Orgasmic migraine aura: Report of two cases

Abstract

Background

Paroxysmal neurological symptoms occurring with sex cause considerable anxiety and sometimes have a serious cause. Thunderclap headache is the most well-known and requires urgent investigation at first presentation for subarachnoid haemorrhage and other significant pathologies. After exclusion of underlying causes, many prove to be primary headache associated with sexual activity. Orgasmic migraine aura without headache is not currently recognised as a clinical entity.

Case reports

We report two patients with acephalgic orgasmic neurological symptoms fulfilling the criteria for migraine aura.

Conclusions

The incidence of acephalgic orgasmic migraine aura is unknown. It should be considered as part of the differential of paroxysmal sex-related neurological symptoms, and clinically differentiated from fixed deficits, reversible cerebral vasoconstriction syndrome and post-orgasmic illness syndrome.

Sudden onset (thunderclap headache) during sex, particularly at the time of orgasm, is distressing and sometimes due to a serious underlying cause, particularly cerebral haemorrhage. Urgent investigation at first presentation is mandatory, especially as 4–12% of subarachnoid haemorrhages secondary to aneurysm rupture are preceded by sexual activity (1).

After excluding a serious underlying cause, most patients have primary headaches associated with sexual activity, at or before orgasm (1–6). The only prospective study, in a Taiwanese specialist headache clinic of 30 patients over 5 years, found 60% of coital headaches were due to reversible cerebral vasoconstriction syndrome, 6.7% due to haemorrhage, and 33% were primary (7). This does not reflect general experience, where most are primary. In a retrospective general medical case series, 11 of 14 sex headaches were primary, and 3 of 14 were low pressure headaches (8).

0.2–1.6% of headache clinic populations report primary headaches associated with sexual activity (5,9–11), as per International Classification of Headache Disorders (ICHD) 3 beta (5). Previous divisions into pre-orgasmic (type 1), or sudden onset, orgasmic headaches (type 2) have been removed in the current classification, as the clinical features are not thought to be distinct (12,13). Primary sex headaches must be distinguished from postural low-pressure headaches, which have a separate classification, specific mechanism and are often associated with hypermobility (5).

Much data on orgasmic headache come from retrospective studies and anecdotal reports. The relationship is complex, as orgasm may also relieve headaches (14). A retrospective study in 83 women at a United States headache clinic demonstrated that orgasm provided migraine relief in 50% of their population, compared with 30% relief with triptans (4). This raises questions about the mechanism through which orgasm may trigger migraine, why the symptomatology is sometimes reversed, and whether there may be gender differences.

Some primary sex headache share features or co-exist with exertional headache (a term embracing headaches associated with coughing, sneezing, Valsalva manoeuvre and straining when passing stool). Mechanisms for primary sex headaches are uncertain and a number of potential factors have been postulated, including autonomic and blood pressure changes (6), muscle contraction (6,15), vasoconstriction (16), and migraine (17).

These two patient reports document reversible symptoms consistent with orgasmic acephalgic aura, fulfilling criteria for ICHD-3 migraine aura (5).

Clinical cases

Case 1: A 23-year-old woman presented with episodic disturbance over the preceding 6 months. During intercourse she experienced weakness of both legs, tremor, oscillopsia, dizziness (a sensation she was spinning) and slurred speech. Symptoms commenced at the onset of orgasm and persisted for half an hour, with full recovery over the next 15 minutes. Symptoms occurred while the patient was lying down, and were not altered by posture. There was no prodrome, no premonitory symptoms, and no correlation with level of exertion.

There was a background history of migraine headache and asthma and a family history of migraine. She never had headaches during or around the time of sex, nor exertional headaches on other occasions. She had no symptoms of hypermobility.

Neurological and general examination was normal, with blood pressure of 110/60 and pulse 88 and regular. Magnetic resonance imaging (MRI) brain scans and magnetic resonance angiography of intracranial vessels (a day after an episode and 3 years later), and blood tests, including full blood count, electrolytes, creatinine, liver function tests, lupus anticoagulants, erythrocyte sedimentation rate, C reactive protein and autoimmune screen were all normal/negative. Cerebrospinal fluid examination 12 hours after an episode was normal (acellular, normal protein and glucose, negative xanthochromia and negative oligoclonal bands). Electroencephalograph was normal. Symptoms resolved with nifedipine 10 mg twice a day. She was able to have sexual intercourse with no further symptomatology and was well at follow-up at 3 years.

