The patient’s past health was good. He had two psychiatric assessments in 1981 and 1996, and three neurological assessments in 1996 and 1997, with a tertiary referral being made to the national Hospital for Neurological Diseases. He has been fully investigated with 24 h electroencephalogram (EEG), magnetic resonance imaging (MRI) and magnetic resonance angiography (MRA) scans of the brain and numerous blood tests. No abnormality or reason for his symptoms could be elucidated.

When he attended this medical centre he was keen to seek further help. Propranolol 10 mg twice daily was prescribed prophylactically at this time but the patient did not persevere with treatment.

He presented again 3 years later, in July 2008. He said he had both good news and bad news. Firstly, 8 weeks into his wife’s and the patient’s own first pregnancy, sexual activity no longer brought on his syndrome. After the baby was born, however, his condition fully returned.

At 8 weeks serum progesterone values rise greatly in a pregnant women and similarly fall after delivery. The patient had done his own research and wanted me to prescribe progesterone. His condition was now also a stress for his wife. I was reluctant to prescribe oral progesterone to a relatively young male. Instead I prescribed progesterone cream 8% which I suggested he apply around the nostril and upper lip area daily. This proved to be ineffective as did a subsequent prescription of a trial of the dopamine agonist, bromocriptine 2.5 mg daily.

In October 2008 I agreed to prescribe oral progesterone. The patient signed a letter of consent after a discussion of possible side effects. I prescribed norethisterone 5 mg (10 tablets). He was to take a tablet around 30 min before sexual activity.

When I saw him again 4 months later, the treatment had been very successful with complete prevention of his attacks. He had obtained a further supply of norethisterone from a colleague at the medical centre in the interim as I was not available, and was “pleased beyond words” (sic.).

He said if he took a norethisterone tablet before the attack it alleviated his symptoms 95%, with only a background headache remaining for about 24 h.

He then usually took a further 5 mg norethisterone daily for the following 2 days to alleviate the residual symptoms and negate the possibility of his symptoms regenerating, although it is not clear in this regard if the extra medication was necessary.

On several occasions he took 10 mg norethisterone within a few minutes after sexual activity, but less than the latent period, and his syndrome did not manifest at all.

Over a 9–10 month period norethisterone was consistently effective. The patient was relieved of more than 30 episodes of his syndrome by the progestogen without exception.

Correspondence from Merck, the manufacturer of norethisterone, at this time confirmed there were no known harmful side effects in males.

During the compilation of this report the patient’s partner became pregnant again. Once more the patient found his condition spontaneously relieved 8–10 weeks into the pregnancy.

Benign coital headache has an incidence of between 0.25–1%, but this could be higher.² The number of self reported cases on internet forums is also rapidly growing. One forum has over 250 members.³ They classify their condition without the emphasis on headache and give their syndrome an alternative name. Two cases are exemplified.⁴ It is distinctly possible that these syndromes are similar, if not the same or part of the same spectrum with similar pathogenesis. Progesterones such as norethisterone may therefore be helpful in these cases also.

No serious pathology underlies the syndrome of benign coital headache, but treatment has been limited.⁵ Different coital positions, analgesics and β-blockers have been reported to be of some help. Sexual abstention has been an unfortunate remedy for others.

Migraine is well documented to reduce in women patients during pregnancy.⁶ This is the first case reported where a woman’s pregnancy has prevented this severe form of benign coital headache syndrome developing in her partner. Close cohabitation and absorption of progesterone through touch and smell could be the beneficial mechanism. Progesterone could also be absorbed per urethra during coitus, but this would not explain the beneficial affects of the compound after non-coital sexual activity.

Serum progesterone concentrations measured in this patient were taken during the second pregnancy. The values were all low or comparatively low compared to the laboratory references quoted earlier. The patient was relieved from his condition at this time. This would suggest that the serum progesterone concentrations of the patient would be even lower during his partner’s non-pregnant state. This could explain why augmentation of serum progesterone concentrations with norethisterone supplementation are effective at this time. A small incremental rise in progesterone may be all that is necessary for its beneficial effect. It would be useful to obtain serum progesterone concentrations in the patient when his partner is no longer pregnant to corroborate this.

Norethisterone was taken during the potential latent phase of his syndrome, suggesting it has a prophylactic effect on the condition. It is possible that norethisterone has a direct ameliorative effect on the condition, as the patient would take it over 3 days, which is the length of time his benign coital headache syndrome would normally last.

Progesterones such as norethisterone have wide pharmacological activity with effects on many tissue types. Norethisterone is a neurosteroid with multiple affects on the central nervous system; it is also a precursor for other powerful neurosteroids such as allopregnanolone. A defect of precursor synthesis could allow for the latency and resultant syndrome as highlighted here.

Certainly further studies of how norethisterone and possibly other progesterones signal relief in benign coital headache may at last throw light on the enigma and the pathos of this condition.