Artieda J, García De Casasola M C, Pastor M A, Alegre M, Urriza J
Servicio de Neurofisiología; Hospital Virgen del Camino, Pamplona, 31008, España.
Rev Neurol. 2001;32(6):549-58.
We review the mechanisms that may involved in the pathophysiology of dystonia.
The role of basal ganglia, spinal and brainstem interneurons, and primary motor cortex in dystonia will be discussed. Abnormalities in the discharge pattern of internal pallidum or thalamus, secondary to basal ganglia disorders might be the cause of disbalance between excitatory and inhibitory mechanisms in motor cortex. Other factors such as excessive repetition of a movement or abnormal sensory afferent discharges may be participating in cortical reorganization.
Overlapping of the cortical representation of dystonic muscles due to enlargement of cortical maps could explain overflow and co-contraction phenomena. The study of the exact role of these factors in each type of dystonia is a challenge for the future that opens the door for new therapeutic approaches.
我们回顾了可能参与肌张力障碍病理生理学的机制。
将讨论基底神经节、脊髓和脑干中间神经元以及初级运动皮层在肌张力障碍中的作用。基底神经节疾病继发的苍白球内部或丘脑放电模式异常可能是运动皮层兴奋和抑制机制失衡的原因。其他因素,如运动的过度重复或异常的感觉传入放电,可能参与皮层重组。
由于皮层图谱扩大导致肌张力障碍肌肉的皮层表征重叠,可以解释溢出和共同收缩现象。研究这些因素在每种类型肌张力障碍中的确切作用是未来的一项挑战,为新的治疗方法打开了大门。