Skip to main content
BMJ Case Reports logoLink to BMJ Case Reports
. 2009 Feb 2;2009:bcr08.2008.0700. doi: 10.1136/bcr.08.2008.0700

Heat stress disorders and headache: a case of new daily persistent headache secondary to heat stroke

C Di Lorenzo 1,2, A Ambrosini 1, G Coppola 2,3, F Pierelli 1,2
PMCID: PMC3029145  PMID: 21686677

Abstract

Headache is considered as a common symptom of heat stress disorders (HSD), but no forms of secondary headache from heat exposure are reported in the International Classification of Headache Disorders-2 Edition (ICHD-II). Heat-stroke (HS) is the HSD most severe condition, it may be divided into two forms: classic (due to a long period environmental heat exposure) and exertional (a severe condition caused by strenuous physical exercises in heat environmental conditions). Here we report the case of a patient who developed a headache clinical picture fulfilling the diagnostic criteria for new daily persistent headache (NDPH), after an exertional HS, and discuss about possible pathophysiological mechanisms and classification aspects of headache induced by heat conditions.

BACKGROUND

The most severe condition among the group of heat stress disorders is heat stroke (HS). It may be divided into two forms: classic and exertional. The former is due to environmental heat exposure and characterised by hyperthermia (above 40°C) and neurological dysfunction (headache, delirium, convulsions and coma). Exertional HS affects subjects performing strenuous exercise in heat environmental conditions and is characterised by more severe symptoms than the classic form. Residual neurological defects have been reported in up to 20% of exertional HS survivors.1

Although headache is reported among HS symptoms, the International Classification of Headache Disorders-second edition (ICHD-II) did not report secondary forms from heat exposure.2

Here we report the case of a patient who developed a headache clinical picture, fulfilling the diagnostic criteria for new daily persistent headache (NDPH) after an exertional HS.

CASE PRESENTATION

A 45-year-old Caucasian woman came to our outpatient headache clinic with a history of chronic headache. Eighteen months before, she presented with an abrupt loss of consciousness during a prolonged physical exercise (trekking), performed at noon on a very hot summer’s day. She received initial treatment at an emergency department where hyperthermia, hypotension, lactic acidosis, breath alkalosis and electrolytic imbalance were observed. The diagnosis was exertional HS and she underwent cooling treatment and rehydration. As she regained consciousness, some hours after admission to the emergency department, motor coordination impairment and headache were present. The patient was discharged after 5 days of clinical observation with full recovery of all physiological parameters and motor coordination. However, headache was still present, and remained constant for the next 18 months. Notably, she had a negative personal anamnesis for headache and was not suffering from other neurological or psychiatric disorders in the period preceding the exertional HS.

Pain was daily and unremitting, bilateral, frontally localised, with pressing quality and mild intensity. During menses or emotional stress it became diffused, with secondary localisation to the upper part of the neck, increased intensity (mild to moderate), occasionally pulsating in quality and accompanied by mild nausea. Headache was not aggravated by routine physical activity or increase in environmental temperature. No other pain associated symptoms were referred.

During the first 6 months of headache, she underwent various pharmacological therapies, including NSAIDs, combination drugs (propyphenazone 375 mg, butalbital 150 mg and caffeine 75 mg), oral prednisone (5 mg/day) and tramadol (up to 200 mg/day). All were ineffective. During the subsequent 12 months no more analgesics were used. A preventive therapy was never started.

INVESTIGATIONS

Physical and neurological examinations were negative. Fundus examination, EEG, cervical and brain enhanced MRI were normal. Moreover, all laboratory examinations were negative: sedimentation rate, fibrinogen, high sensitivity C reactive protein, complete blood count, protein electrophoresis and screening for medical conditions previously reported as precipitating in NDPH (Epstein–Barr virus, cytomegalovirus, Coxsackie A and B virus, Lyme disease and vasculitis).

DIFFERENTIAL DIAGNOSIS

During the time required to perform all of the above mentioned diagnostic procedures, treatment had already been shown to be effective (see below), and this efficacy makes unlikely a secondary form of headache for our patient. For this reason, brain magnetic resonance venography, to exclude cerebral vein thrombosis, and lumbar puncture, to measure CSF pressure and exclude idiopathic intracranial hypertension, were not performed; intracranial hypotension was excluded both by clinical features (headache was not influenced by orthostatic position) and enhanced MRI.

