Coutin-Churchman Pedro, Moreno Rocío
Hospital Psiquiátrico San Juan de Dios, Urb. Campo Claro. Los Curos, Edo. Mérida 5101, Venezuela.
Clin Neurophysiol. 2008 Apr;119(4):948-58. doi: 10.1016/j.clinph.2007.12.013. Epub 2008 Mar 4.
To assess possible differences in intracranial source distribution of surface QEEG power between depressed and non-depressed alcoholic patients in order to find any symptom-related topographic features of physiopathologic relevance.
Low-Resolution Electromagnetic Tomography (LORETA) for the delta, theta, alpha and beta bands of EEG spectra was estimated from 38 alcoholic patients, 20 with and 18 without clinical depression, in which QEEG showed decreased slow and increased beta activity diffusely. Statistical non-parametric mapping was used to compare depressed and non-depressed groups. Measures of intracranial current density in individual patients at areas of significant differences were correlated with BDI scores.
Patients with clinical depression showed areas of significantly lower current density than non-depressed patients in delta band at left anterior temporal, left midtemporal (including amygdala and hippocampus), and both frontopolar cortices mostly on the right; and in theta band at bilateral parietal lobe, anterior cingulate and medial frontal cortex. No differences were found at alpha and beta band. Intracranial current density in delta band at left parahippocampal, left midfrontal cortex and right frontopolar cortex was negatively correlated with BDI score. Theta band also showed negative correlations with BDI at sites of significant differences.
Diffusely decreased delta and theta activity in the surface QEEG of alcoholic patients has a different intracranial distribution linked to the presence or not of clinical depression that seems to reveal a dysfunctional neuronal state at several specific limbic and other cortical locations that have been related to a specific clinical disorder such as depression.
These results provided further evidence on the effects of depression in the context of alcohol dependence, in this case decreased slow activity as a possible marker of neuronal damage secondary to alcohol toxicity, clinically expressed as depressive symptoms when present in structures that are known to be related to clinical depression.
评估抑郁和非抑郁酒精性患者脑电图表面功率的颅内源分布差异，以发现任何与症状相关的具有生理病理相关性的地形学特征。
对38例酒精性患者进行了低分辨率电磁断层扫描（LORETA），以估计脑电图频谱中δ、θ、α和β频段的情况，其中20例有临床抑郁，18例无临床抑郁，这些患者的定量脑电图显示慢波活动普遍减少，β活动增加。采用统计非参数映射来比较抑郁组和非抑郁组。在差异显著区域对个体患者的颅内电流密度测量值与贝克抑郁量表（BDI）评分进行相关性分析。
临床抑郁患者在左侧前颞叶、左侧中颞叶（包括杏仁核和海马体）以及主要位于右侧的双侧额极皮质的δ频段电流密度显著低于非抑郁患者；在双侧顶叶、前扣带回和内侧额叶皮质的θ频段也有此现象。在α和β频段未发现差异。左侧海马旁、左侧额中皮质和右侧额极皮质的δ频段颅内电流密度与BDI评分呈负相关。在差异显著部位，θ频段也与BDI呈负相关。
酒精性患者脑电图表面的δ和θ活动普遍降低，其颅内分布因是否存在临床抑郁而不同，这似乎揭示了几个特定边缘系统和其他皮质区域的神经元功能失调状态，这些区域与诸如抑郁等特定临床疾病有关。
这些结果为酒精依赖背景下抑郁的影响提供了进一步证据，在这种情况下，慢波活动减少可能是酒精毒性继发神经元损伤的标志，当存在于已知与临床抑郁相关的结构中时，临床上表现为抑郁症状。
