Migraine headaches (MH) are an important cause of behavioral limitations, with a lifetime prevalence of 11-32% in several countries and an estimated 7-18% in China. MH is the nineteenth most disabling (disabling or limiting) disease worldwide, and the annual cost of treating MH is approximately $14 billion in the United States. There are two subtypes of MH: those without aura and those with aura.
The aura develops in 5-20 minutes but lasts less than 60 minutes, followed by a migraine attack. One in three migraineurs experience an aura, and MH often occurs in the frontotemporal region, typically unilaterally, and is characterized by recurrent, throbbing, intense headaches with nausea and photophobia.
More than 90% of migraineurs experience incapacity during an attack, and half of these in turn require bed rest. Despite this high rate of attack incapacity, less than 60% of migraineurs have their migraine diagnosis made by a physician. Therefore, many patients do not receive appropriate pain relievers or preventive medications to treat their migraines.
A major barrier to diagnosing headaches in primary care is the time constraints of the visit. Scheduling dedicated time for headache counseling and having patients keep a headache diary that includes headache frequency, severity, and medication use may be helpful in overcoming time constraints and allowing patients to receive an appropriate diagnosis and treatment.
The diagnostic criteria for MH are as follows.
A. at least 5 episodes consistent with B-D
B. Headache lasting 4-72 hours (untreated or unsuccessfully treated)
C. Headache with at least two of the following characteristics: unilateral, throbbing nature, moderate to severe pain level, physical activity that worsens the headache or headache that causes the patient to avoid daily physical activity (e.g., walking or climbing stairs)
D. At least one of the following symptoms during the headache: nausea and/or vomiting, photophobia, fear of sound
E. Does not belong to any of the diseases
Traditional non-surgical treatment of migraine includes both pharmacological and non-pharmacological treatments. Non-pharmacologic treatment involves avoiding other triggers that trigger migraine attacks after diet, usually coffee, alcohol, or tobacco, etc. Medications can be divided into the following categories: emergency pain medications, emergency attack interruption medications, and preventive medications.
Emergency pain management includes pain control with acetaminophen, non-steroidal anti-inflammatory drugs (NSAIDS), analgesics, diazoxide, opioids, and barbiturates. The first-line acute termination of seizures is treated with tritans, although antiemetics and ergometrine are also available. Prophylactic treatments include: ß-blockers, tricyclic antidepressants, and valproic acid.
Although tension headache can be confused with migraine without aura, it is possible to distinguish the two because tension headache is not accompanied by nausea and is not affected by activity. Another group of headaches that needs to be distinguished from migraine is cluster headache. Cluster headaches are characterized by severe pain involving the orbital, infraorbital, or temporal region and are strictly limited to this region. It often lasts 15-180 minutes and is often associated with unilateral autonomic changes such as runny nose, tearing, nasal congestion, frontal-facial sweating, narrow pupils, ptosis, and eyelid edema.
During an episode, the number of headache attacks ranges from once every other day to 8 times daily. In contrast to MH, the typical cluster headache patient often exhibits restlessness and agitation. Non-pharmacologic treatments for cluster headache include avoidance of ethanol, histamine, nitroglycerin, or tobacco. Emergency termination therapy includes 100% oxygen, tretinoin, ergotamine caffeine, and dehydrated ergotamine. Prophylactic treatment includes isoptin, lithium, dimethyl ergometrine, ergotamine tartrate, and prednisone.
Pathophysiology of MH
The exact pathophysiological mechanisms underlying the pathogenesis of MH are not well understood. The currently accepted theory or hypothesis suggests that there are four causal factors in MH. First, MH patients have some experimental evidence of interictal cortical malfunction, particularly high cortical neuronal activity. Second, the periaqueductal gray matter PAG, an antipain modifier, occurs as a progressive dysfunction in MH patients.
Burstein provides evidence that pain receptor sensitivity causes increased neuronal firing, the latter leading to increased perceptibility to all stimuli. Third, the aura is caused by cortical spreading inhibition, which itself can cause irritation of the caudal trigeminal nucleus. Finally, trigeminal nerve provocation leads to the release of substance p, calcitonin gene-related peptide, and neurokinin A in the trigeminal nerve cells. These substances travel along the nerve conduction and produce local meningitis and vasodilatation in the dura mater innervated by the trigeminal nerve, thus causing the onset of MH.