Case 2: A 33-year-old man noted a 4-month history of onset of dizziness (a sensation of the room spinning) at the time of intercourse, starting abruptly at the point of orgasm. On some occasions he noted accompanying visual symptoms, a fortification spectrum over the left visual field. The episodes occurred on multiple occasions and lasted for 10–20 minutes. He did not have any headaches during or around the time of intercourse or orgasm. Symptoms were not positional; there were no premonitory symptoms nor correlation with level of sexual exertion. On other occasions he had episodes of dizziness lasting for up to 10 minutes at a time, unrelated to posture, followed sometimes by a moderate headache which was unilateral, throbbing, lasting 4–6 hours and associated with mild nausea and photophobia. Neurological and general examination was normal, and BP was 126/78. All blood tests, electrocardiogram and magnetic resonance imaging of the brain and intracranial vessels were normal.

He declined preventive treatment. A trial of diclofenac 50 mg stat one hour before sex was tried with success. He remains well at 6 months follow up.

Discussion

Two young patients developed reversible acephalgic orgasmic symptoms fulfilling ICHD-3 criteria of migraine aura (5). The female developed sensory and motor symptoms consistent with a brainstem aura, while the male developed vertigo and typical visual aura. They were of sudden onset, with no associated headache, and were primary, with no evidence of intracranial aneurysm, posterior fossa or other structural pathology or progressive disease.

Before concluding that this phenomenon is migrainous, further investigation of incidence and clinical features in a larger cohort is needed, particularly to examine whether the aura is followed by typical migraine headache in some instances. There are no previous descriptions of acephalgic migraine aura, but post coital migraine with aura was described in a patient with a history of migraine without aura who developed visual fortification spectra 20 minutes after orgasm, followed by a unilateral throbbing headache lasting 4–12 hours (18).

It is unclear how orgasm might trigger the aura phase of migraine. Ictal as well as interictal hypersensitivity to sensory stimulation in migraineurs is important in accompanying features such as photophobia, osmophobia and allodynia (19). For some modalities, aura symptoms can be correlated with the anatomical location of the excitatory and inhibitory processing, such as paraesthesia in the somatosensory cortex (20). Putative networks involved in orgasmic aura are likely to be complex and align better with a model of dysfunction of a neurolimbic network, involving nociceptive, emotional and sensory elements (21). Along with migrainous central sensitization, known limbic activation in both sexual arousal and pain mechanisms may play a role in migraine triggered by orgasm (18,21–23). Increased interictal limbic activation to negative, but not positive, emotional stimuli was recently shown in migraineurs (24). Further functional studies may elucidate how sensory activation and emotional states, including orgasm, trigger aura, and how the migraine process may be attenuated before nociceptor activation.

Sudden onset headache and focal neurological deficits during sex may occur with reversible cerebral vasoconstriction syndrome. Diagnosis may be difficult as it shares clinical features with migraine with aura, and in half of patients the initial MRI brain scan is normal and subsequent angiography is required to identify vascular anomalies (25). Our patients had no thunderclap headache, normal angiography, and no risk factors for this condition, which include pregnancy and vasoconstrictive drugs (26). Furthermore, reversible cerebral vasoconstriction syndrome occurs over days to weeks, in contrast to the time course of migraine aura symptoms.

Post-orgasmic illness syndrome (POIS) shares some clinical features with migraine with aura, including headache, weakness, and visual disturbance (27). Autonomic disturbances such as nasal and sinus congestion, and facial flushing, are seen in in other headache syndromes including migraine, cluster and autonomic cephalalgias (5,28), and there may be a link between POIS and orgasmic aura. A small uncontrolled study found positive skin-prick test with autologous semen in 88% of men with POIS, possibly implicating a hypersensitivity reaction (27). If replicated, this finding would be evidence against a link with orgasmic aura, or would suggest that POIS encompasses more than one pathophysiological process (29).

The evidence for treatment of primary sex headache is limited to case descriptions. One reports success with nimodipine, a calcium channel blocker, in a patient with orgasmic headache and demonstrated vasospasm (putatively blocking the transient cerebral ischaemia and waves of cortical depression) (30). Nifedipine, another calcium channel blocker, was successful in one of our patients. Non-steroidal anti-inflammatories such as diclofenac are a recognised acute treatment for migraine headache but have not been studied in migraine aura (31). This was effective in our second patient. The mechanism of action is unclear.

Orgasmic acephalgic aura is an important differential for paroxysmal symptoms during sex, and fulfils ICHD-3 criteria for migraine aura. Further prospective study is planned to investigate the incidence of this in general populations, and in those with migraine.

Clinical implications

Orgasmic headache or other sudden onset symptoms mandate urgent investigation for serious underlying pathology, particularly intracerebral haemorrhage, but in many the symptoms are primary.

Acephalgic orgasmic aura fulfilling ICHD-3 criteria for migraine aura is described in two patients.