Neuromodulation

Neuromodulation is a new promising treatment for headache disorders. It consists of peripheral nerve neurostimulation and central neurostimulation. © 2016, Touch Briefings. All rights reserved

Preventive treatment of migraine

Migraine is a common episodic pain disorder, the treatment of which can be acute to stop an attack or preventive to reduce the frequency, duration or severity of attacks. Preventive treatment is used when attacks are frequent or disabling. Many different medication groups are used for preventive treatment, including β-blockers, antidepressants and antiepileptic drugs. Their mechanisms of action include raising the threshold to migraine activation, enhancing antinociception, inhibiting cortical spreading depression, inhibiting peripheral and central sensitization, blocking neurogenic inflammation and modulating sympathetic, parasympathetic or 5-HT tone. In this article, I review evidence of the effectiveness of migraine preventive drugs. I also discuss the setting of treatment priorities

Botulinum toxin and other new approaches to migraine therapy

The number of migraine treatments and our understanding of migraine pathophysiology are both increasing. Newer treatments are focusing on migraine prevention. Botulinum toxin (BTX) is a potent neurotoxin that has been used primarily for diseases associated with increased muscle activity. Recently the toxin was found to have antinociceptive effects that are probably independent of its muscle-relaxant action. Recent clinical trials support the efficacy of BTX type-A (and possibly also type-B) in the treatment of migraine. The anticonvulsant topiramate was recently shown to be effective for migraine prevention. With the low doses used for this indication, cognitive side effects are less of a concern. Angiotensin (AT) II receptor blockade is a new approach to migraine prevention that was recently examined. The high tolerability of the AT1 receptor blocker candesartan warrants further studies to assess its role in migraine prevention

Headache management for the pain specialist

Headache is a common symptom caused by a wide variety of diseases. Primary headaches include migraine, cluster headache, tension-type headache and other less common diseases. It is important to differentiate these headaches from secondary headaches caused by vascular, neoplastic, infectious, metabolic and toxic disorders. Most primary headaches have a genetic basis, with environmental factors acting as triggers. Recent advances in basic research resulted in the development of more specific and effective therapies. Medication overuse headache is a very common cause of chronic daily headache. Detoxification from the offending drug is essential for headache improvement. Cervicogenic headache is common and needs to be diagnosed correctly since it may require specific therapy. Nerve blocks are useful for some patients with primary, as well as secondary, headaches

Periodic autonomic dysfunction without pain in a patient with cluster headache

Cluster headache (CH) is characterized by episodes of severe unilateral headache accompanied by symptoms of cranial parasympathetic hyperactivity and sympathetic dysfunction that occur in cluster periods. Positron emission tomography (PET) studies have demonstrated evidence of a central generator of CH attacks located in the posterior-inferior hypothalamus. It has been suggested that the autonomic symptoms in CH result from reflex activation of the superior salivatory nucleus secondary to activation of the trigeminal nucleus caudalis (TNC). However, several cases of CH-like symptoms with no head pain have been documented. We describe a patient who had suffered from typical episodic CH for two decades; it later converted into episodic autonomic dysfunction without head pain

Galcanezumab in episodic migraine: subgroup analyses of efficacy by high versus low frequency of migraine headaches in phase 3 studies (EVOLVE-1 & EVOLVE-2).

BACKGROUND: Patients with high-frequency episodic migraine (HFEM) have a greater disease burden than those with low-frequency episodic migraine (LFEM). Acute treatment overuse increases the risk of migraine chronification in patients with HFEM. Galcanezumab, a humanized monoclonal antibody binding calcitonin gene-related peptide (CGRP), is effective for migraine prevention with a favorable safety profile. Here, we investigate whether there are differences in galcanezumab efficacy in patients with LFEM or with HFEM. METHODS: Data were pooled from two double-blind, placebo-controlled phase 3 trials; EVOLVE-1 and EVOLVE-2. Patients were 18-65 years old, experienced 4-14 monthly migraine headache days (MHDs) for ≥1 year prior, with onset at \u3c 50 years of age. Migraine headaches were tracked via electronic patient-reported outcome system and randomization was stratified by low (LFEM; 4-7 monthly MHDs) or high (HFEM; 8-14 monthly MHDs) frequency. Subgroup analysis compared the HFEM and LFEM subgroups with a linear or generalized linear mixed model repeated measures approach. RESULTS: The intent-to-treat patients (N = 1773) had a mean age of 41.3 years, were mostly white (75%), female (85%), and 66% of patients had HFEM. In both the LFEM and HFEM subgroups, the overall (Months 1-6) and monthly changes from baseline in monthly MHDs and monthly MHDs with acute medication use compared with placebo were statistically significantly reduced for galcanezumab 120-mg and 240-mg. Galcanezumab (120-mg and 240-mg) significantly decreased the overall and monthly MHDs with nausea and/or vomiting, and with photophobia and phonophobia versus placebo in patients with LFEM or HFEM. In both subgroups, the mean overall (Months 1-6) and monthly percentages of patients with ≥50%, ≥75%, and 100% reduction in monthly MHDs from baseline were statistically significantly greater in patients receiving either dose of galcanezumab versus placebo. Galcanezumab (120-mg and 240-mg) significantly improved the Migraine-Specific Quality of Life Questionnaire role function-restrictive domain score as well as the Migraine Disability Assessment total score versus placebo for patients with LFEM or HFEM. There were no significant subgroup-by-treatment interactions. CONCLUSIONS: Galcanezumab was as effective in patients with HFEM as in those with LFEM. Associated symptoms, quality of life, and disability were similarly improved in patients with HFEM or LFEM. TRIAL REGISTRATION: NCT02614183 , NCT02614196

Migraine: association with personality characteristics and psychopathology

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72438/1/j.1468-2982.1995.1505358.x.pd

Zonisamide for migraine prophylaxis in refractory patients

Zonisamide, a new antiepileptic drug, has been approved in the US as adjunctive therapy for the treatment of partial seizures in adults.1,2 Chemically a sulfonamide analogue, zonisamide is thought to have several mechanisms of action, including a rate-dependent blockade of voltage-gated sodium channels and reduction of ion flow through T-type calcium channels.3-5 It is also a weak carbonic anhydrase inhibitor. Zonisamide has a favorable pharmacokinetic profile that includes high oral bioavailability and a long half life (63 hours), permitting a once- or twice-daily dosing regimen.6 There are only a limited number of current migraine preventive medications that have proven efficacy. Their use is often limited because of adverse events (AEs) in a significant number of patients.7 Because of its pharmacologic properties, zonisamide is potentially an effective drug for migraine prevention, and preliminary data suggest that it may be effective for this indication.8-10 The long half life of the drug makes it a good candidate for migraine patients who have poor compliance to preventive therapy that involves multiple daily dosing. The aim of this study was to evaluate the efficacy and tolerability of zonisamide for migraine prophylaxis in refractory patients attending a tertiary headache center

Hemicrania continua-like headache associated with carotid dissection may respond to indomethacin

Hemicrania continua (HC) is an idiopathic, chronic disorder characterized by a continuous, strictly unilateral headache associated with ipsilateral cranial autonomic symptoms. The symptoms of HC typically respond dramatically to indomethacin therapy. We describe a patient with traumatic internal carotid artery (ICA) dissection, who presented with a clinical picture mimicking HC that initially responded to indomethacin. Patients with a clinical picture similar to HC should be managed with a high index of suspicion for a possible cervical arterial dissection