Exactly what initiates trigeminal nerve provocation is not precisely known. Anatomical studies have revealed that the anatomical relationship between trigeminal nerve branches and head and neck musculature provides the basis for the trigger point site of the trigeminal provocation hypothesis. The trigger point is located at the exact location where the nerve is traversed by or in contact with the muscle, thus provoking it.
The suprascapular and supraorbital nerve branches are both branches of the ophthalmic branch of the trigeminal nerve and cross the frown and descending brow muscles. The hypertrophy of the frown muscle in most MH patients provides evidence in support of this hypothesis and is further corroborated by the subsequent results of effective pain relief after botulinum toxin A injection. The zygomaticotemporal branch of the trigeminal nerve (ZMTATN) branches through the temporalis muscle and the occipital major nerve through the cephalic semispinalis muscle. This condition is similar to pear-shaped foramen syndrome, where it is the contraction of the pear-shaped muscle that causes the irritation of the sciatic nerve.
Basic principles of surgical treatment
In 1931, Walter Dandy resected the lower cervical and first thoracic sympathetic ganglia in two migraine patients, and he concluded that the clinical features of migraine were related to the nerve supply. in 1946, Gardner reported the removal of the superficial greater rock nerve in 26 patients. Although he reported some successful cases, he also noted complications such as nasal dryness, decreased tear production, and corneal ulceration. 20 years later, Murillo described temporal neurovascular excision for migraine in 34 patients.
Shortly after, Murphy reported occipital neurectomy for occipital migraine. the common drawbacks of the Murillo and Murphy studies were the short follow-up period in the follow-up data and the sequelae of this procedure such as local numbness after surgery. Although these surgical sequelae have led to unacceptable surgical outcomes, the notion that surgery may have a potential therapeutic effect on migraine has not been abandoned.
Recent clinical observations support a new, safer surgical approach. A chance discovery sparked Dr. Guyuron’s interest in migraine research, and in the fall of 1999, one of Dr. Guyuron’s patients reported complete relief of his migraines six months after a cosmetic forehead surgery that involved primarily the removal of the superior frown muscle. Several other patients have since reported the same results.
To get to the bottom of this, Dr. Guyuron reviewed 314 patients who had undergone the same procedure between 1989 and 1999. He found that a total of 39 patients who also suffered from migraines underwent cosmetic forehead surgery, and that 15 of them (38.5%) had complete resolution of their migraine symptoms and 16 (41%) had “significant improvement”-that is, a reduction in the severity, frequency, and duration of their migraine symptoms. frequency, and duration of migraines by more than 50 percent.
”For each patient, the diagnosis of migraine was made by a neurologist or internist according to the International Headache Society criteria, and to ensure the value of the results, only those with significant improvement or disappearance of migraine were considered, and mild or moderate migraine relief was not considered.” Dr. Guyuron said in a subsequent study.
Speculating that it may be the supraspinatus muscle that compresses the nerve causing neuroinflammation and thus triggering forehead migraine, Dr. Guyuron designed a pioneering study to treat migraine surgically only. After 7-16 months, 21 of the 22 patients reported significant relief of their migraines. This was a great encouragement to Dr. Guyuron.
Dr. Guyuron then designed a further study in which two neurologists identified additional trigger points for migraine and designed surgical techniques to treat migraine. A comprehensive study of surgical procedures including the above four trigger points was completed in 2002. Clinical follow-up data collected at least 1 year after surgery showed that of the 89 patients who underwent surgery and completed follow-up, 82 (92%) achieved complete relief (35%) or significant relief of migraine symptoms (57%).
Dr. Guyuron also performed a double-blind surgical treatment trial on 76 patients. 41 of 75 patients (83.7%) had more than 50% reduction in migraine in 49 real surgeries, of which 28 had complete disappearance of headache (57.1%), while only 1 migraine in the sham surgery group had complete disappearance (3.8%) (p<0.001) [12]. The results demonstrate the effectiveness of nerve decompression surgery and affirm that surgical eradication of peripheral migraine trigger points is an effective treatment option for those patients with frequent moderate to severe migraine and who are difficult to treat with standard methods.