Non-steroidal anti-inflammatory drugs (NSAIDs) are a first-in-line treatment for migraine. They inhibit neurogenic inflammation and central sensitization. Examples: aspirin, ibuprofen, diclofenac, naproxen.

NSAIDs as migraine treatment

A first-in-line treatment for migraine. Although they are less effective than NSAIDs, they do not cause antiplatelet effects or gastric irritation. Acetaminophen can be used in combination with aspirin and caffeine to treat headache.

Acetaminophen as migraine treatment

Triptans are used to treat moderate to severe migraine and are agonists for serotonin receptors.

Triptans as migraine treatment

An older treatment for migraines. Although it has similar effectiveness as triptans, it has less receptor specificity and can result in nausea and leg cramps or tingling extremities due to its vasoconstrictive effects.

Ergotamines as migraine treatment

Activation of the trigeminovascular system involving calcitonin-gene related peptide (CGRP) release plays a key role in migraine. Small molecule CGRP receptor antagonists known as gepants can treat migraines, and monoclonal antibodies can also target CGRP and its receptors. Studies have shown them to be less effective than triptans.

CGRP receptor antagonists as migraine treatment

Sleep is known to consistently relieve migraines. It reduces sensory transmission and responsiveness to painful stimuli. Migraines generally increases non-REM sleep, which indicates that the brain needs more sleep during migraine episodes. Neuropeptides known as orexins, which are involved in wakefulness, also play roles in pain sensation and thus could be targeted in migraine treatments.

Sleep and migraine

* Non-steroidal anti-inflammatory drugs
* Triptans
* CGRP receptor antagonists
* Ergotamines

University of Michigan - Ann Arbor

A migraine is a type of primary headache, thought to be caused by the swelling of blood vessels and an increase in blood flow. It is characterized by severe, often unilateral pain, and can be accompanied by symptoms like an upset stomach, disturbed vision, nausea, and sensitivity to light (photophobia) and sound (phonophobia). Migraines are reported more frequently by women than by men.

Migraine

There are two major theories about the causes of migraine: the neuronal and vascular theories. The neuronal theory - which is more widely accepted today - states that neuronal activity is sufficient to cause a migraine, and is supported by abnormal signal processing and lack of cerebral vasodilation (blood vessel dilation) between episodes, as well as hypothalamic activation during migraines. The vascular theory states that vasodilation is sufficient to cause a migraine, and is supported by the migraine-inducing effects of substances that result in vasodilation and the vasoconstrictive effects of drugs that treat migraines.

Both theories suggest that migraines are associated with the hyperexcitability of local brain tissue due to increased glutamate levels.

Causes of migraine

There are significant genetic factors implicated in migraine. Twin studies have shown a high rate of heritability (about 30-60%). Familial hemiplegic migraine (FHM) is an autosomal dominant form of migraine associated with an aura (visual disturbance) and transient unilateral motor weakness, and is passed down if a person has at least one first or second-degree relative with FHM. The three known genes underlying FHM help control neuronal activity through the availability of glutamate.

Genetics of migraine

An aura describes the visual (most common), sensory or motor symptoms that often characterize migraine. It may be caused by an electrophysiological phenomenon known as cortical spreading depression (CSD), a wave of depolarization that starts in the occipital lobe and slowly spreads before a period of hyperpolarization.

From top-left, clockwise: zigzags, negative scotoma, one-sided loss of perception, positive scotoma.

Migraine aura

1. Premonitory/prodrome: begins up to 3 days before headache and is associated with fatigue, mood changes, muscle tenderness and photophobia (sensitivity to light).
2. Aura: occurs in one-third of migraines. See "Migraine aura" node.
3. Headache: throbbing pain caused by activation of the trigeminovascular pathway, which transmits nociceptive (pain) information 
4. Postdrome: marked by a reduction in headache. Symptoms include soreness in the area.

Stages of migraine

Treatments for migraine

In migraine, light indirectly activates nociceptors (pain receptors) in the eyes; there is cross-talk between vision processing and pain pathways, for which the posterior thalamus has been implicated. Light increases activity in the trigeminovascular neurons of the thalamus.

Neurobiology of photophobia

There is a notable gender disparity in the prevalence of migraines, with women experiencing them more frequently than men.

Gender Differences in Migraine Prevalence

A 34-year-old patient reports experiencing episodes of intense, throbbing pain isolated to the left side of their head. During these episodes, they feel nauseous and find it necessary to retreat to a dark, silent room because ordinary light and sounds are unbearable. Based on this specific combination of symptoms, which condition is the most likely diagnosis?

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