Concentrations of indoleamine metabolic intermediates in the ventricular cerebrospinal fluid of advanced Parkinson's patients with severe postural instability and gait disorders
Concentrations of indoleamine metabolic intermediates in the ventricular cerebrospinal fluid of advanced Parkinson's patients with severe postural instability and gait disorders
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DOI：
10.1007/bf01277663
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发表时间：
1997-01-01
影响因子：
3.3
通讯作者：
Pearlstein, RD
中科院分区：
文献类型：
--
作者：
Iacono, RP;Kuniyoshi, SM;Pearlstein, RD
姿势不稳定和步态障碍（PIGD）是许多但并非所有晚期帕金森病（PD）患者残疾的主要原因。我们测量了10例因PIGD导致严重残疾的PD患者和10例以震颤和左旋多巴诱发的运动障碍为主要运动功能障碍的PD患者脑脊液样本中血清素、5-羟色氨酸（5-HTP）、5-羟基-3-吲哚乙酸（5-HIAA）和同型香草酸（HVA）的浓度。两组在疾病持续时间和年龄方面进行前瞻性匹配。两组间5-HIAA （106 +/- 50 vs. 99 +/- 34）或HVA （1068 +/- 595 vs. 881 +/- 469）的浓度（平均+/- SD (ng/ml)， PIGD优势vs.震颤-运动障碍优势）无显著差异。在以PIGD为主要症状的患者组中，血清素浓度显著降低（0.7 +/- 0.5 vs. 1.5 +/- 0.9）， 5-羟色胺浓度显著升高（684 +/- 1054 vs. 6 +/- 5）。因此，严重PIGD患者的显著特征似乎是芳香氨基酸脱羧酶（AADC）催化的反应步骤中吲哚胺代谢紊乱。这些发现表明，晚期帕金森患者PIGD的加重可能部分与AADC抑制或下调后继发的血清素能传递受损有关。
Postural instability and gait disorders (PIGD) are the primary causes of disability in many but not all advanced Parkinson's disease (PD) patients. We have measured the concentrations of serotonin, 5-hydroxytryptophan (5-HTP), 5-hydroxy-3-indoleacetic acid (5-HIAA), and homovanillic acid (HVA) in samples of ventricular cerebrospinal fluid from ten PD patients with severe disability from PIGD and from ten PD patients with tremor and levodopa induced dyskinesia as their predominant motor dysfunction. The two groups were prospectively matched for duration of disease and age. No significant differences between the two groups were found in the concentration (mean +/- SD in ng/ml, PIGD dominant vs. tremor-dyskinesia dominant) of 5-HIAA (106 +/- 50 vs. 99 +/- 34) or HVA (1,068 +/- 595 vs. 881 +/- 469). Serotonin concentration was significantly lower (0.7 +/- 0.5 vs. 1.5 +/- 0.9) and 5-HTP concentration was substantially higher (684 +/- 1,054 vs. 6 +/- 5) in the patient group with PIGD as their predominant symptoms. Thus, the distinguishing feature of patients with severe PIGD appears to be a derangement in indoleamine metabolism at the reaction step catalyzed by aromatic amino acid decarboxylase (AADC). These findings suggest that aggravation of PIGD in advanced Parkinson's may be related in part to impaired serotonergic transmission secondary to inhibition or down regulation of AADC.