Hoehn M M, Crowley T J, Rutledge C O
Adv Exp Med Biol. 1977;90:243-54. doi: 10.1007/978-1-4684-2511-6_15.
The urinary excretion of free dopamine in 37 untreated parkinsonian patients correlated negatively with the severity of rigidity and akinesia (p less than 0.025) and with total neurologic deficit (p less than 0.05). In a parallel study of psychiatric patients, those with the lowest levels of urinary free dopamine before treatment were the most vulnerable to, and developed the most severe, secondary parkinsonian rigidity (p less than 0.005), akinesia (p less than 0.05), and total deficit (p less than 0.01) when they were subsequently treated for two weeks with trifluoperazine. In neither study was there a significant correlation between free urinary dopamine and tremor. These studies directly associate the level of free dopamine in the urine with the severity of the parkinsonian syndrome. Therefore, although many peripheral sources contribute to urinary free dopamine, a small decrease in the level may actually reflect the severity of the disturbance of central dopamine metabolism and the known deficiency of dopamine in the neurons of the parkinsonian brain.
37例未经治疗的帕金森病患者尿中游离多巴胺的排泄量与强直和运动不能的严重程度呈负相关(p<0.025),与总的神经功能缺损呈负相关(p<0.05)。在一项针对精神病患者的平行研究中,治疗前尿中游离多巴胺水平最低的患者,在随后接受氟哌嗪治疗两周时,最易出现继发性帕金森病强直(p<0.005)、运动不能(p<0.05)和总的功能缺损(p<0.01),且症状最为严重。在这两项研究中,尿中游离多巴胺与震颤均无显著相关性。这些研究直接将尿中游离多巴胺水平与帕金森综合征的严重程度联系起来。因此,尽管尿中游离多巴胺有许多外周来源,但水平的轻微下降实际上可能反映了中枢多巴胺代谢紊乱的严重程度以及帕金森病患者脑中多巴胺神经元已知的缺乏情况。