定量分析在系统性红斑狼疮脑病SPECT脑显像中的应用

目的:探讨定量分析在SPECT脑99mTc-ECD显像检测系统性红斑狼疮(SLE)脑病中的应用价值和目测分析与定量分析方法的相关性.方法:选择年龄匹配的健康人作比较,分别对33例SLE患者和29例正常对照进行SPECT脑血流灌注显像,采用肉眼读片分析及定量分析进行评价,BS软件进行分析.结果:狼疮脑病患者99mTc-ECD显像有脑血流改变,多表现为局部脑血流降低.肉眼读片分析SPECT诊断的SLE脑部受损的阳性率为51.51％,定量分析的阳性率达57.57％.成组t检验示扣带回、颞顶叶等部位最常受累.结论:SPECT脑血流灌注显像可探查到脑组织代谢和功能性损伤以及血流灌注变化,有助于发现SLE患者脑部血流受损情况.联合应用SPECT脑功能显像及BS分析软件可以更方便、快捷地定位大脑功能受损区.视觉分析与定量分析方法有很高的相关性.SPECT脑血流灌注显像对SLE脑病的诊断、治疗有重要的临床价值.     

高压氧治疗外伤性癫痫的临床观察及疗效评价

目的 观察高压氧治疗外伤性癫痫的临床效果,同时应用SPECT脑血流灌注显像技术对高压氧治疗的效果进行评价.方法 将27例临床诊断为脑外伤性的癫痫患者按高压氧治疗的时间分为1疗程治疗组和2疗程治疗组,并分别于治疗前、后进行SPECT脑血流灌注显像检查,对比治疗前、后脑血流灌注的变化情况.结果 27例患者接受高压氧治疗后脑血流低灌注较治疗前有所改善;2个疗程高压氧治疗组患者的脑血流低灌注改善明显高于1个疗程治疗组.SPECT疗效评价与临床疗效判定指标相符.结论应用高压氧治疗外伤性癫痫有效;SPECT脑血流灌注显像能有效应用于高压氧治疗脑外伤性癫痫的疗效判断.     

帕金森病合并抑郁与脑血流灌注的关系及经颅磁刺激的影响

目的：应用CT灌注成像技术观察帕金森病合并抑郁患者局灶脑血流灌注的特点,进一步探讨抑郁症发生与脑血流的关系.方法：将41例帕金森患者根据是否合并抑郁症分为帕金森病组22例、帕金森病合并抑郁症者为抑郁组19例、其中抑郁组分为经颅磁刺激（rTMS）治疗前组、治疗后组,3组均进行CT局部脑血流灌注显像,半定量分析各脑区血流灌注情况.结果：帕金森合并抑郁症组患者双侧额叶、颞叶和基底节的脑血流量测定（CBF）较帕金森病组显著下降（P＜0.05）;抑郁组左、右侧脑血流低灌注存在不对称性,左侧额叶、顶叶的CBF较右侧显著下降（P＜0.01）;rTMS治疗后脑血流灌注较治疗前改善,HAMD评分改善（P＜0.05）.结论：帕金森患者存在局灶性脑血流灌注降低,合并抑郁症患者额、顶叶下降更明显,经颅磁刺激治疗后脑血流低灌注改善.     

正常小型家猪脑血流灌注特征的SPECT/CT研究

目的:探讨采用SPECT/CT获得小型家猪脑血流灌注特征的方法和可行性.方法:对8头健康小型家猪进行SPECT/CT脑显像,进行图像预处理,自动提取脑相同感兴趣的相对血流量和相对离散度.结果:正常小猪脑不同感兴趣区相对血流量存在较大差异(P<0.05),相对脑血流量值以颞顶叶最高,其次是额顶叶,小脑最低.正常小猪脑各感兴趣内的相对离散度有统计学差异(P<0.05),相对离散度小脑感兴趣区最高,额叶感兴趣区最低.结论:SPECT/CT可用于半定量评价小型家猪脑血流灌注.     

