To observe the therapeutic efficacy of Jin-3-needling therapy (J3N) on generalized anxiety disorder (GAD) through clinical global impression scale (CGI)

and to explore the mechanism by measuring the plasma levels of corticosteroid (CS)

adrenocorticotrophic hormone (ACTH)

and platelet 5-hydroxytryptamine (5-HT) before and after treatment. Eighty-six GAD patients with the diagnosis agreeing with the inclusion criteria were assigned

according to the sequence of visiting time

to three groups. The 29 patients in the Western medicine group were treated mainly with fluoxetine or paroxetine

Alprazolam might be given additionally in severe conditions if necessary; the 29 patients in the needling group received J3N therapy with Sishenzhen

Dingshenzhen

Neiguan (PC6)

Shenmen (HT7) and Sanyinjiao (SP6) as the chief acupoints selected; and the 28 patients in the combined treatment group were treated with both drugs and needling in the same way as applied in the above two groups. The therapeutic course for all was 6 weeks. Conditions of patients were evaluated before and after treatment with CGI

and levels of CS

ACTH as well as 5-HT were measured by high performance liquid chromatography-electrochemistry. By CGI scoring

the scores of severity index and the general index were not different significantly in the three groups

but the efficacy index proved to be the highest in the needling group

the second in the combined trentment group

and the lowest in the drug group. Plasma level of ACTH and platelet content of 5-HT were lowered in all the three groups after treatment

showing statistical significance (P<0.05)

but no significant change was found in CS level (P>0.05). The therapeutic efficacy of J3N in treating GAD is equivalent to

but with the efficacy index significantly higher than

that of conventional treatment. Moreover

when combined with drugs

needling might effectively prevent the side effect of the routinely used Western drugs. The regulatory action of needling on platelet 5-HT and plasma ACTH is probably one of the acting pathways for J3N treatment on GAD.