The effects of classic antipsychotic haloperidol plus the extract of Ginkgo biloba on superoxide dismutase in patients with chronic refractory schizophrenia
Df. Zhou et al., The effects of classic antipsychotic haloperidol plus the extract of Ginkgo biloba on superoxide dismutase in patients with chronic refractory schizophrenia, CHIN MED J, 112(12), 1999, pp. 1093-1096
Objectives To explore the association between schizophrenic symptoms and su
peroxide dismutase (SOD), and to investigate the effect of classic antipsyc
hotic haloperidol plus the extract of Ginkgo biloba (EGb) on SOD.
Methods In 54 patients with chronic refractory schizophrenia, 27 were treat
ed with haloperidol plus EGb (group 1), and the rest received haloperidol p
lus placebo (group 2). Superoxide dismutase (SOD) levels of these patients
were measured before and after treatment and compared with the levels of 25
healthy volunteers. Therapeutic efficacy was equated with a change in clin
ical rating scores assessed by standardized measurement tools including the
Scale for Assessment of Positive Symptoms (SAPS) and the Scale for Assessm
ent of Negative Symptoms (SANS).
Results Patients in group 1 improved significantly as demonstrated by score
s from both SAPS and SANS, while those in group 2 only by scores from SANS.
Assessed by SAPS, the response of patients receiving haloperidol plus EGb
was more significant than those receiving haloperidol only. SOD levels befo
re treatment in all patients were significantly higher than those in normal
controls. After treatment, SOD levels decreased significantly in group 1 b
ut not in group 2. In addition, before treatment, SOD levels in all patient
s correlated significantly with SAPS score. The levels of SOD measured befo
re treatment were also correlated with the improvement of patients as measu
red by SAPS and SANS after 12 weeks.
Conclusions EGb may enhance the efficacy of classic antipsychotic haloperid
ol on schizophrenia, especially on positive symptoms. It may work through a
n antioxidant efficacy that is involved in the therapeutic mechanism.