Mechanism and the treatment of central deafferentation pain

中枢性传入神经阻滞疼痛的机制及治疗

• 批准号: 03454354
• 负责人: TSUBOKAWA Takashi
• 金额: $ 3.52万
• 依托单位: Nihon University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for General Scientific Research (B)
• 财政年份: 1991
• 资助国家: 日本
• 起止时间: 1991 至 1993
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-03454354/
• 关键词: Deafferentation Pain; Central Pain; Morphine; Ketamine; Barbiturate; Thalamic Pain; Motor Cortex; Thalamic pain; Central Pain; Motor Cortex; Stimulatio Therapy; cytochrome oxydase; somatosensory cortex; thalamus; thalamic pain; pain; hyper

Deafferentation of the sensory pathways within the peripheral and central nervous systems has been demonstrated to cause hyperactivity of neurons within the sensory pathways above the level of deafferentation. Such hyperactivity has been implicated in the mechanism of deafferentation pain observed clinically. In this studies ; 1) We recorded single neuron activities within the thalamic nucleus ventralis posterolateralis (VPL) after transection of the spinithalamic tract (STT) and within the sensory cortex after VPL lesions. Sensory cortex neurons became hyperactive after VPL lesions, and VPL neurous became hyperactive after STT transection through recruitment of NMDA recetors. The hyperactibities of VPL and sonsory cortex neurons were inhibited by the motor cortex stimulation. 2) After unilateral lesions restricted to the posterior ventrobasal region of the thalamus, CYO activity decreased rapidly in layr IV of the sensorimotor cortex at lesioned side. Segmentations normally seen in layr IV corresponding to barrels remained absent. While less marked decreases were also noted in other layrs, obvious recovery was subsequently obserbed. These changes in metabolic activity reflect the process of reorganization of neural circuits after tha lamocortical deafferentation from which thalamic pain is sometime produced. 3) In clinical studies, we concluded that pharmacoligical classification of deafferentation pain is useful for finding the deafferentation pain and for predicting the efficiency of chronic brain stimuration therapy, 4) Based on these results, We treated 12 cases of thalamic pain syndrome by chronic motor cortex stimulation employing epidural plate electrodes. Good pain control was obtained without any complication and side effects.

已经证明，外周和中枢神经系统内的感觉通路的传入神经阻滞会导致感觉通路内的神经元在传入神经阻滞水平之上的活动过度。这种活动过度与临床上观察到的去传入疼痛的机制有关。在这项研究中;（1）脊髓丘脑束（STT）切断后，在丘脑腹后外侧核（VPL）和感觉皮质内记录单个神经元的活动。VPL损伤后感觉皮层神经元变得过度活跃，STT切断后VPL神经元通过募集NMDA受体变得过度活跃。刺激运动皮层可抑制VPL和感觉皮层神经元的过度活动。2)单侧丘脑后腹基底区损伤后，损伤侧感觉运动皮层IV层CYO活性迅速下降。通常在Layr IV中看到的与桶相对应的节段仍然不存在。虽然在其他层也观察到不太明显的下降，但随后明显恢复。这些代谢活动的变化反映了丘脑皮层传入神经阻滞后神经回路的重组过程，丘脑痛有时也是由其引起的。3)在临床研究中，我们认为传入阻滞痛的药理学分类有助于发现传入阻滞痛和预测慢性脑刺激治疗的疗效。4）在此基础上，我们采用硬膜外板电极慢性运动皮层刺激治疗了12例丘脑痛综合征。疼痛控制良好，无并发症及副作用。

项目成果

Takashi Tsubokawa: "Neurosurgical management of deafferentation pain" Crit.Rev.Neurosurg.3. 325-331 (1993)

Takashi Tsubokawa：“传入神经阻滞疼痛的神经外科治疗” Crit.Rev.Neurosurg.3。

Fujii M., Katayama Y., Makiyama Y., Maejima S., Tsudokawa T.: "Dynamic changes in cytichrome oxidase activity in the rat somatosensory cortex following thalamocortical deafferentation." Neurological Research. 15. 384-388 (1993)

Fujii M.、Katayama Y.、Makiyama Y.、Maejima S.、Tsudokawa T.：“丘脑皮质传入神经阻滞后大鼠体感皮层细胞色素氧化酶活性的动态变化。”

Motonobu Fujii: "Dynamic changes in cytochrome oxidase activity in the rat somatosensory cortex following thalamocortical deafferentation" Neurological Research. 15. 384-388 (1993)

Motonobu Fujii：“丘脑皮质传入神经阻滞后大鼠体感皮层细胞色素氧化酶活性的动态变化”神经学研究。

Seigou Koyama: "Thalamic neuronal hyperactivity following transection of the spinothalamic tract in the cat: involvement of N-methyl-D-aspartate receptor" Brain Research. 612. 345-350 (1993)

Seigou Koyama：“猫脊髓丘脑束横断后丘脑神经元过度活跃：N-甲基-D-天冬氨酸受体的参与”大脑研究。

Yoichi Katayama: "Treatment of thalamic pain with chronic motor cortex stimulation." Paicing and Clinical Electrophysiology. 14. 131-134 (1991)

Yoichi Katayama：“通过慢性运动皮层刺激治疗丘脑疼痛。”