CT灌注成像技术在脑肿瘤中的临床应用

Axel等于20世纪80年代初提出了CT灌注(CTperfu sion)成像理论,近年来随着CT扫描技术的发展及高速和多排螺旋CT的出现,基于该理论的临床应用与研究,尤其以观察脑组织血流灌注状况及组织血管化程度来揭示脑肿瘤的病理解剖、病理生理、判断肿瘤生物学行为及预后情况为目的的脑CT灌注成像研究日益增多。研究现状尽管SPECT和PET在评价脑血流动力学状态方面具有极佳的优势。但其价格昂贵、成像时间长、图像空间分辨率差,有核放射性等缺点,限制了其临床应用[1]。MR灌注成像也能提供脑血流动力学信息,但要求MR设备具有EPI功能,EPI技术所…     

基于动脉自旋标记技术的内侧颞叶癫痫病人脑血流灌注成像研究北大核心CSCD

基于动脉自旋标记(arterial spin labeling,ASL)技术,分析内侧颞叶癫痫(mesialtemporal lobe epilepsy,mTLE)患者大脑血流灌注(perfusion)的改变情况。在静息态下,采集了30例内侧颞叶癫痫伴单侧海马硬化发作间期患者(其中左侧16例,右侧14例)及22例健康志愿者的ASL数据,并通过计算获取其相对脑血流量(relative CBF,rCBF)及灌注不对称率(asymmetric index,AI)。癫痫病人与正常人的比较结果表明:左侧mTLE患者在两侧海马旁回、梭状回、额叶、颞叶和患侧海马回及岛叶,右侧mTLE患者在两侧海马回、海马旁回、额叶、颞叶和患侧杏仁核及岛叶,rCBF均有所下降,且患侧的下降程度和范围均大于对侧。说明mTLE患者的海马硬化可能导致了痫灶区功能异常,并通过癫痫的发作影响到全脑。     

抑郁症患者的脑CT灌注成像特征与认知功能的相关性

摘要 目的：探讨抑郁症患者的脑CT灌注成像特征与认知功能的相关性。方法：选取我院2020年1月到2023年1月收治的90例抑郁症患者作为研究对象,将其分为观察组,另选取同期来我院体检的90名健康志愿者作为对照组。收集所有受检者脑CT灌注成像检查数据,分析抑郁症患者的脑CT灌注成像特征,并建立受试者工作特征（ROC）曲线分析脑CT灌注成像对抑郁症的诊断效能。随后对观察组和对照组受检者均进行认知功能评估,其中包括连线检测（TMT）、视觉再生测验（VRT）、言语流畅性测验（VF）、数字广度测验（DST）以及数字符号测验（SDMT）,并分析脑CT灌注成像与抑郁症认知功能的相关性。结果：观察组与对照组受检者rCBV、rCBF、MTT、TIP、右枕叶、左枕叶、右颞叶、左颞叶、右顶叶、左顶叶CT值对比无明显差异（P＞0.05）,观察组与对照组受检者右额叶、左额叶CT值对比差异显著,观察组明显低于对照组（P＜0.05）;90例抑郁症患者经过汉密尔顿抑郁量表（HAMD）评估后分数均＞20分,确定存在抑郁症状,脑CT灌注成像与HAMD评分诊断抑郁症的准确性、灵敏度、特异性、阳性预测值和阴性预测值对比无明显差异（P＞0.05）,脑CT灌注成像的曲线下面积为83.89,最佳诊断着色界限值为82.53%,HAMD评分的曲线下面积为84.26,最佳诊断着色界限值为87.57%;观察组与对照组受检者连线提笔数、连线错误数、视觉再生检测结果对比无明显差异（P＞0.05）,观察组与对照组受检者连线、言语流畅性、数字广度、数字符号检测结果对比差异显著（P＜0.05）;Spearman相关分析结果表明：连线提笔数、连线错误数、视觉再生与脑CT灌注参数均无明显相关性（P＞0.05）,连线、言语流畅性、数字广度、数字符号与rCBV、rCBF、MTT、TIP、右枕叶、左枕叶、右颞叶、左颞叶、右顶叶、左顶叶CT值无明显相关性（P＞0.05）,连线与右额叶、左额叶CT值呈负相关（P＜0.05）,言语流畅性、数字广度、数字符号与右额叶、左额叶CT值呈正相关（P＜0.05）。结论：抑郁症患者的脑CT灌注成像与健康群体呈现差异,其中右额叶、左额叶差异情况最为显著,提示抑郁症患者可能存在大脑额叶功能改变,另外,抑郁症患者的大脑额叶功能与认知功能变化具有明显相关性。     

