changes were associated with accelerated cognitive decline. To quantify brain structure, three-dimensional T1−weighted MRI scans were performed at baseline and again after a minimum of 24 months in 25 patients with PTSD (PTSD+) and 22 controls (PTSD−). Longitudinal changes in brain volume were measured using deformation morphometry. For the group as a whole, PTSD+ patients did not show significant ongoing brain atrophy compared to PTSD−. PTSD+ patients were then subgrouped into those with decreasing or increasing symptoms. We found little evidence for brain markers of accelerated atrophy in PTSD+ veterans whose symptoms improved over time, with only a small left parietal region showing greater ongoing tissue loss than PTSD−. PTSD patients whose symptoms increased over time showed accelerated atrophy throughout the brain, particularly brainstem and frontal and temporal lobes. Lastly, for the sample as a whole, greater rates of brain atrophy were associated with greater rates of decline in verbal memory and delayed facial recognition.     

Reduced hippocampal volume and total white matter volume in posttraumatic stress disorder.

BACKGROUND: Reduced hippocampal volumes in posttraumatic stress disorder (PTSD) patients are thought to reflect specific changes of this structure. Previous magnetic resonance imaging (MRI) studies have not consistently examined indices of overall brain atrophy, therefore it cannot be completely ruled out that hippocampal changes are explained by whole-brain atrophy. The purpose of this study was to assess hippocampal and whole-brain volume in civilian PTSD. METHODS: Twelve subjects with PTSD and 10 control subjects underwent brain MRI. Hippocampal volumes were visually quantified using a computerized volumetric program. Whole-brain volumes were obtained with automated k-means-based segmentation. RESULTS: No differences were found in intracranial volumes (ICV). Subjects with PTSD had higher cerebrospinal fluid (CSF)/ICV ratios and lower white matter/ICV ratios, consistent with generalized white matter (WM) atrophy. The effect of age on CSF/ICV was more pronounced in the PTSD group. Subjects with PTSD had smaller absolute and normalized bilateral hippocampal volumes. These differences persisted after adjusting for lifetime weeks of alcohol intoxication. Posttraumatic stress disorder and depression scores correlated negatively with left hippocampal volume, but PTSD scores were a better predictor of hippocampal volumes. CONCLUSIONS: Our results replicate previous findings of reduced hippocampal volume in PTSD but also suggest independent, generalized, white matter atrophy.     

矿难后急性重性创伤后应激障碍症状激发和创伤有关短期记忆提取的功能性磁共振成像研究

目的 探讨急性重性创伤后应激障碍(post traumatic stress disorder,PTSD)患者的脑功能及执行记忆功能时的脑反应.方法 采用功能磁共振成像技术,对经历矿难的10例急性重性PTSD患者(PTSD组)和7例非PTSD对照(非PTSD组)执行症状激发任务,并首次采用1项创伤有关的短期记忆提取任务...     

The Neurofunctional Mechanisms of Traumatic and Non-Traumatic Memory in Patients with Acute PTSD Following Accident Trauma

Neurofunctional alterations in acute posttraumatic stress disorder (PTSD) and changes thereof during the course of the disease are not well investigated. We used functional magnetic resonance imaging to assess the functional neuroanatomy of emotional memory in surgical patients with acute PTSD. Traumatic (relative to non-traumatic) memories increased neural activity in the amygdala, hippocampus, lateral temporal, retrosplenial, and anterior cingulate cortices. These regions are all implicated in memory and emotion. A comparison of findings with data on chronic PTSD suggests that brain circuits affected by the acute disorder are extended and unstable while chronic disease is characterized by circumscribed and stable neurofunctional abnormalities.     

