Abstract
Hot bath-related headache (HBRH) was described only recently, and has been rarely reported in the literature. Typical HBRH is provoked by pouring hot water on oneself or soaking in a hot bath, and lasts from 10 min to several hours (1–4). The headache develops rapidly and reaches a peak level of pain within a minute (1–4). HBRH has a bursting and pulsatile character and is seldom accompanied by nausea, vomiting, photophobia or phonophobia (2–4). Most HBRH attacks last up to several weeks and disappear spontaneously. Some HBRH is associated with cold stimulus headache (CSH), whereby headache is provoked by a cold stimulus (1, 3). The pathogenic mechanism of HBRH has not yet been established. Nimodipine, amitryptiline and valproate are known therapeutic options if symptoms do not improve spontaneously (2, 3, 5, 6). In this report, we describe the case of a woman who was relatively young at the onset of HBRH, with a long symptomatic period of typical HBRH accompanied by CSH and a dramatic response to oral topiramate.
Case report
A 34-year-old woman presented with a 6-year history of intermittent headache. When she took a hot bath, symptoms gradually occurred in both occipital areas and spread to the whole head. The headache reached maximum intensity within 2–3 min and lasted for approximately 3–4 days. At that time, another type of headache also developed. When she went out in cold weather, she experienced sudden headache as soon as cold air came into contact with her head and face, with the pain rapidly becoming very severe. The nature of the headache was similar to HBRH and distributed throughout the head from the onset. The pain induced by cold temperature was more abrupt and severe than HBRH. The patient's CSH persisted 1–2 days, shorter than HBRH. She had no history of head trauma, drug addiction, infection or other illness.
After the first episodes, she experienced headaches of a similar pattern whenever she poured hot water over her body or exposed herself to low temperature. The headache was not provoked by exposure to a hair dryer or other types of heat. Once evoked, headaches were always severe in intensity, throbbing in nature and sometimes associated with facial flushing, nausea and vomiting. She did not have photophobia or phonophobia. Once symptoms developed, she could not maintain her normal daily lifestyle. As a result, she had tried not to take a bath with hot water and not to go out in cold weather to prevent the headaches. This approach proved successful. She had adopted these preventive measures over the last 4 years. However, a hot bath or exposure to cold temperature has always triggered a headache. She did not take any medication to control the headache, including analgesics, narcotics and non-steroidal anti-inflammatory drugs (NSAIDs), because she was very reluctant to take medication. Recent recurrences of symptoms associated with a hot bath brought her to the clinic. She was a non-smoker and drank an average of two units of alcohol a month. Her blood pressure was 110/70 mmHg and other vital signs were normal. Her body weight was 55 kg and height 165 cm.
Considering the chronicity and frequency of headache, we commenced, empirically, oral topiramate. After a regime of 25 mg topiramate per day, headache induced by hot baths became less severe and shorter in duration, although the frequency did not change. After 4 weeks, the dosage was increased to 50 mg a day. Since that time, headache was not triggered by a hot bath for >6 months. During the last 2 months of follow-up, HBRH recurred 15 days after she stopped the medication on her own. Headache began when she took a hot bath and its nature and intensity were similar to previous headache. Therefore, she again started to take topiramate 50 mg a day. When she tried a hot bath 10 days later, headache developed again but was less severe and shorter in duration. There was also no more recurrence of severe headache 10 days after the reinstitution of topiramate. One week later, headache was not triggered by a hot bath when she re-tried hot bath. After that time, the headache has not recurred. The responsiveness of CSH to topiramate could not be determined because the treatment was between spring and autumn.
Discussion
We report a 34-year-old female patient with repetitive and stereotypical headaches provoked by hot bathing and cold exposure over a period of 6 years, which had initially developed at 28 years of age.
The nature and pattern of headache were compatible with previously reported cases of HBRH (1–4). She had a paroxysmal, throbbing and intense headache recurrently triggered by hot water immersion. The headache started in both occipital areas and expanded to the entire head, reaching its peak within 2–3 min.
However, this patient is unique in some aspects. First, 28 years is an earlier age of onset than is typically observed. HBRH usually develops in middle-aged woman, aged in their 50 s and 60 s (2–4), although a few patients with early onset have been reported (4). Second, the duration of each headache episode was relatively long, lasting 3–4 days. Moreover, her headache susceptibility had persisted for 6 years. In the previously reported cases, each headache episode had usually lasted 30 min to several hours, with episodes generally remitting after several months without treatment, although there are some reports of cases with a long history (3–15 years) of symptoms before remission (2–4). Third, HBRH was combined with CSH in the present patient. HBRH combined with CSH has rarely been reported. The diagnostic criteria of CSH have not been established. Previously reported cases of CSH combined with HBRH are not throbbing in nature and have a moderate to severe intensity lasting 1–9 h (1–3). In this case, the patient had very severe throbbing headaches that were associated with nausea. The duration of symptoms, about 1–2 days, was longer than previously reported cases. Fourth, headache showed a good response to oral topiramate. Previous reports of HBRH have assessed the effectiveness of various forms of medication in the alleviation of severe pain or prevention of further attacks (2, 3, 5, 6). Some medication can relieve the headache temporarily, but the response to analgesics, narcotics and NSAIDs has been poor (2, 3). Among these medications, nimodipine has been the most frequently used. Because there are some reports showing transient vasospasm in cerebral arteries and reversible posterior leukoencephalopathy (2, 3), nimodipine, a calcium channel antagonist, could be effective in treating HBRH, as it can relieve vasospasm (5, 6). Nevertheless, the efficacy of nimodipine in HBRH is unclear. Topiramate has been used for the prevention of migraine headache. The efficacy and safety of topiramate have, to some degree, been demonstrated for patients with migraine headache (7–10). Topiramate has significant effects on the blockade of neuronal excitability and on excitatory amino acids, which are considered to be implicated in the pathophysiology of migraine (7). Topiramate has shown significant efficacy in migraine prevention at a dose of 100–200 mg a day (8–10), but the effect of topiramate on HBRH has not yet been reported. In our case, we empirically assessed its effectiveness. A relatively low dosage (50 mg a day) brought complete remission of symptoms despite repetitive exposure to the trigger of a hot bath.
Improvement after topiramate therapy should be differentiated from the natural course, because HBRH usually has a self-limiting course. However, immediate recurrence of symptoms after topiramate withdrawal and their remission after its reinstitution supports that topiramate was an effective preventive agent in this patient.
In summary, this patient had a relatively young age of onset, long duration of each headache episode and persistence of symptoms over a number of years. Her headache was, however, completely prevented by topiramate. This is the first report suggesting that topiramate is an effective therapy in persistent HBRH.