Teaching case presentation--primary thunderclap headache.

CASE PRESENTATION A 67-year-old woman presented to the emergency department for the evaluation of a new suddenonset headache. The headache began suddenly while she was seated at a meeting on July 30, 2008. No preceding event was identified before the onset of the headache such as trauma, infection, coughing, sexual activity, Valsalva maneuver, exertion, or sleep. The headache was excruciating and explosive in quality, reaching maximum intensity within seconds. The pain began in the occipital and nuchal regions bilaterally, with radiation throughout the entire head. The headache continued for 4 hours at maximal intensity. She denied any associated symptoms of photophobia, phonophobia, nausea, vomiting, weakness, numbness, brainstem signs, autonomic features, or constitutional symptoms. She had no aura or premonitory symptoms prior to the headache. There was no positional component associated with the headache. She could not identify any alleviating or worsening factors. Her past medical history was significant for arthritis, hyperlipidemia, and sinus tachycardia. She had a full cardiologic work-up for the sinus tachycardia including cardiac catheterization, which was unremarkable. She was currently taking Lipitor 10 mg daily and Atenolol 50 mg daily for sinus tachycardia. She denied any other prescribed or alternative medications. She endorsed no symptoms of anxiety or depression, but reported some difficulty with falling and staying asleep. She drank 1-2 alcoholic beverages per month, but had no history of drug or tobacco use. Her caffeine intake was minimal. Her mother had a history of migraine headaches. Examination in the emergency department revealed normal and stable vital signs, with an unremarkable general physical and neurological examination. Specifically, there was no evidence of fever or meningeal signs. Given the absence of a prior history of headaches and the presence of a sudden-onset explosive headache that rapidly reached peak intensity within seconds, extensive diagnostic testing was performed to exclude secondary causes of headache. An unenhanced computed tomography (CT) scan of the brain was normal. Following this study, a lumbar puncture under CT guidance was performed with a normal opening pressure of 150 mm of cerebrospinal fluid (CSF). Her CSF analysis showed clear and colorless fluid with no evidence of xanthochromia, normal protein, normal glucose, and 1 white blood cell (WBC) and 3 red blood cells (RBC) in tube 1 and no WBCs or RBCs in tube 4. Gram stain and bacterial, viral, and fungal cultures were negative; CSF testing for cryptococcal antigen and acid-fast bacilli was similarly negative. An electrocardiogram and routine laboratory studies, including a complete blood count, basic metabolic panel, coagulation profile, liver function tests, thyroid function tests, erythrocyte sedimentation rate, antinuclear antibodies, cyanocobalamin level, cardiac enzymes, urine analysis, and serum and urine protein electrophoresis, were all normal. Magnetic resonance imaging (MRI) of the brain and cervical spine, magnetic resonance angiography (MRA) of the brain and neck, and magnetic resonance venography (MRV) of the brain were all normal. Specifically, there was no evidence of ISSN 0017-8748 doi: 10.1111/j.1526-4610.2009.01504.x Published by Wiley Periodicals, Inc. Headache © 2009 the Author Journal compilation © 2009 American Headache Society