应用脑电阻图法测定家兔的局部脑血流

脑电阻图法在临床上作为脑血管疾病的辅助诊断手段已有较长历史,但其应用主要限于对整体血流的研究。有关国内外在实验动物身上开展脑电阻图方面的工作报道,迄今也不多见。尤其是利用脑电阻图对局部脑血流的测定,特别对在急性低氧条件下局部脑血流搏动性变化的测定,国内尚未见报道。我们对此进行了初步探索,试图为今后的局部脑血流研     

SPECT心肌灌注显像对急性心肌梗死患者PCI术后疗效评估

目的:探讨用单光子发射型计算机断层(single photon emission computedtomography,SPECT)心肌灌注显像,评估心肌梗死(AMI)经冠脉介入治疗(PCI)后的心肌灌注疗效。方法:采用99mTc-tetrofosmin(P53)SPECT心肌灌注显像对54例行PCI治疗的AMI患者评估心肌灌注情况,并追踪记录6个月内心脏事件发生率。结果:SPECT显示无复流组22例,有复流组32例,两组心肌梗死患者近期预后差异有统计学意义(P<0.05)。无复流组不良事件发生率较有复流组有增加趋势;另外,急诊PCI组的预后明显好于择期PCI组,差异有统计学意义(P<0.05)。结论:SPECT心肌灌注显像可对AMI患者梗死相关血管(IRA)再通治疗疗效进行可靠的无创性评价。     

单光子发射计算机断层扫描肺灌注显像(SPECT/CT)在肺恶性肿瘤放疗中 的应用进展

放射性肺损伤是肺恶性肿瘤放疗后常见的并发症,其限制肺恶性肿瘤的放疗剂量并影响总体疗效及患者生存质量。本文复习放射性肺损伤发生机制及影响因素,分析剂量体积直方图、肺功能测定、TGF-β1等临床常用放射性肺损伤评估指标的利弊。参考近年文献,总结了单光子发射计算机断层扫描肺灌注显像(SPECT/CT)在肺恶性肿瘤放疗中的应用,从其原理、区域肺功能的显像、对放疗的评估与指导应用几方面阐述。认为SPECT/CT能实时反映区域肺功能、肺功能改变以及其解剖定位,可在放疗中起监测作用,对准确评估肺功能、预测放疗后肺损伤,优化放疗计划有重要价值。SPECT/CT肺灌注显像还需要多中心、大样本、长时间随访资料进一步深入研究。     

Differential neural responses to food images in women with bulimia versus anorexia nervosa

Background

Previous fMRI studies show that women with eating disorders (ED) have differential neural activation to viewing food images. However, despite clinical differences in their responses to food, differential neural activation to thinking about eating food, between women with anorexia nervosa (AN) and bulimia nervosa (BN) is not known.

Methods

We compare 50 women (8 with BN, 18 with AN and 24 age-matched healthy controls [HC]) while they view food images during functional Magnetic Resonance Imaging (fMRI).

Results

In response to food (vs non-food) images, women with BN showed greater neural activation in the visual cortex, right dorsolateral prefrontal cortex, right insular cortex and precentral gyrus, women with AN showed greater activation in the right dorsolateral prefrontal cortex, cerebellum and right precuneus. HC women activated the cerebellum, right insular cortex, right medial temporal lobe and left caudate. Direct comparisons revealed that compared to HC, the BN group showed relative deactivation in the bilateral superior temporal gyrus/insula, and visual cortex, and compared to AN had relative deactivation in the parietal lobe and dorsal posterior cingulate cortex, but greater activation in the caudate, superior temporal gyrus, right insula and supplementary motor area.

Conclusions

Women with AN and BN activate top-down cognitive control in response to food images, yet women with BN have increased activation in reward and somatosensory regions, which might impinge on cognitive control over food consumption and binge eating.     

