Headache, also known as cephalalgia, is one of the most common reasons patients seek medical attention. It may simply be a symptom that affects a person’s functionality and Quality of Life (primary headache) or it may be a symptom of an underlying disease, potentially life-threatening to the patient (secondary headache).
Headaches are included among the top 20 diseases in the world by the World Health Organization that seriously impair people’s ability to function.
The time and mode of headache onset is very important diagnostic component.
Acute onset of severe headache raises the suspicion of vascular damage (subarachnoid hemorrhage, intracerebral hemorrhage, brain tumor hemorrhage), underlying malignancy, carcinomatous or infectious meningitis (lumbar puncture [spinal tap]), or even brain abscess. To rule out the aforementioned conditions, patients should always undergo paraclinical testing (brain CT or MRI).

Diagnostic approach to headache

According to the classification of the International Headache Society, the diagnosis of primary headache syndromes is phenomenological and, thus, obtaining a detailed patient history helps deliver the diagnosis in most of the cases.
When obtaining a medical history, the following are of particular importance:

  • Age and mode of headache onset (acute, subacute, or chronic)
  • Headache frequency pattern
  • Location and extension of the pain
  • Pain type (throbbing, pressing, stabbing headache), duration, intensity, and any changes thereof
  • Time of pain onset
  • Factors affecting pain intensity
  • Search for precursor symptoms, aura, and accompanying symptoms (nausea, vomiting, phonophobia, photophobia)
  • Association of headache with menstruation
  • Patient behavior and attitude during the headache
  • Impact of pain on patient functionality
  • Previous treatments and drug effectiveness
  • Medical history
  • Family headache history
  • History of abuse (alcohol, drugs)
  • Mental history
    Patients with headache should then undergo a physical examination and, depending on the findings, paraclinical testing should be considered.
  • Migraine
  • Without aura
  • With aura
  • Tension headaches
  • Episodic
  • Chronic
  • Cluster headache and other types of headaches related to the trigeminal and autonomic nervous system


Primary headaches


Migraine is an episodic headache, with neurological signs and symptoms from the digestive and the autonomic nervous systems. First-degree relatives have been found to have a higher relative risk of migraine, which is particularly prevalent in cases of migraine with aura. It is divided into migraine without aura and migraine with aura.


Migraine aura

Migraine aura usually precedes a headache, but can also occur during the headache (it cannot be subsequent to the headache). It does not always occur in migraine attacks, while the presence of only 2 aura episodes is sufficient to characterize migraine with aura. Typically, the aura is visual (photopsias, scotomas, blurred vision, zig-zag lines), but it can also appear as sensory symptoms (unilateral dysesthesias or numbness), or in the form of speech disorders (aphasia).

Migraine with aura

It is a relapsing disorder manifested by reversible neurological symptoms that gradually appear within 5-20 minutes and last for less than 60 minutes (aura). Next, a migraine follows with the characteristics of migraine without aura.


Migraine without aura

These are recurrent headache episodes that last 4-72 hours. Common features of headache include contralateral location, throbbing character, moderate or severe pain intensity, and worsening after light physical activity. Another feature is the coexistence with nausea and/or photophobia and phonophobia. If a migraine attack occurs 15 or more days a month, it is considered chronic.

Migraine attack stages

Precursor symptoms precede pain and can be either negative (e.g., fatigue, yawning, decreased appetite, drowsiness, intolerance, depression, or hypoactivity) or positive (e.g., irritability, well-being, increased appetite, hyperactivity, increased sensitivity to light and noises). Precursor symptoms are independent of the aura, precede the migraine, and are not always present.

  • Migraine aura
  • Headache and accompanying symptoms (nausea, vomiting, phonophobia, photophobia, osmophobia)
  • Resolution of pain


General guidelines for treating migraines

The accurate diagnosis of a migraine using the International Headache Society’s criteria is the first step in therapy. This is followed by patient awareness and education on how to look for migraine triggers, keep track with the headache diary, and change of lifestyle (exercise, avoiding skipping meals, good sleep). Treatment is divided into symptomatic (treatment of migraine attacks) and chronic prophylaxis.