TREATMENT

Amitriptyline was introduced in increasing doses up to 40 mg/day over 4 weeks. Headache disappeared after a 2-month full dose period. After a 3 month pain free period, amitriptyline was reduced to 20 mg/day, and an episodic headache, fulfilling tension-type headache (TTH) criteria,2 slowly appeared. After 2 months, and without analgesic overuse, headache became chronic again (20 days/month), and restoring the dosage of amitriptyline to 40 mg/day did not produce any remarkable clinical change. The patient could not tolerate further dosage increase, so gabapentin (300 mg/day) was then introduced and increased by 300 mg weekly. At the end of the fourth week, pain was completely alleviated. During the subsequent 6 month period she received daily amitriptyline 40 mg and gabapentin 1200 mg. Amitriptyline was then tapered over a 1 month period and, after another 6 months, gabapentin was also discontinued.

OUTCOME AND FOLLOW-UP

After a 1 year therapy free period, and periodical clinical observations, headache attack frequency was less than 1 per month, and the clinical features fulfilled the ICHD-II criteria for infrequent episodic TTH.2 The patient denied being affected by this type of headache prior to HS development.

DISCUSSION

Fulfilling the ICHD-II criteria,1 the patient’s headache was diagnosed as NDPH. The recent finding of an increase in tumour necrosis factor α(TNFα) in the CSF of NDPH patients3 is in line with the idea that cytokine fluctuations may play a role in the pathogenesis of headache. In our patient, this mechanism could account for the clinical features of her headache, as TNFα elevation is also reported in HS.1

The 10th chapter of ICHD-II includes headache forms attributed to disorders of homeostasis, but no forms of headache secondary to heat exposure, or heat related, were codified. However, dehydration was previously reported to be a precipitating factor in headache, by alteration in homeostasis.4 We cannot exclude the fact that our case shares several pathophysiological aspects with dehydration headache, although they are different in quality, intensity and duration.

A further type of rare headache related to heat exposure is the so-called “bath related headache”: patients experience recurrent headache every time they take a bath or pour hot water over themselves.5 This headache is not related to homeostatic, or cytokine, alterations, but is due to an exaggerated neurogenic vasomotor reflex triggered by unexpected direct skin caloric stimulation. Heat alone is insufficient to provoke an attack: for this reasons, our patient’s headache does not have to be considered as a clinical variant of this form.

In conclusion, according to ICHD-II criteria, we consider that our patient was suffering from NDPH, and hypothesise that headache was induced by HS, adding “heat” to the several acute precipitating factors of the NDPH. Moreover, we encourage publication of other cases regarding the relationship between headache and heat exposure, as we believe that by increasing attention on this topic, a revision of the 10 chapter of ICHD-II could be considered.

LEARNING POINTS

  • The most severe condition among the group of heat stress disorders is heat stroke (HS). It may be divided into two forms: classic and exertional.

  • The 10th chapter of the International Classification of Headache Disorders – second edition (ICHD-II) is devoted to headache forms attributed to disorders of homeostasis, but did not report secondary forms of headache heat related, even though headache forms due to dehydration were previously reported.

  • Here a case of new daily persistent headache (NDPH) after an exertional HS is described.

Acknowledgments

This article has been adapted with permission from Di Lorenzo C, Ambrosini A, Coppola G, Pierelli F. Heat stress disorders and headache: a case of new daily persistent headache secondary to heat stroke. J Neurol Neurosurg Psychiatry 2008;79:610–11.

Footnotes

Competing interests: None.

REFERENCES

  • 1.Bouchama A, Knochel JP. Heat Stroke. N Engl J Med 2002; 346: 1978–88 [DOI] [PubMed] [Google Scholar]
  • 2.Headache Classification Subcommittee of the International Headache Society The International Classification of Headache Disorders, 2nd Edn Cephalalgia 2004; 24(suppl 1): 1–151 [DOI] [PubMed] [Google Scholar]
  • 3.Rozen T, Swidan SZ. Elevation of CSF tumor necrosis factor alpha levels in new daily persistent headache and treatment refractory chronic migraine. Headache 2007; 47: 1050–5 [DOI] [PubMed] [Google Scholar]
  • 4.Blau JN, Kell CA, Sperling JM. Water-deprivation headache: a new headache with two variants. Headache 2004; 44: 79–83 [DOI] [PubMed] [Google Scholar]
  • 5.Rossi P, Nappi G. Bath-related headache: the first European case. Cephalalgia 2006; 26: 1485–6 [DOI] [PubMed] [Google Scholar]

Articles from BMJ Case Reports are provided here courtesy of BMJ Publishing Group

RESOURCES