Saadé N E, Al Amin H, Abdel Baki S, Chalouhi S, Jabbur S J, Atweh S F
Department of Human Morphology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon.
Exp Neurol. 2007 Mar;204(1):205-19. doi: 10.1016/j.expneurol.2006.10.009. Epub 2006 Nov 28.
Thalamic somatosensory nuclei have been classified into medial and lateral systems based on their role in nociception. An imbalance between these two systems may result in abnormal somatic sensations and spontaneous pain. This study aims to investigate the effects of transient or permanent block of the medial and intralaminar nuclear groups on the neuropathic-like behavior in a rat model for mononeuropathy.
Neuropathy was induced on one hind paw in different groups of rats following the spared nerve injury model. When the resulting hyperalgesia and allodynia (tactile and cold) reached a maximum plateau, the rats received either chemical or electrolytic lesion or lidocaine (2%) microperfusion, placed in the various thalamic nuclear groups.
All procedures produced transient but significant decrease of neuropathic manifestations. The magnitude and duration of decrease depended on the type and the site of the block. These effects can be ranked in increasing order as follows, electrolytic<chemical<lidocaine micro-perfusion according to the procedure, and as rostro-medial<ventro-median<parafascicular nuclei, according to the site of the block. Thermal hyperalgesia was the most affected while cold allodynia showed the least attenuation. Neuropathic manifestations returned to their pre-lesion levels after 2-3 weeks, along with frequently observed delayed hyper-responsiveness to the hotplate test.
The observed results demonstrate the involvement of the medial and intralaminar thalamic nuclei in the processing of neuropathic-like manifestations, and the reversibility of the effects suggests the flexibility of the neural network involved in supraspinal processing of nociceptive information.
丘脑体感核团已根据其在伤害感受中的作用分为内侧和外侧系统。这两个系统之间的失衡可能导致躯体感觉异常和自发痛。本研究旨在探讨内侧和板内核群的短暂或永久性阻断对单神经病变大鼠模型中神经病理性样行为的影响。
按照保留神经损伤模型在不同组大鼠的一侧后爪诱导神经病变。当由此产生的痛觉过敏和异常性疼痛（触觉和冷觉）达到最大平台期时，大鼠接受化学或电解损伤或利多卡因（2%）微灌注，分别置于不同的丘脑核团。
所有操作均使神经病理性表现产生短暂但显著的降低。降低的幅度和持续时间取决于阻断的类型和部位。根据操作方法，这些效应按升序排列如下：电解<化学<利多卡因微灌注；根据阻断部位，按升序排列如下： Rostro - medial<ventro - median<束旁核。热痛觉过敏受影响最大而冷觉异常性疼痛减弱最少。2 - 3周后神经病理性表现恢复到损伤前水平，同时经常观察到对热板试验的延迟高反应性。
观察结果表明内侧和板内核团参与神经病理性样表现的处理，且效应的可逆性提示参与伤害性信息脊髓上处理的神经网络具有灵活性。
