1129 the T.S.H. response to T.R.H.,’ whereas bromocriptine lowers the raised T.S.H. found in hypothyroid patients6 but does not influence T.S.H. in normal people.’ We have examined the T.S.H. response to T.R.H. stimulation in nine severe postencephalitic Parkinson’s disease patients before and after three months of bromocriptine therapy (mean dosage 45 mg daily). The pretreatment T.S.H. was normal. Although the T.S.H. response to T.R.H. after bromocriptine treatment suggested a partial suppression, this was not statistically significant. The normal thyroid function in parkinsonism and the negligible effect of bromocriptine on T.S.H. secretion suggest that direct dopaminergic mechanisms within the hypothalamus and pituitary do not greatly influence the regulation of T.S.H. release and that the effects of levodopa and dopamine probably involve in-

termediate mechanisms.3 Departments of Endocrinology and Neurology,

University College Hospital, London WC1E 6AU

K. M. SHAW

A. J. LEES G. M. STERN

HYPERTHYRODDISM SiR,—The case described by Dr Turner and his colleagues (Aug. 20, p. 410) shows that hyperthyroidism can recur after l2SI-induced hypothyroidism. A confirmed primary hypothyroidism,is usually permanent, but progression to thyrotoxicosis Case1 had bilateral proptosis in March, 1975. Serum-thyroxine (T4) was 2-9 g/dl (normal 4-5-10), resin-T3 test 0.72 (normal 0-80-1-25), serum thyroid-stimulating horand long-acting thyroid mone (T.S.H.). 49 U/ml (normal