NEUROPSYCHOLOGICAL, ANATOMICAL, AND PHYSIOLOGICAL CORRELATES OF MOOD DISORDERS

神经心理学测试显示，情感疾病患者 在霍尔斯特德类别测试和识别中的表现受损 与未受损的语言表达相比， 情绪识别任务。 面部情绪识别障碍 是与状态相关的;即，在表达过程中比“好”更深刻- 间隔”之间的插曲。 患者还报告终身困扰 在日常生活的任务和活动中，包括视觉空间 处理，但不是那些在口头模式。 的神经基质 这些缺陷正在被各种各样的 技术包括使用015血流研究测试患者 采用PET方法（参见MH 02636-02 BPB和MH 02638-02 BPB）。 早些时候 CAT扫描研究显示，情感障碍患者的VBR增加， 与病程无关的疾病，但与 年龄，皮质醇分泌过多的测量，以及霍尔斯特德的损害 类别测试 最近的MRI研究表明， 与对照组相比，有情感疾病的受试者的颞叶。 在T2时，在BP-I患者中观察到脑室周围异常 加权扫描;这些发现与增加的 双极-I型患者的CSF蛋白也是如此。 正面的证据 PET扫描研究显示原发性高血压患者存在低代谢 情感障碍以及与癫痫相关的抑郁症。 这 与汉密尔顿抑郁量表评定的抑郁严重程度相关 规模 颞叶和顶叶的变化也很明显。 正面 低代谢预测对尼莫地平（和安非他酮或 文拉法辛），多动，特别是在颞叶 叶，与卡马西平的反应有关。 我们希望看到 神经心理学特征是否也可以预测对锂的反应 还有这些探员 像这样的癫痫患者， 在他们的治疗过程中， 初步证据表明，这与急性发作无关。 抗抑郁或抗躁狂反应，并 矛盾的是，长期服用卡马西平的患者， 长期预防。

Neuropsychological testing has revealed that affectively ill patients have impaired performance on the Halstead Category Test and recognition of facial emotional expression, in contrast with unimpaired verbal emotion recognition tasks. The impairment in facial emotion recognition is state-related; i.e., more profound during expression than the "well- interval" between episodes. Patients also report lifetime disturbances in tasks and activities of daily living including visual spatial processing, but not those in the verbal mode. The neural substrates of these deficits are being systematically explored by a variety of techniques including testing patients utilizing 015 blood flow studies with PET methodology (see MH 02636-02 BPB and MH 02638-02 BPB). Earlier CAT scan studies have revealed increased VBR in patients with affective disorders unrelated to the course of illness, but positively related to age, measures of cortisol hypersecretion, and impairment on the Halstead Category Test. More recent MRI studies suggest decreased area and volume of the temporal lobe in affectively ill subjects compared with controls. Periventricular abnormalities have been observed in BP-I patients on T2 weighted scans; these findings are of interest in relation to increased CSF protein in bipolar-I patients as well. Evidence of frontal hypometabolism is revealed on PET scan studies in patients with primary affective disorders as well as depression associated with epilepsy. This correlated with severity of depression rated on the Hamilton Depression Scale. Temporal and parietal alterations are also evident. Frontal hypometabolism predicts response to nimodipine (and bupropion or venlafaxine in outpatients), hyperactivity, particularly in temporal lobes, is associated with response to carbamazepine. We wish to see whether neuropsychological profiles can also predict response to lithium and these agents. Affectively ill patients like these with epilepsy have a high incidence of paroxysmal psychosensory symptoms during their episodes; preliminary evidence suggests that this is unrelated to acute antidepressant or antimanic response to carbamazepine, and is paradoxically associated with a poorer response to carbamazepine in long- term prophylaxis.