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患有“癔症性”麻醉的慢性疼痛患者中枢体感处理的改变

Altered central somatosensory processing in chronic pain patients with "hysterical" anesthesia.

作者信息

Mailis-Gagnon A, Giannoylis I, Downar J, Kwan C L, Mikulis D J, Crawley A P, Nicholson K, Davis K D

机构信息

Comprehensive Pain Program, Toronto Western Hospital, Ontario, Canada.

出版信息

Neurology. 2003 May 13;60(9):1501-7. doi: 10.1212/wnl.60.9.1501.

DOI:10.1212/wnl.60.9.1501
PMID:12743239
Abstract

OBJECTIVE

The authors hypothesized that central factors may underlie sensory deficits in patients with nondermatomal somatosensory deficits (NDSD) and that functional brain imaging would reveal altered responses in supraspinal nuclei.

BACKGROUND

Patients with chronic pain frequently present with NDSD, ranging from hypoesthesia to complete anesthesia in the absence of substantial pathology and often in association with motor weakness and occasional paralysis. Patients with pain and such pseudoneurologic symptoms can be classified as having both a pain disorder and a conversion disorder (Diagnostic and Statistical Manual of Mental Disorders-IV classification).

METHODS

The authors tested their hypothesis with functional MRI (fMRI) of brush and noxious stimulation-evoked brain responses in four patients with chronic pain and NDSD.

RESULTS

The fMRI findings revealed altered somatosensory-evoked responses in specific forebrain areas. Unperceived stimuli failed to activate areas that were activated with perceived touch and pain: notably, the thalamus, posterior region of the anterior cingulate cortex (ACC), and Brodmann area 44/45. Furthermore, unperceived stimuli were associated with deactivations in primary and secondary somatosensory cortex (S1, S2), posterior parietal cortex, and prefrontal cortex. Finally, unperceived (but not perceived) stimuli activated the rostral ACC.

CONCLUSIONS

Diminished perception of innocuous and noxious stimuli is associated with altered activity in many parts of the somatosensory pathway or other supraspinal areas. The cortical findings indicate a neurobiological component for at least part of the symptoms in patients presenting with nondermatomal somatosensory deficits.

摘要

目的

作者推测中枢因素可能是导致非皮节性躯体感觉障碍(NDSD)患者感觉缺陷的基础,并且功能性脑成像将揭示脊髓上核团的反应改变。

背景

慢性疼痛患者常伴有NDSD,表现为从感觉减退到完全麻醉,而无明显病理改变,且常伴有肌无力和偶尔的瘫痪。伴有疼痛和此类假性神经症状的患者可被归类为患有疼痛障碍和转换障碍(《精神疾病诊断与统计手册》第四版分类)。

方法

作者通过对4例慢性疼痛和NDSD患者进行功能性磁共振成像(fMRI),检测刷擦和有害刺激诱发的脑反应,来验证他们的假设。

结果

fMRI结果显示特定前脑区域的躯体感觉诱发反应发生改变。未被感知的刺激未能激活被感知的触觉和疼痛所激活的区域:特别是丘脑、前扣带回皮质(ACC)后部区域以及布罗德曼44/45区。此外,未被感知的刺激与初级和次级躯体感觉皮质(S1、S2)、顶叶后皮质和前额叶皮质的失活有关。最后,未被感知(但非被感知)的刺激激活了ACC喙部。

结论

对无害和有害刺激的感知减弱与躯体感觉通路或其他脊髓上区域许多部位的活动改变有关。皮质层面的研究结果表明,至少部分非皮节性躯体感觉障碍患者的症状存在神经生物学成分。

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