CAJ | 학술논문

目的探讨慢性压迫性脊髓症不同体感诱发电位(somatosensory evoked potential,SEP)变化对应的病理学机制.方法 20只SD大鼠经后路手术、颈椎管内(C5～C6水平)植入吸性聚氨酯胶片,该植入体在硬膜外逐渐吸水膨胀,形成对脊髓的慢性持续压迫.术前和造模后6个月检测SEP,并对慢性压迫脊髓行Micro-CT、组织学(HE染色)和组织化学(FLB染色)检测.结果 20只造模大鼠脊髓均出现侧后方明显压迫性形态学改变,Micro-CT显示脊髓灰质和白质扭曲变形.依据SEP变化分为Ⅰ(n=6)、Ⅱa(n=5)、Ⅱb(n=4)、Ⅲ(n=5)、Ⅳ(n=0)5类.SEP异常者脊髓后索髓鞘FLB染色显著减少(SEP异常:106±27;SEP正常:121±8;P=0.036),Micro-CT显示脊髓后索对比剂密度明显增加(SEP异常:95±5;SEP正常:87±6;P=0.041),后角内神经元也明显较少[SEP异常:(21±8)/mm2;SEP正常:(29±6)/mm2;P＞0.05].病理学上,SEP-Ⅰ型表现为脊髓中央管扩大;Ⅱa型表现为灰质内出血、静脉扩张和中央管缩小;Ⅱb型表现为灰质、白质排列紊乱,血管增生;Ⅲ型表现为神经元明显减少、白质-灰质结构不清,基质海绵样变.结论慢性压迫性脊髓症不同类型的SEP变化反映了脊髓后索和灰质神经元损伤的严重程度,SEP作为脊髓功能预后评估的判断指标具有相应的病理学特征.
목적 탐토만성압박성척수증불동체감유발전위(somatosensory evoked potential,SEP)변화대응적병이학궤제.방법 20지SD대서경후로수술、경추관내(C5～C6수평)식입흡성취안지효편,해식입체재경막외축점흡수팽창,형성대척수적만성지속압박.술전화조모후6개월검측SEP,병대만성압박척수행Micro-CT、조직학(HE염색)화조직화학(FLB염색)검측.결과 20지조모대서척수균출현측후방명현압박성형태학개변,Micro-CT현시척수회질화백질뉴곡변형.의거SEP변화분위Ⅰ(n=6)、Ⅱa(n=5)、Ⅱb(n=4)、Ⅲ(n=5)、Ⅳ(n=0)5류.SEP이상자척수후색수초FLB염색현저감소(SEP이상:106±27;SEP정상:121±8;P=0.036),Micro-CT현시척수후색대비제밀도명현증가(SEP이상:95±5;SEP정상:87±6;P=0.041),후각내신경원야명현교소[SEP이상:(21±8)/mm2;SEP정상:(29±6)/mm2;P＞0.05].병이학상,SEP-Ⅰ형표현위척수중앙관확대;Ⅱa형표현위회질내출혈、정맥확장화중앙관축소;Ⅱb형표현위회질、백질배렬문란,혈관증생;Ⅲ형표현위신경원명현감소、백질-회질결구불청,기질해면양변.결론 만성압박성척수증불동류형적SEP변화반영료척수후색화회질신경원손상적엄중정도,SEP작위척수공능예후평고적판단지표구유상응적병이학특정.
Objective To evaluate the altered somatosensory evoked potential (SEP) as related to pathological mechanisms of chronic spinal cord compression induced myelopathy. Methods A total of 20 rats were implanted with water-absorbing polymer sheet in the cervical spinal canal (C5-C6 level), which would expand outside the dura mater gradually to produce chronic compression to the spinal cord. Before and at 6 months after surgery, SEP, Micro-CT, HE-staining histology and FLB-staining histochemistry of spinal cord under chronic compression were measured. Results In all of the 20 rat models, typical morphology of chronic compression was seen posterolateral to the spinal cord, as reflected by distorted gray matter and white matter of spinal cord demonstrated at Micro-CT. The abnormal SEP responses were categorized into 5 types:Ⅰ (n=6), Ⅱ a (n=5), Ⅱ b (n=4), Ⅲ (n=5), and Ⅳ (n=0). Compared with normal group, altered SEP responses were associated with significantly less FLB-stained myelin of posterior column ( 106±27 vs 121±8;P=0.036, ＜ 0.05), higher contrast medium density in posterior dorsal colunn (95±5 vs 87±6; P=0.041 )and fewer neurons within posterior horn [ (21 ± 8)/mm2 vs (29 ± 6)/mm2, P＞0.05] by Micro- CT.Histopathologically, type Ⅰ SEP was associated with central canal enlargement of the spinal cord; type Ⅱ a with intra-gray matter bleeding, phlebectasia and constriction of central canal; type Ⅱ b with distortion of gray and white matters, and increase of blood vessels; and type Ⅲ with loss of white-gray matter structure,fewer neurons and even cavernous degeneration of the matrix. Conclusions Different SEP responses to chronic compression-induced myelopathy may reflecte the severity of damage to posterior tract and neurons in gray matter of the spinal cord. As a prognostic indicator, SEP is shown to be correlated well with certain pathological characteristics.