Provocation of Symmetry/Ordering Symptoms in Anorexia nervosa: A Functional Neuroimaging Study

Anorexia nervosa (AN), obsessive–compulsive disorder (OCD), and obsessive–compulsive personality disorder (OCPD) are often co-morbid; however, the aetiology of such co-morbidity has not been well investigated. This study examined brain activation in women with AN and in healthy control (HC) women during the provocation of symmetry/ordering-related anxiety. During provocation, patients with AN showed more anxiety compared to HCs, which was correlated with the severity of symmetry/ordering symptoms. Activation in the right parietal lobe and right prefrontal cortex (rPFC) in response to provocation was reduced in the AN group compared with the HC group. The reduced right parietal activation observed in the AN group is consistent with parietal lobe involvement in visuospatial cognition and with studies of OCD reporting an association between structural abnormalities in this region and the severity of ‘ordering’ symptoms. Reduced rPFC activation in response to symmetry/ordering provocation has similarities with some, but not all, data collected from patients with AN who were exposed to images of food and bodies. Furthermore, the combination of data from the AN and HC groups showed that rPFC activation during symptom provocation was inversely correlated with the severity of symmetry/ordering symptoms. These data suggest that individuals with AN have a diminished ability to cognitively deal with illness-associated symptoms of provocation. Furthermore, our data also suggest that symptom provocation can progressively overload attempts by the rPFC to exert cognitive control. These findings are discussed in the context of the current neurobiological models of AN.     

Human and nonhuman primate brains: Are they allometrically scaled versions of the same design?

Allometric analyses of brain structure sizes across the primate order demonstrate that human, ape, and other anthropoid brains are not simply allometrically scaled versions of the same generalized design. Both human and ape brains exhibit specializations with respect to other anthropoid brains. Ape specializations include elaboration of the cerebellum (all apes) and frontal lobes (great apes only), and probably connectivity between them. Human brain specializations include an overall larger proportion of neocortex, with disproportionate enlargement of prefrontal and temporal association cortices; an apparent increase in cerebellar connections with cerebral cortical association areas involved in cognition; and a probable augmentation of intracortical connectivity in prefrontal cortex.     

Altered Resting-State Functional Connectivity of the Frontal-Striatal Reward System in Social Anxiety Disorder

We investigated differences in the intrinsic functional brain organization (functional connectivity) of the human reward system between healthy control participants and patients with social anxiety disorder. Functional connectivity was measured in the resting-state via functional magnetic resonance imaging (fMRI). 53 patients with social anxiety disorder and 33 healthy control participants underwent a 6-minute resting-state fMRI scan. Functional connectivity of the reward system was analyzed by calculating whole-brain temporal correlations with a bilateral nucleus accumbens seed and a ventromedial prefrontal cortex seed. Patients with social anxiety disorder, relative to the control group, had (1) decreased functional connectivity between the nucleus accumbens seed and other regions associated with reward, including ventromedial prefrontal cortex; (2) decreased functional connectivity between the ventromedial prefrontal cortex seed and lateral prefrontal regions, including the anterior and dorsolateral prefrontal cortices; and (3) increased functional connectivity between both the nucleus accumbens seed and the ventromedial prefrontal cortex seed with more posterior brain regions, including anterior cingulate cortex. Social anxiety disorder appears to be associated with widespread differences in the functional connectivity of the reward system, including markedly decreased functional connectivity between reward regions and between reward regions and lateral prefrontal cortices, and markedly increased functional connectivity between reward regions and posterior brain regions.     

Cholecystokinin, vasoactive intestinal peptide and peptide histidine methionine responses to feeding in anorexia nervosa.

Anorexia nervosa (AN) is a syndrome of unknown cause characterized by voluntary starvation. Cholecystokinin has been implicated as a neuroendocrine regulatory factor in control of satiety. Relatively little information is known about gastrointestinal hormone responses to feeding in subjects with anorexia nervosa. In the present studies, we examine fasting and postprandial levels of cholecystokinin (CCK), vasoactive intestinal peptide (VIP) and peptide histidine methionine (PHM) in anorexia nervosa subjects and in control individuals. Results of these studies indicate that plasma CCK response to a liquid meal (Ensure Plus) in untreated AN subjects was distinctly different from that observed in healthy controls, both in terms of temporal pattern of peptide released and the amount of CCK secreted into the circulation. Peak levels of CCK release occurred at 30 min following meal ingestion in AN patients and at 60 min in control subjects. Integrated CCK release in untreated AN patients was approximately twice that measured in control individuals. Renutrition therapy was associated with reversion of the pattern of CCK release to that observed in control subjects. Plasma VIP levels were unchanged following meal ingestion in both control and anorexic subjects. In contrast, PHM levels in AN subjects were significantly greater than that observed in control individuals. The pattern of PHM release following liquid meal ingestion was similar to that observed with plasma CCK; namely, peak release of peptide was observed at 30 min which was significantly greater than corresponding control values (P less than 0.05). In conclusion, these results demonstrate distinctive differences in plasma CCK and PHM levels in response to feeding in AN subjects when compared to control individuals. These findings suggest that the earlier and greater rise in plasma CCK levels in AN subjects following meal ingestion may contribute to the abnormal sensation of satiety in this condition.     

