Case Presentation

An overweight 28-year-old female presents to your office with complaints of 1-2 severe, debilitating headaches per month for the last 2 years. The headaches last 1-2 days. They are occasionally localized bifrontally, but more often localized to the right temple, right frontal and behind the right eye. There is frequently nasal rhinorrhea with her headaches. She denies any prodromal or aura type symptoms. The pain is usually a deep ache, but throbbing when severe. She denies vomiting and inconsistently gets mild nausea. She always has to wear sunglasses and go to a quiet room when the headaches occur. She says they “knock her out of commission” and she is unable to do anything because activity makes the headache worse. She recently got a new job at a law firm and these headaches are beginning to interfere with her job.

1. What is the most likely diagnosis and would it be classified as a primary or secondary headache disorder?

  1. Cluster headache
  2. Intermittent sinus headache
  3. Episodic tension headache
  4. Idiopathic intracranial hypertension (pseudotumor cerebri)
  5. Episodic migraine

2. Which of the following is NOT included in the IHS (International Headache Society) criteria for episodic migraine?

  1. Nausea/vomiting
  2. Photophobia/phonophobia
  3. Osmophobia
  4. Symptom relation to activity
  5. Pain severity/characterization

3. She says she has been reading up on different headache types and asks you if this could be tension type headache. Which one of the following symptoms she described could also be included in the International Headache Society (IHS) criteria for episodic tension type headache?

  1. Photophobia
  2. Throbbing/pulsating pain
  3. Aggravation by routine physical activity
  4. Nausea
  5. Vomiting

4. Which of the following is the first step in the proposed pathophysiology of migraine?

  1. Release of vasoactive neuropeptides from trigeminal sensory nerves
  2. Meningeal blood vessel dilation
  3. Activation of trigeminal sensory afferents in the meningeal vessels
  4. Cortical spreading depression
  5. Meningeal blood vessel constriction

5. What is the best choice of treatment at this time, assuming there are no contraindications?

  1. Prescribe an abortive agent (triptan) and NSAID to take immediately today
  2. Prescribe a preventative agent
  3. Give her a DHE infusion today in the office
  4. Follow her over the next couple months before prescribing anything
  5. Prescribe an abortive agent (triptan) and NSAID to use as needed as well as a preventative agent

6. What is the best choice of treatment at this time, assuming there are no contraindications?

  1. Increase her Topiramate dosing and have her take another triptan
  2. Change her preventative agent since it does not appear to be working
  3. Give an IV DHE infusion
  4. Change her triptan therapy and have her to take one now
  5. Noncontrast CT brain for the paresthesias on exam

7. Which of the following is NOT a typical “red flag” in evaluation of this case?

  1. Age
  2. Family history of brain tumor
  3. Fever
  4. Weight loss
  5. Neurologic symptoms

8 What is the most likely diagnosis that should be first considered?

  1. Tension type headache
  2. Brain tumor
  3. Episodic migraine
  4. Cluster headache
  5. Temporal arteritis

9. What would be the next step in treatment based on your suspicion?

  1. B-blocker
  2. Prednisone
  3. Triptan
  4. Ca-channel blocker
  5. Tricyclic antidepressant

10. He says he has been reading about headaches himself and asks if this could be cluster headache. You begin educating him on cluster headache. According to IHS criteria, the duration of a cluster headache is:

  1. 4-72 hours
  2. 1-60 minutes
  3. 1-60 seconds
  4. 15-180 minutes
  5. 1-12 hours

Key Points

  1. Primary headache disorders are not associated with an underlying pathologic process and include migraine, tension, cluster and other trigeminal autonomic cephalgias. Baseline neurologic exam is normal and diagnostic work-up is negative.
  2. Secondary headache disorders have extensive possible etiologies and are related to an underlying pathologic process. They are associated with an abnormal neurologic exam and/or abnormal diagnostic work-up.
  3. The current theory of migraine pathophysiology states that migraine is initiated with cortical spreading depression followed by meningeal vasodilation and trigeminal activation, leading to release of vasoactive neuropeptides and resulting in sterile neurogenic inflammation. These vasoactive neuropeptides result in further vasodilation and trigeminal afferent activation leading to worsening of pain symptoms.
  4. It is crucial to treat migraine at the earliest symptoms identified. Optimal abortive treatment includes administration of NSAID with a triptan. The purpose of the NSAID is to decrease the neurogenic inflammation which leads to worsening of migraine symptoms. The purpose of the triptan is to counteract the meningeal vasodilation as well as the release of vasogenic neuropeptides from the trigeminovascular system. The longer a patient waits to treat a migraine, the less effective these treatments will be.
  5. In general, preventative therapy should be initiated in migraine if they are significantly debilitating, very severe (including presence of uncommon migraine findings such as hemiplegic migraine, basilar migraine, migrainous infarction, etc.), interfering with daily activities/jobs and if there are >4 migraines per month. Preventative therapy should be tailored towards comorbidities