Symptomatic treatment

To treat seizures, a medication of choice and a second “escape” medication (an alternate medication used if a patient does not respond to the medication of choice) are selected. If the pain is still severe after 2 hours, the “escape” medicine is administered. In the event of a relapse (recurrence of the headache that had resolved with the first medication), the medication of choice is administered again.
Migraine-specific treatments include triptans.
Non-migraine-specific treatments are:
• Regular pain relievers (Paracetamol, Aspirin)
• Non-steroidal anti-inflammatory drugs (Naproxen, tolfenamic acid, indomethacin, diclofenac sodium. They are not recommended for long-term use because they cause rebound headache when overused.
• Dopamine antagonists (Metoclopramide, Domperidone, Chlorpromazine)

Chronic migraine prophylaxis

Chronic prophylaxis aims to reduce the frequency, duration, and intensity of migraine attacks and, thus, improve a patients’ functionality and Quality of Life. It is recommended for patients who experience frequent migraine attacks (2-3 monthly), do not respond well to symptomatic treatment, and often resort to escape medication as well as for patients who experience side effects from the use of symptomatic treatment or overuse of medications. The duration of prophylaxis ranges from 6 months to one year.
Prophylaxis medications:

  • Beta-adrenergic receptor antagonists (Propranolol)
  • Anticonvulsants (Sodium Valproate, Topiramate)
  • Antidepressants (Amitriptyline)

Tension headache

It can occur at any age and is either episodic (less than 15 days per month) or chronic (more than 15 days per month). It is located frontally, cervically, occipitally and, rarely, unilaterally, and it is sensed in the form of pressure or tightness. It can last from a few hours to a whole day. It develops with no precursor symptoms, aura or nausea and vomiting. Patients with tension headaches are advised to change their lifestyle (stress, poor sleep, sedentary lifestyle) and exercise more. Symptomatic treatment includes regular plain relievers and anti-inflammatories as well as prophylaxis such as amitriptyline, propranolol, SSRIs.

Cluster headache

Men between the ages of 30 and 40 are more likely to experience it, with an average of 1 to 3 attacks occuring every day for approximately 6 weeks. It is usually unilateral, around the eyes, unbearably painful, and lasts from anywhere between 30 minutes and 2 hours. It is typically accompanied by drooping eyelids, tearing, eye redness, and rhinorrhea. During a cluster headache crisis, oxygen 7-10 lt/min is administered for 15-30 minutes or sumatriptan subcutaneously. Verapamil tolithium and prednisone are recommended as prophylaxis medications.

Trigeminal neuralgia

It is characterized by intermittent, brief—up to 2 minutes—paroxysmal frontal or facial pain attacks.
Pain should manifest with at least 4 of the following characteristics:

  • It is located in the region of one or more trigeminal branches
  • It is sudden, sharp, superficial, and feels like burning or stabbing.
  • It is very intense
  • It is caused by regular activities or by irritated particular areas (feeding, brushing teeth)
  • Between attacks, patients are asymptomatic.
  • Each patient experiences the same attacks in a predictable personal pattern.

Trigeminal neuralgia can be idiopathic (of unknown etiology) or symptomatic (secondary). Secondary trigeminal neuralgia is due to either lesions compressing the trigeminal ganglion (arteriosclerotic vessel loop, basilar artery aneurysm, cerebellopontine angle tumors) or demyelinating lesions (axon hyperexcitability). Treatment comprises anticonvulsants (carbamazepine, phenytoin, gabapentin, pregabalin, sodium valproate, lamotrigine, oxcarbazepine) or non-anticonvulsants (baclofen, amitriptyline), and surgery (transcutaneous thermocoagulation of the trigeminal ganglion, percutaneous glycerol injection, microvascular nerve decompression).