Migraine headaches affect more than 35 million Americans and are ranked the third-highest cause of disability worldwide, resulting in decreased quality of life and serious economic consequences. There are 4 types of migraine headaches: frontal, temporal, occipital, and rhinogenic. Each type has a well-described trigger site. Migraines headaches often are refractory to medical therapy and may respond well to botulinum toxin type A. Migraine surgery is another option to release trigger sites. A systematic review of the migraine surgery literature found an average success rate of 90%, with elimination or greater than 50% improvement of migraine headaches after migraine surgery.
Key points
- •
Migraine headaches affect 35 million American and are ranked the third-highest cause of disability worldwide, resulting in serious economic burdens, with loss of work days and productivity.
- •
There are 4 types of migraine headaches, with well-described trigger sites associated with each type of migraine headache.
- •
Migraines headaches often are refractory to medical therapy and may respond well to botulinum toxin type A administered to specific trigger sites.
- •
Literature found an average success rate of 90% with either elimination or greater than 50% improvement of migraine headaches after migraine surgery.
Migraine headache treatment
Introduction
Migraine headaches cause significant suffering and disability at the national and global levels. Headaches and migraines are leading causes of outpatient and emergency department visits and remain an important public health problem. In the Global Burden of Disease Study 2010, migraine headache was ranked the third most prevalent disorder in the world. In 2015, it was ranked the third-highest cause of disability worldwide in both men and women under the age of 50 years. Approximately 35 million Americans suffer from migraine headaches, approximately 1 out of every 7. This includes 19% of all women and 9% of all men. This results in extreme economic consequences. There are 112 million collective workdays lost, an estimated $1 billion in medical costs, and $16 billion productivity loss in the United States annually. The theory behind migraine pathophysiology has evolved over the past several decades, and literature is rapidly accumulating supporting that migraine headaches are the consequence of compression or traction and subsequent irritation to peripheral nerves in the head and neck. Advances in the underlying pathophysiology have led to newer and promising treatment modalities, such as botulinum toxin type A (BTX-A) injections and migraine surgery, both of which provide relief to the peripheral nerves associated with the migraine.
Diagnostic Criteria for Migraine Headaches
In 2018, the Headache Classification Committee of the International Headache Society released the International Classification of Headache Disorders , 3rd edition, with diagnostic criteria for migraine headaches. This helps delineate migraine headaches from other headaches, such as cluster or tension headaches.
To be diagnosed with migraine headaches there must be at least 5 attacks meeting the following criteria :
- •
Headache attacks lasting 4 hours to 72 hours (when untreated or unsuccessfully treated)
- •
Headaches having 2 of the following 4 characteristics:
- ○
Unilateral location
- ○
pulsating quality
- ○
moderate/severe pain intensity
- ○
aggravation by or causing avoidance of routine physical activity (eg, walking or climbing stairs)
- •
During headache at least 1 of the following:
- ○
Nausea and/or vomiting
- ○
Photophobia and phonophobia
- ○
- •
Not better accounted for by another diagnosis or disorder
Nonsurgical Treatment
Nonsurgical treatment of migraine headaches consists of 2 categories, nonpharmacologic and pharmacologic. Nonpharmacologic treatment of migraine headaches consists of behavior modifications, such as avoidance of triggers. , Other nonpharmacologic treatments like application of pressure, cold or heat, and acupuncture can mitigate or abort the migraine headaches. ,
Current forms of pharmacologic treatments of migraine headaches include prophylactic and abortive medications.
