667 much more likely to be investigation of avoidance behaviour
pharmacological manipulations, fruitful than the
earnest
are
in rats. The two-process theory, incidentally, was not "proposed" by Hebb as you assert. It was current in the 19th century, and is usually attributed to William James, although James himself
drew offer
heavily from other writers.14 Hebb’s contribution was to a neurophysiological hypothesis to account for the two
processes."
son
for this is
not
known, and it remains
lowering the serum-prolactin
will influence
to
seen
whether
sperm pro-
duction. Institute of Medical
P. FALASCHI G. FRAJESE A. Rocco
Pathology II,
University of Rome, Rome, Italy Departments of Endocrinology and Chemical Endocrinology, St. Bartholomew’s Hospital,
G.M.BESSER L. H. REES
London EC1A 7BE
Kingston Hospital, Kingston on Thames, Surrey KT2 7QB
be
mature
MICHAEL KOPELMAN
REPLACEMENT THERAPY IN UNCOOPERATIVE PATIENTS WITH ENDOCRINE-DEFICIENCY PROLACTIN AND IDIOPATHIC OLIGOSPERMIA
STATES
SIR,-Serum-prolactin levels in patients with oligospermia and azoospermia have been reported to be above the normal range.’2 To verify this observation we examined a group of men with idiopathic oligospermia. The criteria for oligospermia in the 23 patients were low sperm concentration (30x 106/ml or less) with normal libido and potency, normal serum basal luteinising hormone, folliclestimulating hormone, and testosterone levels, without any urological or chromosomal abnormalities, and with a testicularbiopsy evidence of maturation arrest at the spermatid level. As controls we studied 23 healthy volunteers of similar age. Serum-prolactin was measured by a specific double-antibody radioimmunoassay on blood-samples taken between 8 and 10 A.M. The laboratory upper limit of normal for men is less than 360 mU/1. Seminal-fluid analyses were done on samples collected after 3 days of sexual abstinence.
SIR,-Dr Nathan and colleagues (Feb. 10, p. 319) report a twice-weekly regimen for replacement therapy in an uncooperative patient with hypopituitarism. We have had a similar experience with a supervised regimen in a patient with Addison’s disease and autoimmune hypothyroidism. In July, 1967, a 50-year-old woman presented with classical features of Addison’s disease with gross pigmentation, hypotension (systolic blood-pressure 80 mm Hg), and hyponatrxmia (110 mmol/1). She improved rapidly with intravenous saline and hydrocortisone. Subsequent corticotrophin stimula-
SERUM-PROLACTIN VALUES IN
23
CONTROLS AND
successful
tion showed no adrenal response and her serum contained antibodies to adrenal cortex. She was stabilised on cortisone acetate 37.5 mg daily and discharged. She attended clinics regularly at first and, although remaining pigmented, was otherwise clinically normal with normal electrolytes. However, she was admitted in 1970 in addisonian crisis, thought to have been precipitated by a chest infection, and in 1972 was lost to
follow-up.
23
She
OLIGOSPERMIC PATIENTS
*p