A frontal variant of Alzheimer's disease exhibits decreased calcium-independent phospholipase A2 activity in the prefrontal cortex

A frontal variant of Alzheimer's disease (AD) has recently been identified on neuropathological and neuropsychological grounds (Johnson, J.K., Head, E., Kim, R., Starr, A., Cotman, C.W., 1999. Clinical and pathological evidence for a frontal variant of Alzheimer Disease. Arch. Neurol. 56, 1233-1239). Frontal AD differs strikingly from typical AD by the occurrence of neurofibrillary tangle densities in the frontal cortex as high or higher than in the entorhinal cortex. Since cerebrocortical membranes are commonly abnormal in Alzheimer's disease (AD), we assayed frontal AD cases for enzymes regulating membrane phospholipid composition. We specifically measured activity of phospholipase A2s (PLA2s) in dorsolateral prefrontal and lateral temporal cortices of frontal AD cases (n=12), which have respectively high and low densities of neurofibrillary tangles. In neither cortical area was Ca(2+)-dependent PLA2 activity abnormal compared to controls (n=12). In contrast, a significant 42% decrease in Ca(2+)-independent PLA2 activity was found in the dorsolateral prefrontal, but not the lateral temporal, cortex of the frontal AD cases. Similarly, the dorsolateral prefrontal cortex, but not the lateral temporal cortex of the frontal AD cases suffered a 42% decrease in total free fatty acid content, though neither that decrease nor those in any one species of free fatty acid was significant. The observed biochemical changes probably occurred in neurons given (a) our finding that PLA2 activity of cultured human NT2 neurons is virtually all Ca(2+)-independent and (b) the finding of others that nearly all Ca(2+)-independent PLA2 in brain gray matter is neuronal. The decrease in Ca(2+)-independent PLA2 activity is not readily attributable to Group VI or VIII iPLA2s since neither NT2N neurons nor our brain homogenates were greatly inhibited by drugs potently suppressing those iPLA2s. Decreased Ca(2+)-independent PLA2 activity in frontal AD may reflect a compensatory response to pathologically accelerated phospholipid metabolism early in the disorder. That could cause an early elevation of prefrontal free fatty acids, which can stimulate polymerization of tau and thus promote the prefrontal neurofibrillary tangle formation characteristic of frontal AD.     

Cerebral Inefficient Activation in Schizophrenia Patients and Their Unaffected Parents during the N-Back Working Memory Task: A Family fMRI Study

Background

It has been suggested that working memory deficits is a core feature of symptomatology of schizophrenia, which can be detected in patients and their unaffected relatives. The impairment of working memory has been found related to the abnormal activity of human brain regions in many functional magnetic resonance imaging (fMRI) studies. This study investigated how brain region activation was altered in schizophrenia and how it was inherited independently from performance deficits.

Method

The authors used fMRI method during N-back task to assess working memory related cortical activation in four groups (N = 20 in each group, matching task performance, age, gender and education): schizophrenic patients, their unaffected biological parents, young healthy controls for the patients and older healthy controls for their parents.

Results

Compared to healthy controls, patients showed an exaggerated response in the right dorsolateral prefrontal cortex (brodmann area [BA] 46) and bilateral ventrolateral prefrontal cortex, and had reduced activation in bilateral dorsolateral prefrontal cortex (BA 9). In the conjunction analysis, the effect of genetic risk (parents versus older control) shared significantly overlapped activation with effect of disease (patients versus young control) in the right middle frontal gyrus (BA 46) and left inferior parietal gyrus (BA 40).

Conclusions

Physiological inefficiency of dorsal prefrontal cortex and compensation involvement of ventral prefrontal cortex in working memory function may one physiological characteristics of schizophrenia. And relatively inefficient activation in dorsolateral prefrontal cortex probably can be a promising intermediate phenotype for schizophrenia.     

