neurologic disorders
Migraine
Treatment of Migraine
Elimination of obvious triggers Relaxation techniques, yoga, or behavioral interventions For mild headaches,acetaminophenor nonsteroidal anti-inflammatory drugs (NSAIDs) For acute attacks, triptans,lasmiditan, gepants, ordihydroergotamineplus adopamineantagonist antiemetic Neuromodulatory devices for acute treatment and prevention A thorough explanation of the disorder helps patients understand that although migraine cannot be cured, it can be controlled, enabling them to better participate in treatment. Patients are urged to keep a written headache diary to document the number and timing of attacks, possible triggers, and response to treatment. Identified triggers are eliminated when possible. However, elimination of triggers can be overdone. may be used ( Treatment references ). If patients wish to avoid medications or if medications have been ineffective, Patients who frequently (eg, > 2 days/week) use medications to treat their acute migraine attacks (particularly analgesics that contain butalbital, triptans,ergotamine, or opioids) should be treated with preventive migraine drugs combined with a program for stopping overused analgesics. Clinicians sometimes recommend behavioral interventions (biofeedback, stress management, psychotherapy) to manage migraine, especially when stress is a major trigger or when analgesics are being overused. Yoga can reduce headache frequency and intensity; it enhances vagal tone and decreases sympathetic drive, thus improving cardiac autonomic balance. Relaxation techniques can reduce sympathetic nervous system activity, ease muscle tension, and alter brain wave activity. NSAIDs oracetaminophenis used to treat mild to moderate migraine attacks. If these drugs are ineffective, clinicians should consider using triptans ordihydroergotamine. A good response todihydroergotamineor a triptan should not be interpreted as diagnostic for migraine because these drugs may relieve headache due to subarachnoid hemorrhage or other structural abnormalities. If mild attacks worsen or if attacks are severe from the onset, triptans ordihydroergotaminecan be used. When nausea is prominent, combining a triptan with an antiemetic at the onset of attacks is effective. Triptans are selective serotonin 1B,1D receptor agonists. They are not analgesic per se but specifically block the release of neuropeptides that trigger migraine pain. Triptans are most effective when taken at the onset of attacks. They are available in oral, intranasal, and subcutaneous forms; subcutaneous forms are more effective but have more adverse effects. Overuse of triptans can also lead to Medication Overuse Headache . Triptans and Lasmiditan(a new selective serotonin [5-HT] 1F receptor agonist) or a gepant, such asubrogepantorrimegepant, can be used when triptans ordihydroergotamineare contraindicated because of cardiovascular disorders.Lasmiditan, which has a much greater affinity for serotonin 1F receptors than for 1B receptors, has no cardiovascular contraindications. (Triptans cause vasoconstriction by activating 5-HT1B receptors.) As of this time, gepants have no cardiovascular precautions or contraindications and have no known serious cardiovascular o gastrointestinal effects. An antiemetic (eg,metoclopramide,prochlorperazine) alone may be used to relieve mild or moderate attacks.Prochlorperazinesuppositories (25 mg) or tablets (10 mg) are an option for patients who cannot tolerate triptans and other vasoconstrictors. Evidence supports use of neuromodulatory devices for acute attacks and prevention of migraine headaches. IV fluids (eg, 1 to 2 L of 0.9% normal saline solution) can help relieve headache and increase a sense of well-being, especially in patients who are dehydrated from vomiting. IVdihydroergotaminewith adopamineantagonist antiemetic (eg,metoclopramide10 mg IV,prochlorperazine5 to 10 mg IV) helps abort very severe, persistent attacks.Dihydroergotamineis also available in a subcutaneous form and as a nasal spray. Opioids should be used as a last resort (rescue drug) for severe headache when other measures are ineffective. The same medications used to prevent episodic migraine, including monoclonal antibodies that block CGRP, are used to treat chronic migraine. Also, supporting evidence is strong foronabotulinumtoxinAandtopiramate. Evidence supports use of neurostimulation for acute treatment and prevention of chronic migraine headaches. Noninvasive options include supraorbital stimulation, vagus nerve stimulation, single-pulse transcranial magnetic stimulation, and remote electrical stimulation. Neuromodulatory treatments, which affect brain activity through electrical currents or magnetic fields, can be noninvasive, using commercially available devices. They can also be used to treat attacks and to prevent them. Noninvasive transcranial magnetic stimulation, using a handheld device applied to the back of the head may relieve acute migraine ( Treatment references ). A device that uses an armband to deliver a nonpainful electrical skin stimulus (called remote electrical neuromodulation) can relieve acute migraine pain. A handheld device that delivers noninvasive Trigeminal nerve stimulation, with a device applied to the forehead, can be used in patients who are ≥ 18 to treat acute migraine attacks (with or without an aura) or to reduce the frequency of attacks. Noninvasive neuromodulatory devices have no significant adverse effects. Invasive treatments tend to be available only at specialized centers and have greater risks than noninvasive treatments. 1.Marmura MJ, Silberstein SD, Schwedt TJ: The acute treatment of migraine in adults: The American Headache Society evidence assessment of migraine pharmacotherapies.Headache55 (1):3–20, 2015. 2.Miller S, Sinclair AJ, Davies B, Matharu M: Neurostimulation in the treatment of primary headaches.Pract Neurol16 (5):362–375, 2016. doi: 10.1136/practneurol-2015-001298 3.Lipton RB, Dodick DW, Silberstein SD, et al: Single-pulse transcranial magnetic stimulation for acute treatment of migraine with aura: A randomised, double-blind, parallel-group, sham-controlled trial.Lancet Neurol9:373–380, 2010. doi: 10.1016/S1474-4422(10)70054-5 