Two-year prospective evaluation of the relationship between acute stress disorder and posttraumatic stress disorder following mild traumatic brain injury

OBJECTIVE: To assess the ability of acute stress disorder to predict posttraumatic stress disorder (PTSD), the relationship between acute stress disorder and PTSD over the 2 years following mild traumatic brain injury was determined. METHOD: Survivors of motor vehicle accidents who sustained mild traumatic brain injuries were assessed for acute stress disorder within 1 month of the trauma (N=79) and for PTSD at 6 months (N=63) and 2 years (N=50) posttrauma. RESULTS: Acute stress disorder was diagnosed in 14% of the patients. Among the patients who participated in all three assessments, 80% of the subjects who met the criteria for acute stress disorder were diagnosed with PTSD at 2 years. Of the total initial group, 73% of those diagnosed with acute stress disorder had PTSD at 2 years. CONCLUSIONS: This study provides further support for the utility of the acute stress disorder diagnosis as a predictor of PTSD but indicates that the predictive power of the diagnostic criteria can be increased by placing greater emphasis on reexperiencing, avoidance, and arousal symptoms.     

The neurofunctional mechanisms of traumatic and non-traumatic memory in patients with acute PTSD following accident trauma

Neurofunctional alterations in acute posttraumatic stress disorder (PTSD) and changes thereof during the course of the disease are not well investigated. We used functional magnetic resonance imaging to assess the functional neuroanatomy of emotional memory in surgical patients with acute PTSD. Traumatic (relative to non-traumatic) memories increased neural activity in the amygdala, hippocampus, lateral temporal, retrosplenial, and anterior cingulate cortices. These regions are all implicated in memory and emotion. A comparison of findings with data on chronic PTSD suggests that brain circuits affected by the acute disorder are extended and unstable while chronic disease is characterized by circumscribed and stable neurofunctional abnormalities.     

Neural correlates of declarative memory for emotionally valenced words in women with posttraumatic stress disorder related to early childhood sexual abuse.

BACKGROUND: Animal studies have shown that early stressors result in lasting changes in structure and function of brain areas involved in memory, including hippocampus and frontal cortex. Patients with childhood abuse-related posttraumatic stress disorder (PTSD) have alterations in both declarative and nondeclarative memory function, and imaging studies in PTSD have demonstrated changes in function during stimulation of trauma-specific memories in hippocampus, medial prefrontal cortex, and cingulate. The purpose of this study was to assess neural correlates of emotionally valenced declarative memory in women with early childhood sexual abuse and PTSD. METHODS: Women with early childhood sexual abuse-related PTSD (n = 10) and women without abuse or PTSD (n = 11) underwent positron emission tomographic (PET) measurement of cerebral blood flow during a control condition and during retrieval of neutral (e.g., "metal-iron") and emotionally valenced (e.g., "rape-mutilate") word pairs. RESULTS: During retrieval of emotionally valenced word pairs, PTSD patients showed greater decreases in blood flow in an extensive area, which included orbitofrontal cortex, anterior cingulate, and medial prefrontal cortex (Brodmann's areas 25, 32, 9), left hippocampus, and fusiform gyrus/inferior temporal gyrus, with increased activation in posterior cingulate, left inferior parietal cortex, left middle frontal gyrus, and visual association and motor cortex. There were no differences in patterns of brain activation during retrieval of neutral word pairs between patients and control subjects. CONCLUSIONS: These findings are consistent with dysfunction of specific brain areas involved in memory and emotion in PTSD. Regions implicated in this study of emotionally valenced declarative memory are similar to those from prior imaging studies in PTSD using trauma-specific stimuli for symptom provocation, adding further supportive evidence for a dysfunctional network of brain areas involved in memory, including hippocampus, medial prefrontal cortex, and cingulate, in PTSD.     

Alterations in brain structure and function associated with post-traumatic stress disorder.

Neuroimaging studies in post-traumatic stress disorder (PTSD) have revealed changes in brain structure and function that may underlie the symptoms of PTSD. Two brain areas that have been consistently implicated in PTSD include the hippocampus and prefrontal cortex. Several studies showed that PTSD is associated with reduction in volume of the hippocampus, a brain area involved in learning and memory, as measured with magnetic resonance imaging (MRI). Positron emission tomography (PET) studies showed dysfunction of medial and orbital prefrontal cortex during PTSD symptom provocation and in response to traumatic reminders. Decreased benzodiazepine receptor binding was found in the medial prefrontal cortex as measured with neuroimaging in PTSD. The hippocampus and medial prefrontal cortex play important roles in memory and emotional regulation, and dysfunction in these areas may underlie memory deficits and pathological emotions in PTSD.