- •
Prophylactic: lessen the frequency and severity of the migraine attacks
- ○
Antihypertensives
- ▪
β-blockers
- ▪
Calcium channel blockers
- ▪
Angiotensin-converting enzyme inhibitors
- ▪
- ○
Antidepressants
- ○
Anticonvulsants
- ○
Antihistamines
- ○
- •
Abortive: prevent a migraine attack or to stop it once it starts
- ○
Triptans
- ○
Nonsteroidal anti-inflammatory drugs
- ○
Acetaminophen
- ○
Combination (acetaminophen, caffeine, and aspirin)
- ○
Narcotics
- ○
Pathophysiology
Over the past 20 years there have been advances in the understanding of migraine headaches and their cause. There has been a shift from a vascular theory to neuronal theory involving the central nervous system, peripheral nervous system, or both as the cause of migraine headaches. These newer theories have brought forth the concept of peripheral trigger points involving branches of the trigeminal nerve and greater occipital nerve and their muscular investments and surrounding structures.
Pain from migraine headaches is thought to be the result of increased activity of nociceptors that innervate the meninges and their blood vessels. The peripheral branches of the trigeminal and occipital nerve encounter muscles at defined trigger points. Subsequent muscle contraction causes compression or traction of the nerve branches leading to nerve irritation. Although compression of the nerves is the most widely believed cause of nerve irritation, it has been noted that the involved nerves do not show the classic appearance of a compressed nerve, as would be seen in the median nerve of carpal tunnel syndrome, such as the hourglass deformity or color change from myelin loss. Because of this, another theory for nerve irritation suggests traction on the nerve branches rather than a pure nerve compression.
In the trigger point theory, the activation is mechanical stimulation of branches of the trigeminal nerve, which causes the nerve fibers to release vasoactive chemicals, such as substance P and calcitonin gene–related peptide (CGRP). The theory is that these vasoactive substances are released in the cell bodies of the trigeminal nerve and travel proximally, causing local meningitis and dilation of trigeminal nerve-innervated vessels and dura mater and project to the trigeminal nucleus caudalis. Studies of peptide release have shown, however, that substance P is not elevated but CGRP is elevated in patients during migraine attacks. This observation has given rise to development and testing of medical therapies that target CGRP, the most abundant neuropeptide in the trigeminal nerve. The theory is that the more specific action on the trigeminal pain system will more effectively treat migraine pain with little to no adverse effects, as is common with many of the current day pharmacologic treatments. CGRP antagonists, known as gepants, are used for acute relief of migraines. Monoclonal antibodies against CGRP or targeting the CGRP receptor prevent migraine attacks. There have been promising results in phase 3 trials. ,
Types of Migraine Headaches
Frontal migraine headaches
Frontal migraine headaches are characterized by frontal pain, typically occur in the late afternoon, and are associated with stress. Patients with these headaches tend to have hypertrophy of the furrowing muscles, including the corrugator supercilii. Eyebrow ptosis and eyelid ptosis are other possible clinical manifestations of frontal migraines. ,
Frontal migraines originate secondary to irritation of supraorbital and supratrochlear nerves. Frontal trigger is the most common trigger site. The supraorbital nerves have 3 muscular trigger sites: the corrugator supercilii, depressor supercilii, and procerus muscles. There are 4 branching types of the supraorbital nerve relative to the corrugator muscle. The supraorbital nerve also may be irritated by the supraorbital artery and at the entrance into the brow through the supraorbital forearm or a narrow supraorbital notch. The supratrochlear nerve has 3 branching patterns relative to the corrugator muscles. Additional points of irritation include corrugator supercilii and the frontal notch. ,
Temporal migraine headache
Temporal migraine headaches are located in the temple area, lateral and superior to the lateral canthus. They frequently occur in the morning, are related to stress, and are associated with clenching of teeth. Patients often wake up in the morning with pain after grinding teeth while asleep and may have worn dental facets on examination. Migraine headaches in this location also are associated with trigger point tenderness as well as temporomandibular joint pain. ,
Temporal migraine headaches are caused by compression or traction of the zygomaticotemporal branch of the trigeminal nerve (ZTBTN). Trigger sites include the exit point of the nerve through the zygomatic bone, 17 mm lateral to and 7 mm superior to the lateral canthus. In addition, the ZTBTN may be compressed by temporalis muscle, deep temporal fascia and superficial temporal artery. The temporal trigger is the second most common trigger area. Temporal region migraines occasionally are caused by the irritation of the auriculotemporal nerve (ATN) as it runs superior to the ear.