Thinking about eating food activates visual cortex with reduced bilateral cerebellar activation in females with anorexia nervosa: an fMRI study

Background

Women with anorexia nervosa (AN) have aberrant cognitions about food and altered activity in prefrontal cortical and somatosensory regions to food images. However, differential effects on the brain when thinking about eating food between healthy women and those with AN is unknown.

Methods

Functional magnetic resonance imaging (fMRI) examined neural activation when 42 women thought about eating the food shown in images: 18 with AN (11 RAN, 7 BPAN) and 24 age-matched controls (HC).

Results

Group contrasts between HC and AN revealed reduced activation in AN in the bilateral cerebellar vermis, and increased activation in the right visual cortex. Preliminary comparisons between AN subtypes and healthy controls suggest differences in cortical and limbic regions.

Conclusions

These preliminary data suggest that thinking about eating food shown in images increases visual and prefrontal cortical neural responses in females with AN, which may underlie cognitive biases towards food stimuli and ruminations about controlling food intake. Future studies are needed to explicitly test how thinking about eating activates restraint cognitions, specifically in those with restricting vs. binge-purging AN subtypes.     

Altered brain levels of arachidonic acid-derived inflammatory eicosanoids in a rodent model of anorexia nervosa

Increasing evidence underline the role of inflammation in the behavioral, emotional and cognitive dysregulations displayed in anorexia nervosa (AN). Among the inflammatory mediators acting at both peripheral and central levels, growing attention receives a class of lipids derived from arachidonic acid (AA), called eicosanoids (eiCs), which exert a complex, multifaceted role in a wide range of neuroinflammatory processes, peripheral inflammation, and generally in immune system function. To date, little is known about their possible involvement in the neurobiological underpinnings of AN. The present study evaluated whether the activity-based model of AN (ABA) may alter AA-metabolic pathways by changing the levels of AA-derived eiCs in specific brain areas implicated in the development of the typical anorexic-like phenotype, i.e. in prefrontal cortex, cerebral cortex, nucleus accumbens, caudate putamen, amygdala, hippocampus, hypothalamus and cerebellum. Our results point to brain region-specific alterations of the cyclooxygenase (COX), lipoxygenase (LOX) and cytochrome P450 epoxygenase (CYP) metabolic pathways rendering altered levels of AA-derived eiCs (i.e. prostaglandins, thromboxanes and hydroxyeicosatetraenoic acids) in response to induction of and recovery from the ABA condition. These changes, supported by altered messenger RNA (mRNA) levels of genes coding for enzymes involved in eiCs-related methabolic pathways (i.e., PLA₂, COX-2, 5-LOX and 15-LOX), underlie a widespread brain dysregulation of pro- and anti-inflammatory eiC-mediated processes in the ABA model of AN. These data suggest the importance of eiCs signaling within corticolimbic areas in regulating key neurobehavioral functions and highlight eiCs as biomarker candidates for monitoring the onset and development of AN, and/or as possible targets for pharmacological management.     

Dynamic Changes in Brain Activations and Functional Connectivity during Affectively Different Tactile Stimuli

In the present study, we compared brain activations produced by pleasant, neutral and unpleasant touch, to the anterior lateral surface of lower leg of human subjects. It was found that several brain regions, including the contralateral primary somatosensory area (SI), bilateral secondary somatosensory area (SII), as well as contralateral middle and posterior insula cortex were commonly activated under the three touch conditions. In addition, pleasant and unpleasant touch conditions shared a few brain regions including the contralateral posterior parietal cortex (PPC) and bilateral premotor cortex (PMC). Unpleasant touch specifically activated a set of pain-related brain regions such as contralateral supplementary motor area (SMA) and dorsal parts of bilateral anterior cingulated cortex, etc. Brain regions specifically activated by pleasant touch comprised bilateral lateral orbitofrontal cortex (OFC), posterior cingulate cortex (PCC), medial prefrontal cortex (mPFC), intraparietal cortex and left dorsal lateral prefrontal cortex (DLPFC). Using a novel functional connectivity model based on graph theory, we showed that a series of brain regions related to affectively different touch had significant functional connectivity during the resting state. Furthermore, it was found that such a network can be modulated between affectively different touch conditions.