Abstract
Introduction
Migraine with aura (MA) is a primary headache infrequently induced by specific triggers, the most peculiar of which being exposure to bright light (1). The role of other factors, such as stress and mental tension, physical activity, tiredness, etc., found in a retrospective study (1), should be confirmed by a prospective diary survey.
Orgasm is not considered a trigger factor for MA. Here we report the case of a woman who complained of a typical MA attack shortly after orgasm.
Case report
A 36-year-old woman presented with a history of visual phenomena followed by throbbing headache attacks starting soon after sexual intercourse exclusively. Two to five minutes after every orgasm, she suddenly began to experience blurred vision in the left or right side of the visual field, developing into a flickering zigzag line together with pinpoint circles of red and blue light. Around these fortification spectra, hemianopsia developed. These positive and negative signs lasted 20–30 min and were immediately followed by a mild to severe throbbing pain in the frontal-temporal region contralateral to the side of aura. Pain was accompanied by photophobia and phonophobia. The headache duration was 4–12 h. The visual symptomatology was perceived with a great feeling of anxiety and fear, so much that, after a few months, she decreased the frequency of sexual intercourse and, during them, she behaved in a way to avoid orgasm. She had tried flunarizine and propranolol without any improvement. Afterwards she was put on carbamazepine (800 mg daily) and subsequently on valproate (1000 mg daily) with no effect.
In 1996, 3 years after the beginning of the attacks, she came under our care. She had suffered since the age of 12 from migraine without aura (attacks characterized by unilateral throbbing severe pain, accompanied by photophobia, phonophobia, nausea and vomiting, lasting 1 day, not precipitated by any trigger factor), with a frequency of one attack per month. Pathological history was otherwise unremarkable. Physical and neurological examinations were normal, as well as EEG and brain magnetic resonance imaging. Routine blood tests were also normal. We treated the patient with lamotrigine, at the dosage of 100 mg daily (after a period of titration), obtaining the complete disappearance of MA attacks related to orgasm. In the first 6 months, the drug was stopped twice and MA attacks promptly recurred. Treatment with lamotrigine was restarted, with complete success. The patient withdrew treatment after 2 years, without any recurrence in a 30-month follow-up.
Discussion
To our knowledge, this is the first case in which MA attacks were triggered by orgasm. The short time elapsing between orgasm and aura and the consistency of attack occurrence strongly suggest a cause–effect relationship.
Three types of sexual headache are recognized in the classification of the International Headache Society (2). The first is described as a dull ache in the head and neck, that intensifies on sexual excitement (3). Type 2 is a sudden severe (‘explosive’) headache occurring at orgasm (4). Type 3 is a postural headache resembling that of low CSF pressure developing after coitus (5). Attacks of our patient started soon after orgasm and therefore could be included in type 2 sexual headache. However, there are several differences, besides the occurrence of aura: type 2 sexual headaches are more frequent in men, usually bilateral, explosive in onset, of short duration (minutes to 3 h) and always severe. Moreover, they start at or immediately before the orgasm, while in our patient the attacks began 2–5 min after (6). Therefore we believe that our patient experienced attacks of typical migraine with aura triggered by orgasmic phase of sexual intercourse.
The physiological mechanisms of female sexual arousal and orgasm are poorly understood. It has been hypothesized that the female sexual response is related to the activation of the medial preoptic, anterior hypothalamic region and related limbic-hippocampal structures (7). Among other hypotheses, we can speculate that the activation of limbic structures, putatively involved in the pathophysiology of migraine (8), may have triggered MA attacks in this particular case. The effectiveness of lamotrigine in this drug-resistant patient further supports the utility of this drug in the prophylaxis of migraine with aura (9).