Occipital migraine headaches
The pain of occipital migraines is located in the upper neck and occipital region. These headaches are associated with stress, upper neck and occipital pain, muscle tightness, and trigger point tenderness and may be related to heavy exercise. Patients may have a history of whiplash. ,
Compression of the greater occipital nerve by the semispinalis capitis is thought to be responsible for migraine headaches at this location. The occipital nerve is compressed as it pierces the semispinalis capitis muscles. Mosser and colleagues performed an anatomic study of the nerve’s relation to the muscle, demonstrating that the nerve can reliably be found 3 cm inferior to the occipital protuberance and 1.5 cm lateral to the midline. The nerve also may be compressed by trapezius, obliquus capitis muscles, and nuchal fascia. ,
Rhinogenic migraine headaches
Rhinogenic migraine headaches are characterized by retrobulbar pain behind the eye. They often occur in the early morning and are related to weather, allergies, and hormones. The headaches often are cyclic in nature. A trial of nasal sprays can be used.
Intranasal triggers lead to impingement and irritation of the terminal trigeminal branches and can be diagnosed by evidence of nasal septum deviation, turbinate hypertrophy, and/or mucosal inflammation on an intranasal examination. Further diagnostic support of these migraine headaches may be provided by computed tomography (CT) of the face with evidence of contact points, including septal spurs or septal deviation.
Nonsurgical Treatment of Migraine Pain
Nonsurgical treatment of migraines consists of chemodenervation with BTX-A.
BTX-A has a defined intracellular mechanism of action, impairing the soluble N -ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-mediated synaptic vesicle fusion to nerve terminals. BTX-A prevents the release of acetylcholine at the neuromuscular junction, thus inhibiting initiation of the action potential and firing of the affected muscle. It is thought that the inhibition of muscle contraction that follows then reduces compression and irritation of the nerve associated with the trigger point.
The entire mode of action of BTX-A in migraine headaches, however, is not fully understood. Studies have shown that in addition to the extracranial effects, BTX-A may effect modulation of neurotransmitter release and changes in surface expression of receptors and cytokines as well as enhancement of opioidergic transmission. There is reduced sensory transduction of suprathreshold mechanical stimuli associated with processing mechanical pain but not sensory transduction of threshold tactile mechanosensitivity. The peripherally delivered BTX-A is taken up by sensory afferents and may undergo transcytosis to cleave SNAREs in second-order neurons in the ganglion and trigeminal nucleus caudalis or in adjacent afferent terminals and prevent evoked afferent release and downstream activation.
BTX-A was first demonstrated to reduce the severity and frequency of migraines headaches by Binder and colleagues, in 2000, in their landmark study that demonstrated complete resolution of migraines in 55% of migraine patients and partial reduction in 38%. This study came after years of successful treatment with BTX-A in other ailments associated with muscular dystonia. The study was followed by a double-blind randomized trial of 123 patients with moderate to severe migraines and provided further evidence for the ability of BTX-A to alleviate migraines. A great deal of work has been done to study the role for BTX-A in migraine headaches, however, likely none more impactful than the 2010 Phase III Research Evaluating Migraine Prophylaxis Therapy 1 trial that provided the convincing and rigorous evidence for the efficacy of BTX-A as a prophylactic treatment of migraine headaches, which was largely responsible for the subsequent Food and Drug Administration (FDA) approval of the therapy in 2010. ,
Low doses of BTX-A ( Table 1 ) are injected directly into the muscle site that has been identified as a trigger point. Trigger points are identified during the initial work-up through history, physical examination, and often a headache diary, in which the patient keeps track of headaches for at least 1 month, carefully recording the characteristics of the migraines. The trigger points then are systematically injected from most to least likely source, and the results are logged by the patient. An added benefit of this approach is that it can provide a reliable source of the trigger point for future surgical intervention if indicated.
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
