I realized today that it has been almost 4 years ago since I started writing regularly on this blog. Many things have changed, including medications, treatments and my knowledge about headaches. In the interim, I even managed to write a practical manual about caring for kids and teens with headaches. Much of the new information is regarding migraines. I thought this might be a nice opportunity to revisit the migraine blog posts, update and incorporate new information around pediatric migraine.
Here we go…..
The 3 most common subtypes of primary headaches commonly seen in pediatric patients are: migraine, tension-type, and chronic daily headache, including chronic mixed type headache and new daily persistent headache. Children often have a combination of types, such as chronic mixed type headache, which generally combine migraine and tension-type headache. All primary headaches present differently and are often treated differently. Migraine is a well-known type of headache, will be covered here in a number of posts. There are also migraine variants, particular to children, such as abdominal migraine and cyclic vomiting syndrome.
Migraine is a neurological disorder, characterized by headache attacks. Migraines are episodic or chronic, are recurrent, can last from 4-72 hours, with moderate to severe throbbing pain. In pediatric patients, pain can be felt in one location, such as behind the eyes or temples, or one-sided, or everywhere (holocephalic). In adults the pain is generally one-sided. Pain can occur suddenly or be preceded by warning symptoms, called an aura. Along with head pain, patients can experience nausea and/or vomiting, photophobia, phonophobia, osmophobia (sensitivity to smell), pallor, lightheadedness or dizziness, visual changes (blurred vision, loss of vision, seeing colors), hearing changes (tinnitus), paresthesias, focal numbness, fatigue, sweating, and scalp sensitivity (allodynia). The only constant in migraine is that every migraine patient experiences their migraines differently- different location, constellation of symptoms, triggers.
Here is the up-to-date current information about the basic pathophysiology of migraine.
Currently the research suggests that migraine occurs when there is a primary neuronal dysfunction that leads to sequential changes in the brain, both intracranial and extracranial. There is a chain reaction which involves several parts.
Cortical spreading depression is a self-propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex. It is thought to be the cause of migraine aura, can activate trigeminal nerve afferents, and can alter the blood-brain barrier permeability.
The Trigeminal vascular system (small sensory neurons that originate from the trigeminal ganglion and upper cervical dorsal roots) innervates large cerebral vessels, pial vessels, dura mater, and large venous sinuses, both through the ophthalmic division of the trigeminal nerve (anterior) and the upper cervical roots (posterior). Activation of this system happens at the trigeminal nucleus caudalis and spreads throughout the brain.
Stimulation of the trigeminal ganglion results in release of vasoactive neuropeptides (substance P, calcitonin gene-related peptide, and neurokinin A), and is associated with neurogenic inflammation. The main components of this inflammatory process are vasodilation and plasma protein extravasation. Neurogenic inflammation can prolong and intensify migraine pain, and lead to sensitization.
Sensitization occurs when the neurons become increasingly more responsive to both nociceptive and non-nociceptive stimulation. This increased responsiveness or sensitivity is thought to increase perception of pain and can lead to the transformation from episodic to chronic migraine. Sensitization may be responsible for the throbbing quality of the pain, the worsening of pain with movement or coughing, hyperalgesia (pain out of proportion), and allodynia (pain with non-noxious stimulation).
The calcitonin gene-related peptide (CGRP) is expressed in the trigeminal ganglia nerves and is a potent vasodilator of cerebral and dural vessels. Elevated CGRP levels can be seen in chronic migraine patients, and those elevated levels can become normal after the use of a triptan medication. Medications that block these peptides are now available, but not approved for those under age 18.
Genetics: Migraine is often found within families, passed genetically through generations. The incidence is more common in women (17%) than men (6%). Most people have their first migraine between the ages of 6 and 25 years, so it is likely that their pediatric provider will be the first person to evaluate for migraine. Imaging is not required to diagnose migraine, especially if there is a strong family history. However, imaging (MRI) can be helpful for presentations without family history, unusual, complex or variant-like symptoms. Most families are comfortable without imaging when there is family history of migraine.
Most migraineurs have missed school, social or sports activities, or work during a migraine, and about 50% have difficulty functioning at all during an attack. As you can imagine, having 1 migraine episode per week and having to miss 1 day/week of school, is going to have significant consequences.
The next step, after making the diagnosis, is to decide on a treatment plan. Does this patient need a preventive or daily medication? What is the rescue plan? And even more importantly, what about the lifestyle factors that can trigger migraine or reduce the incidence of migraine? I will start to cover these topics in my next post.
HeadFirst PNP 