Chudler Eric H, Dong Willie K
Department of Anesthesiology and Multidisciplinary Pain Center, University of Washington, Seattle, WA 98195, USA.
Pain. 1995 Jan;60(1):3-38. doi: 10.1016/0304-3959(94)00172-B.
The involvement of the basal ganglia in motor functions has been well studied. Recent neurophysiological, clinical and behavioral experiments indicate that the basal ganglia also process non-noxious and noxious somatosensory information. However, the functional significance of somatosensory information processing within the basal ganglia is not well understood. This review explores the role of the striatum, globus pallidus and substantia nigra in nociceptive sensorimotor integration and suggests several roles of these basal ganglia structures in nociception and pain. Electrophysiological experiments have detailed the non-nociceptive and nociceptive response properties of basal ganglia neurons. Most studies agree that some neurons within the basal ganglia encode stimulus intensity. However, these neurons do not appear to encode stimulus location since the receptive fields of these cells are large. Many basal ganglia neurons responsive to somatosensory stimulation are activated exclusively or differentially by noxious stimulation. Indirect techniques used to measure neuronal activity (i.e., positron emission tomography and 2-deoxyglucose methods) also indicate that the basal ganglia are activated differentially by noxious stimulation. Neuroanatomical experiments suggest several pathways by which nociceptive information may reach the basal ganglia. Neuroanatomical studies have also indicated that the basal ganglia are rich in many different neuroactive chemicals that may be involved in the modulation of nociceptive information. Microinjection of opiates, dopamine and gamma-aminobutyric acid (GABA) into the basal ganglia have varied effects on pain behavior. Administration of these neurochemicals into the basal ganglia affects supraspinal pain behaviors more consistently than spinal reflexive behaviors. The reduction of pain behavior following electrical stimulation of the substantia nigra and caudate nucleus provides additional evidence for a role of the basal ganglia in pain modulation. Some patients with basal ganglia disease (e.g., Parkinson's disease, Huntington's disease) have alterations in pain sensation in addition to motor abnormalities. Frequently, these patients have intermittent pain that is difficult to localize. Collectively, these data suggest that the basal ganglia may be involved in the (1) sensory-discriminative dimension of pain, (2) affective dimension of pain, (3) cognitive dimension of pain, (4) modulation of nociceptive information and (5) sensory gating of nociceptive information to higher motor areas. Further experiments that correlate neuronal discharge activity with stimulus intensity and escape behavior in operantly conditioned animals are necessary to fully understand how the basal ganglia are involved in nociceptive sensorimotor integration.
基底神经节在运动功能中的作用已得到充分研究。最近的神经生理学、临床和行为实验表明，基底神经节也处理无害和有害的躯体感觉信息。然而，基底神经节内躯体感觉信息处理的功能意义尚未得到很好的理解。本综述探讨了纹状体、苍白球和黑质在伤害性感觉运动整合中的作用，并提出了这些基底神经节结构在伤害感受和疼痛中的几种作用。电生理实验详细描述了基底神经节神经元的非伤害性和伤害性反应特性。大多数研究一致认为，基底神经节内的一些神经元编码刺激强度。然而，这些神经元似乎不编码刺激位置，因为这些细胞的感受野很大。许多对躯体感觉刺激有反应的基底神经节神经元仅被有害刺激激活或对其有不同反应。用于测量神经元活动的间接技术（即正电子发射断层扫描和2-脱氧葡萄糖方法）也表明，基底神经节对有害刺激有不同的激活反应。神经解剖学实验提出了伤害性信息可能到达基底神经节的几种途径。神经解剖学研究还表明，基底神经节富含许多不同的神经活性化学物质，这些物质可能参与伤害性信息的调制。向基底神经节微量注射阿片类药物、多巴胺和γ-氨基丁酸（GABA）对疼痛行为有不同影响。将这些神经化学物质注入基底神经节对脊髓上疼痛行为的影响比对脊髓反射行为的影响更一致。电刺激黑质和尾状核后疼痛行为的减轻为基底神经节在疼痛调制中的作用提供了额外证据。一些患有基底神经节疾病（如帕金森病、亨廷顿病）的患者除了运动异常外，还存在疼痛感觉改变。这些患者经常有难以定位的间歇性疼痛。总体而言，这些数据表明基底神经节可能参与（1）疼痛的感觉辨别维度，（2）疼痛的情感维度，（3）疼痛的认知维度，（4）伤害性信息的调制，以及（5）伤害性信息向更高运动区域的感觉门控。需要进一步的实验，将神经元放电活动与操作性条件反射动物的刺激强度和逃避行为联系起来，以充分了解基底神经节如何参与伤害性感觉运动整合。
