Arciniegas D B, Topkoff J L, Rojas D C, Sheeder J, Teale P, Young D A, Sandberg E, Reite M L, Adler L E
Research, Radiology, and Psychiatric Services, Denver Veterans Affairs Medical Center, CO, USA.
J Neuropsychiatry Clin Neurosci. 2001 Spring;13(2):213-21. doi: 10.1176/jnp.13.2.213.
Traumatic brain injury (TBI) may produce persistently impaired auditory gating. This cholinergic-dependent, hippocampally mediated preattentive cognitive function that facilitates filtering of auditory stimuli may be indexed by the P50 evoked waveform to paired auditory stimuli. Abnormal P50 suppression post TBI is believed to result from injury to the hippocampus and/or its afferent cholinergic projections. This hypothesis was tested by comparing hippocampal and total brain volumes on MRI between ten P50-nonsuppressing TBI patients and ten normal control subjects matched for age, gender, and education. TBI subjects had highly significant bilateral hippocampal volume reductions, even when covaried for reductions in total brain volume. Degree of volume loss was not correlated with initial TBI severity. Findings support the hypothesis that hippocampal injury underlies P50 nonsuppression post TBI and suggest that such structural abnormalities may be observed even in "mildly" injured persons.
创伤性脑损伤(TBI)可能导致听觉门控持续受损。这种依赖胆碱能、由海马介导的前注意认知功能有助于过滤听觉刺激,可通过对成对听觉刺激诱发的P50波形来衡量。创伤性脑损伤后P50抑制异常被认为是海马及其传入胆碱能投射受损所致。通过比较10例P50无抑制的创伤性脑损伤患者与10例年龄、性别和教育程度相匹配的正常对照受试者的MRI海马体积和全脑体积,对这一假设进行了验证。创伤性脑损伤受试者双侧海马体积显著减小,即使在对全脑体积减小进行协变量分析时也是如此。体积损失程度与初始创伤性脑损伤严重程度无关。研究结果支持这样的假设,即海马损伤是创伤性脑损伤后P50无抑制的基础,并表明即使在“轻度”受伤者中也可能观察到这种结构异常。