Cerebral Structural And Metabolic Correlates Of Aggressive Or Addictive Behavior

攻击性或成瘾行为的大脑结构和代谢相关性

• 批准号: 7591910
• 负责人: Daniel W Hommer
• 金额: $ 86.3万
• 依托单位: NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM
• 依托单位国家: 美国
• 资助国家: 美国
• 起止时间: 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/7591910
• 关键词: Accounting; Addictive Behavior; Adolescent; Affect; Aggressive behavior; Alcohol consumption; Alcoholism; Brain; Brain Mapping; Cerebrospinal Fluid; Cerebrum; Child; Corpus striatum structure; Data; Development; Family history of; Fathers; Female; Genetic; Glucose; Gray unit of radiation dose; Growth; Heavy Drinking; Human; Impulsive Behavior; Left; Life; Magnetic Resonance Imaging; Measurement; Measures; Mental disorders; Metabolic; Methods; Motivation; Nucleus Accumbens; Patients; Positron-Emission Tomography; Process; Research; Risk; Score; Social Behavior; Substance Abuse, Other; Weight; Woman; brain size; brain volume; design; early onset; frontal lobe; gray matter; human subject; male; men; mind control; neurochemistry; non-alcoholic; problem drinker; programs; white matter

We collected full, volumetric T-1 weighted MR images using a 1.5 T scanner to measure intracranial volumes in 350 alcoholics (248 males and 112 females) and 163 healthy, non-alcoholic comparison subjects (82 males and 81 females). An automated segmentation program was used to divide the intracranial contents into CSF, gray and white matter (Human Brain Mapping, 5:194-205, 1997). When we measure brain volume we are measuring the combined effect of two processes: growth and degeneration. Growth determines maximum brain size achieved during life. Maximal brain growth can be estimated by intracranial volume (ICV) and since ICV remains constant throughout life, brain In additiondegeneration can be measured by the ratio of cerebral volume or gray matter or white matter volume to the remainder of the intracranial contents. Alcoholics show greater brain degeneration than non-alcoholics. Alcoholic women are more affected than alcoholic men. Alcoholics also show significantly greater brain shrinkage than controls by their mid to late twenties. In addition, alcoholics have smaller intracranial volumes than controls suggesting that pre-morbid differences in brain size may contribute to the risk for alcoholism. Despite the significant difference in intracranial volume brain, degeneration accounts for a greater amount of the difference in brain volume between alcoholics and controls than brain growth does. Similarly, presence or absence of co-morbid psychiatric disorder or other substance abuse does not affect brain shrinkage among alcoholics. Over the past year we have made several methodological advances in the automated measurement of brain volumes. An automated method for dividing the brain into right and left hemispheres was developed and validated. In addition, we have developed an automated method for measuring the volume of mesial and orbital frontal cortex, as well as the entire striatum. These regions are known to be involved in motivation and social behavior. We have begun to investigate the normal and pathological development of the striatum. It appears that children and adolescents at risk for the development of alcoholism have significantly smaller striatums, including nucleus accumbens, than child not at high risk for the development of alcoholism. In addition, we have also examined how a family history (FH) of heavy drinking affects both brain shrinkage as measured by the ratio of brain volumes to intracranial volume as well as maximal brain growth as measured by ICV in early-onset and late-onset alcoholics. FH positive alcoholic patients have significantly smaller ICVs than FH negative patients, suggesting smaller premorbid brain growth among alcoholics with a heavy drinking motr or father. Brain shrinkage was not affected by FH. Late-onset alcoholics show a greater difference in ICV between FH positive and FH negative patients than early-onset alcoholics. Late-onset FH positive patients also have significantly lower IQ scores than late-onset FH negative patients, and IQ scores are correlated with ICV. These data provide evidence that heavy parental alcohol use may increase risk for alcoholism in offspring in part by a genetic and/or environmental effect resulting in reduced brain growth.

我们使用1.5T扫描仪收集了完整的T-1加权磁共振图像，测量了350名酗酒者(248名男性和112名女性)和163名健康的非酒精对照组(82名男性和81名女性)的颅内体积。使用自动分割程序将颅内内容分为脑脊液、灰质和白质(人脑图谱，5：194-205,1997)。当我们测量大脑体积时，我们是在测量两个过程的综合影响：生长和退化。生长决定了一生中所能达到的最大大脑大小。脑的最大增长可以通过颅内体积(Icv)来估计，由于icv在一生中保持不变，因此可以通过脑体积或灰质或白质体积与剩余的颅内内容的比率来衡量大脑的额外退化。酗酒者比非酗酒者表现出更大的大脑退化。酗酒的女性比酗酒的男性更容易受到影响。到了二十五岁左右，酗酒者的大脑萎缩程度也明显高于对照组。此外，酗酒者的颅内体积比对照组的小，这表明患病前大脑大小的差异可能是酗酒的风险所在。尽管酗酒者和对照组的脑体积存在显著差异，但与脑生长相比，变性在脑体积差异中所占的比例更大。同样，存在或不存在共病精神障碍或其他物质滥用也不会影响酗酒者的大脑萎缩。在过去的一年里，我们在自动测量大脑体积方面取得了几项方法学上的进步。开发了一种自动将大脑划分为左右半球的方法，并进行了验证。此外，我们还开发了一种自动测量内侧和眼眶额叶皮质以及整个纹状体体积的方法。众所周知，这些区域与动机和社会行为有关。我们已经开始研究纹状体的正常和病理发育。看来，有酗酒风险的儿童和青少年的纹状体，包括伏隔核，比不是酗酒高危儿童的纹状体要小得多。 此外，我们还研究了大量饮酒的家族史(FH)如何影响早发性和晚发性酗酒者的脑萎缩(通过脑体积与颅内体积的比率衡量)和最大脑发育(由ICV衡量)。FH阳性的酗酒患者的ICV明显小于FH阴性的患者，这表明有酗酒史或父亲的酗酒者病前脑发育较小。FH对脑萎缩无明显影响。晚发性酒精者FH阳性与FH阴性患者的ICV差异明显大于早发性酒精者。晚发型FH阳性患者的智商得分也显著低于晚发型FH阴性患者，且IQ得分与ICV呈正相关。这些数据提供了证据，证明父母大量饮酒可能会增加子女酗酒的风险，部分原因是遗传和/或环境影响导致大脑发育减慢。