Sebum secretion was measured on the forehead of 47 patients with idiopathic Parkinson's disease before and after treatment with anticholinergic (biperiden), levodopa + AAID and bromocriptine, by the osmic acid technique. Another 100 patients under biperiden, levodopa 4- AAID or association of both, for at least one year, were also evaluated. The male parkinsonian «de novo» patients have shown greater sebum secretion than female patients. It was also concluded that biperiden failed to reduce sebum secretion rate. On the other hand, it was found that L-dopa + AAID reduces the sebum secretion (CL = casual level and SER = sebum excretion rate) on both male and female patients. Bromocriptine (10mg/day) was the second dopaminergic therapy employed in the present work. Similarly to L-dopa, this dopaminergic agonist was able to significantly reduce sebum secretion (both CL and SER) of male patients. There was a positive and significant correlation for the 50-59 years old male patients «de novo» between CL and tremor, hypokinesia, gait and posture or functional incapacity, before treatment. After a period of treatment correlation was no more found. In relation to parkinsonians under chronic treatment was found a positive and significant correlation between sebum secretion and hypokinesia. The level of sebum secretion on parkinsonian «de novo:» patients before treatment was equal to parkinsonian patients under chronic treatment regardless the treatment, except for > 60 years old parkinsonians who have shown CL and SER higher than «de novo» parkinsonian patients with the same age but without treatment. The treatment with L-dopa + AAID significantly decreased both CL and SER of «de novo» parkinsonian patients. No difference of sebum secretion was found between parkinsonian «de novo» patients before treatment and patients under treatment, regardless the, drugs, but after treatment with L-dopa + AAID, «de novo» patients have shown significant lesser sebum secretion than patients under the same treatment for at least one year. It is discussed whether the suppressive effect of the dopaminergic drugs may be explained through dopamine hypothalamic dysfunction.