Battistella P A, Bordin A, Cernetti R, Broetto S, Corrà S, Piva E, Plebani M
Department of Pediatrics, University of Padua, Padova, Italy.
Headache. 1996 Feb;36(2):91-4. doi: 10.1046/j.1526-4610.1996.3602091.x.
Interictal serum levels of serotonin and plasma and mononuclear cell concentrations of beta-endorphin were measured in 20 juvenile patients (13 suffering from migraine without aura and 7 from episodic tension-type headache) before and after 3 months of L-5-hydroxytryptophan treatment (5 mg/kg/day) and compared with a control group of 17 headache-free healthy subjects. While no significant differences in serum serotonin levels emerged between the three groups (migraine 104.6 +/- 26 micrograms/L, tension-type headache 90.7 +/- 26.2 micrograms/L, controls 96 +/- 32.9 micrograms/L), significantly lower plasma and mononuclear cell concentrations of beta-endorphin were found in both patient groups by comparison with the healthy controls (beta-endorphin in plasma: migraine sufferers 16.2 +/- 4.2 pmol/L [P < 0.05], tension-type headache subjects 14.5 +/- 1.7 pmol/L [P < 0.001] vs controls 21.3 +/- 4.6 pmol/L and respectively, beta-endorphin in mononuclear cells: migraine sufferers 110.5 +/- 16.4 pmol/10(6) GB/L [P < 0.001], tension-type headache subjects 142.3 +/- 22.7 pmol/10(6) GB/L [P < 0.001] vs controls 359.3 +/- 31.6 pmol/10(6) GB/L). No differences emerged between the two clinical forms of headache for the plasma and mononuclear cell concentrations of beta-endorphin. After L-5-hydroxytryptophan treatment, serum serotonin and both plasma and mononuclear cell beta-endorphin levels tended to be higher, though not significantly so, than prior to treatment, and the clinical score (frequency x intensity of headache attacks) was significantly lower in both headache groups than at the baseline. This study supports the theory that opiate analgesic system function is abnormally low in juvenile primary headache as in adults, and confirms that administering serotoninergic precursor drugs increases beta-endorphin, even in the peripheral blood, and may favorably affect clinical symptoms.
在20名青少年患者(13名无先兆偏头痛患者和7名发作性紧张型头痛患者)中,于L - 5 - 羟色氨酸治疗(5毫克/千克/天)3个月前后测量了发作间期血清5 - 羟色胺水平以及血浆和单核细胞中β - 内啡肽的浓度,并与17名无头痛的健康受试者组成的对照组进行比较。三组之间血清5 - 羟色胺水平无显著差异(偏头痛组104.6±26微克/升,紧张型头痛组90.7±26.2微克/升,对照组96±32.9微克/升),但与健康对照组相比,两个患者组的血浆和单核细胞中β - 内啡肽浓度均显著降低(血浆中β - 内啡肽:偏头痛患者16.2±4.2皮摩尔/升[P < 0.05],紧张型头痛患者14.5±1.7皮摩尔/升[P < 0.001],对照组21.3±4.6皮摩尔/升;单核细胞中β - 内啡肽分别为:偏头痛患者110.5±16.4皮摩尔/10⁶GB/升[P < 0.001],紧张型头痛患者142.3±22.7皮摩尔/10⁶GB/升[P < 0.001],对照组359.3±31.6皮摩尔/10⁶GB/升)。两种临床类型的头痛在血浆和单核细胞β - 内啡肽浓度方面无差异。L - 5 - 羟色氨酸治疗后,血清5 - 羟色胺以及血浆和单核细胞β - 内啡肽水平均趋于高于治疗前,但差异不显著,且两个头痛组的临床评分(头痛发作频率×强度)均显著低于基线水平。本研究支持这样一种理论,即与成年人一样,青少年原发性头痛患者的阿片类镇痛系统功能异常低下,并证实给予5 - 羟色胺能前体药物可增加β - 内啡肽,甚至在外周血中,且可能对临床症状产生有利影响。