Nearly 1: 7 adults have migraine headaches. Migraine is known as asoroben in Twi-language
Migraine tends to run in families. Environmental factors play a role in causing migraine headaches.
Pathophysiology of migraine
Migraine with Aura (classic migraine)
Migraine with aura occurs in persons with low levels of ATP (the energy storehouse of cells) in their brain neurons. Energy that drives cellular metabolism is stored as ATP in all cells.
The Na+-K+ ATPase pump moves potassium and sodium ions in and out of cells, across the cell membranes.
In the absence of adequate supply of ATP in the cells, the sodium-potassium pump breaks down.
A breakdown in the sodium-potassium pumping activity allows more potassium ions to enter the neuronal cells.
As more potassium ions enter the neuronal cells, an Action Potential is generated causing a wave of slow depolarization across the cerebral cortex.
The wave of depolarization that spreads across the cortex is known as Cortical Spreading Depolarization (CSD)
Low blood glucose and low oxygen levels in the brain neurons are the usual causes of a reduction in cellular ATP generation.
The CSD is a self-propagating wave of depolarization responsible for the Aura experienced in migraine.
Hypoglycemia increases one’s susceptibility to CSD
Adequate levels of neuronal glucose, and oxygen maintain cellular ATP generation and prevent CSD development.
Migraine suffers typically have almost 16% reduction in ATP levels in the brain (1)
B. Calcitonin Gene Related Peptide (CGRP) As a cause of Common migraine.
Several areas in the brain are involved in migraine headaches.
Such areas include the sensory nerves in the cerebral cortex, the pons and the trigeminal ganglion.
The sensory nerves in the brain and, and around blood vessels produce and release a chemical protein known as Calcitonin Gene Related Peptide (CGRP).
Calcitonin gene related peptide (CGRP) causes migraine through several mechanism.
CGRP is a very potent vasodilator.
CGRP also causes the release of inflammatory chemicals like TNF-alfa which in turn mediates the production (transcription) and release of more CGRP in sensory nerves
CGRP also causes mast cells to release inflammatory chemicals like Histamine, Nitric oxide, Tumor necrosis factor-alfa.
These chemicals sensitize pain-nerves in the brain, especially the trigeminal afferents and around meningeal blood vessels to generate the characteristic headaches associated with migraine
CLINICAL FEATURES OF MIGRAINE
For a headache to be labeled as a typical Migraine, a person must have had at least, 5 episodes of the same type of headaches in the past. The headache must have these characteristics:
1.One-sided throbbing headache that may last from 4 hours to 72 hrs. if left untreated.
2.The headache that is worsened by loud noise (Phonophobia)
3.The headache is worsened by bright light (photophobia), affected persons prefer dark rooms, and quite areas
4. The headache has moderate to severe intensity or disabling
5. A typical Migraine headache worsens with activity.
6. Autonomic dysfunction: Nausea, and vomiting.
The most frequent migraine triggers are: Fasting & Skipping meals, Sleep deprivation and Emotional stress.
Migraine with Aura
About 30% of migraine sufferers experience an aura, during, and or up to one hour before the onset of the pulsatile headache. (70% of migraines do not have an aura, such migraines are known as Common migraine)
The typical aural symptoms involve the following:
Visual: flashing of light or zigzag lights in the vision that either moves or gets larger.
Sensory: tingling, numbness that travels up one arm towards one side of the face.
Speech/Language symptoms: trouble producing words (even though they clearly know what to say); trouble understanding what people are saying.
Each aura symptom is fully reversible; they each last less than one hour.
NB. Weakness in any parts of the body is not a typical migraine with aura symptom.
Treatment of acute migraine
Mild headache, no vomiting/nausea.: Aspirin or NSAIDs.
Moderate to severe migraine:
Small molecule CGRP-Antagonist (termed as “gepants”)example Ubrogepant, and Rimegepant OR
A combination of Triptans plus NSAIDS, example sumatriptan + naproxen.
(The triptan medications are vasoconstrictors that block the release of CGRP from sensory neurons)
If the person with migraine has nausea/vomiting,
. Add Antiemetics (metoclopramide, prochlorperazine). And use parenteral preparations of the acute migraine medications. In such case subcutaneous sumatriptan, with its rapid onset is very appropriate. Intra-nasal forms of Sumatriptan are the fastest for pain relieve.
All patients with migraine headaches should maintain a headache diary to determine the frequency, severity, and duration of headaches
The following persons need to be placed on Migraine-prevention medications if
. Headaches that occur on 10 or more days per month
. An episode of disabling headaches that occurs more than once a week
. If abortive headaches medications are used more than 8 days per month
The efficacy of migraine-prevention medications can be assessed only after 2-3 months trial.
It may sometimes take 6months to study a full trial.
Preventive therapy involves the use of a single medication that is started at a lower dose and titrated upwards.
Beta blockers like propranolol, metoprolol. Atenolol, timolol
Anticonvulsants. Depakote (divalproex sodium)
Tricyclic antidepressant like Amitriptyline
SNRI-antidepressant like venlafaxine.
Monoclonal antibodies that block CGRP receptors: an example is Erenumab injected monthly for migraine prevention
ALEX SARKODIE MBChB.