Abstract
Liao et al. (1) describe four middle-age Taiwanese women with bathing headache – a thunderclap headache triggered by bathing in warm water. This report complements an earlier series of 3 middle-age Japanese women reported by Negoro et al. (2) who also experienced recurrent sudden severe headaches provoked by bathing. It is worth pointing out that among these seven pateints, some of the headaches were also triggered by diving into cold water, brushing teeth with cold water, walking into cold wind, and coughing. In Liao's series, two patients were hypertensive at the time of presentation, and one patient had diffuse cerebral vasospasm, posterior leukoencephalopathy, and suffered a residual symptomatic cerebellar infarction. Because each of the patients reported in Liao's report clinically resembled and met the proposed criteria for idiopathic thunderclap headache (ITH), the authors suggested that Bathing headache is a variant of ITH (3, 4).
As more cases of idiopathic thunderclap headache are reported, a definite clinical picture is beginning to emerge. As these and other cases in the literature demonstrate, ITH appears to be a predominantly uniphasic headache syndrome which may occur spontaneously or be provoked by a variety of factors (e.g. bathing, valsalva, sexual intercourse and other forms of intense exertion, postpartum period) in predisposed individuals during a period of vulnerability (5). During this period, patients experience recurrent thunderclap headaches over a period of 1–2 weeks and may or may not have hypertension, posterior leukoencephalopathy, and diffuse reversible cerebral vasospasm (6, 7). In rare circumstances, transient neurological deficits or cerebral infarction may occur, presumably in cases where vasospasm is sufficiently severe and prolonged to produce cerebral ischemia (8, 9). In some cases of ITH with reversible vasospasm, CSF pleocytosis and protein elevation have been noted (10).
Idiopathic thunderclap headache, whether triggered by temperature changes or occurring spontaneously without obvious provocation, appears to be an autonomic neurovascular reflex. Vasospasm is uncommon and very rarely does cerebral infarction occur. As described in the report by Liao et al. (1), nimodipine has been advocated for patients with vasospasm and symptoms of cerebral ischemia. Even though neurological sequelae in this syndrome are rare, a brief course of nimodipine appears prudent in patients with documented vasospasm, especially in the setting of focal neurological symptoms.