Sage Jacob I.
Department of Neurology, Robert Wood Johnson Medical School, University of Medicine and Dentistry of New Jersey, 97 Patterson Street, New Brunswick, NJ 08901, USA.
Curr Treat Options Neurol. 2004 May;6(3):191-200. doi: 10.1007/s11940-004-0011-x.
Pain is reported by nearly 50% of patients with Parkinson's disease. In some patients, it can be more debilitating than the motor deficits. In order to identify the appropriate treatment strategy for each patient, it is useful to categorize pain syndromes as follows: 1) low DOPA (end of dose wearing off, diphasic, or early morning) painful states are associated with inadequate levels of dopamine receptor stimulation; 2) high DOPA (peak dose) painful states occur at times of maximum levodopa efficacy; and 3) many patients report pain that has no obvious relation to dopaminergic medications or may even be caused by other conditions. Low DOPA painful states are best treated by trying to provide more continuous dopaminergic stimulation and thereby reduce or prevent the number and duration of "off" periods. Adding or increasing the dose of direct-acting dopamine receptor agonists or of catechol-o-methyl transferase inhibitors is the best first-line strategy. Other approaches include increasing the frequency of immediate-release levodopa preparations or using controlled-release preparations. More invasive approaches should be considered only when simpler methods fail. These include deep brain stimulation to the pallidum or the subthalamic nucleus, or direct duodenal continuous infusion of levodopa in patients who are unable to undergo surgery. Pain associated with excessive dopaminergic stimulation usually is a result of dystonia or severe chorea. Reduction of levodopa is the first step in attempting to diminish high DOPA states, followed by reduction or cessation of other dopaminergic agents such as selegiline, catechol-o-methyl transferase inhibitors, or direct-acting dopamine receptor agonists. Adding amantadine can reduce chorea significantly and it should be tried if the potential and actual side effects are tolerable to the patient. Deep brain stimulation is a good final option if medication adjustments are ineffective. Nonspecific pains of Parkinson's disease can be difficult to treat. The effective use of central pain suppressant or analgesics is anecdotal and difficult to verify. In untreated early disease, generalized pain or pain related to joint or muscle immobility may be reduced by effective treatment of the underlying Parkinson's disease.
近50%的帕金森病患者报告有疼痛。在一些患者中，疼痛可能比运动功能障碍更使人衰弱。为了为每位患者确定合适的治疗策略，将疼痛综合征分类如下是有用的：1）低多巴胺（剂末现象、双相现象或清晨）疼痛状态与多巴胺受体刺激水平不足有关；2）高多巴胺（峰值剂量）疼痛状态发生在左旋多巴疗效最大时；3）许多患者报告的疼痛与多巴胺能药物无明显关系，甚至可能由其他病症引起。低多巴胺疼痛状态最好通过尝试提供更持续的多巴胺能刺激来治疗，从而减少或预防“关”期的次数和持续时间。添加或增加直接作用的多巴胺受体激动剂或儿茶酚-O-甲基转移酶抑制剂的剂量是最佳的一线策略。其他方法包括增加速释左旋多巴制剂的给药频率或使用控释制剂。只有在较简单的方法失败时才应考虑更具侵入性的方法。这些方法包括对苍白球或丘脑底核进行深部脑刺激，或对无法接受手术的患者进行十二指肠左旋多巴持续输注。与多巴胺能刺激过度相关的疼痛通常是肌张力障碍或严重舞蹈症的结果。减少左旋多巴是试图减轻高多巴胺状态的第一步，随后减少或停用其他多巴胺能药物，如司来吉兰、儿茶酚-O-甲基转移酶抑制剂或直接作用的多巴胺受体激动剂。添加金刚烷胺可显著减轻舞蹈症，如果患者能耐受潜在的和实际的副作用，应尝试使用。如果药物调整无效，深部脑刺激是一个很好的最终选择。帕金森病的非特异性疼痛可能难以治疗。使用中枢性疼痛抑制剂或镇痛药的有效性只是传闻，难以证实。在早期未治疗的疾病中，有效的帕金森病基础治疗可能会减轻全身性疼痛或与关节或肌肉活动减少相关的疼痛。
