gammaCore®

gammaCore® therapy is delivered via a non-invasive vagus nerve stimulator intended for use by the  patient.  The gammaCore device is intended for non-invasive stimulation of the vagus nerve in the neck. In Canada gammaCore is indicated for the acute and/or prophylactic treatment of Cluster Headache and for the treatment of Migraines in adults.

Features of the gammaCore therapy:

• Neuro modulation
• Non-Invasive
• Non-Pharmaceutical
• Easy-to-Use
• Portable

ABOUT CLUSTER HEADACHES

Cluster headache typically involves intense pain that is almost always experienced on one side of the head.  The pain produced by cluster headache is often described by doctors, physicians and sufferers as the most intense of all pains including child birth, burns and broken bones.

Dr. Peter Goadsby, Professor of Clinical Neurology at University of California, San Francisco, a leading researcher on the condition has commented:

“Cluster headache is probably the worst pain that humans experience. I know that’s quite a strong remark to make, but if you ask a cluster headache patient if they’ve had a worse experience, they’ll universally say they haven’t. Women with cluster headache will tell you that an attack is worse than giving birth. So you can imagine that these people give birth without anesthetic [several] times a day. Many cluster headache sufferers have committed suicide, leading to the nickname “suicide headaches” for cluster headaches. Cluster headaches often occur periodically: spontaneous remissions interrupt active periods of pain, though there are about 20% of suffers whose cluster headaches never remit. The cause of the condition is currently unknown. It affects approximately 0.1% of the population, and men are more commonly affected than women.”[1]

It is estimated that approximately 0.1% of the population suffers from cluster headaches suggesting, in Canada, there are approximately 35,000 individuals managing this problem

ABOUT MIGRAINES

The World Health Organization (WHO) has estimated a worldwide prevalence of current migraine of 10%, and a lifetime prevalence of 14%. WHO further classifies individuals who are suffering with migraines as debilitated as a quadriplegic. In the US it is estimated that more than 100,000 migraines occur every day.  These attacks on an annual basis, leads to more than 150 million lost workdays and a loss of national productivity measured in tens of billions of dollars. Estimates of the total cost of migraine across Europe place loss at over 25 Billion Euros(2).  Similar economic data for Canada has not been located.

Migraine is a term used to describe a category of recurrent headaches that are typically one-sided but may also occur bilaterally.  These headaches may occur with or without familiar warning signs, including either prodromal symptoms or an aura.  Prodromal symptoms consist of altered mood, irritability, depression or euphoria, fatigue, dizziness and other visceral symptoms preceding the headache by several hours or days.  The aura phase, present in 20-30% of migraineurs, is a neurological symptom that generally precedes the migraine attack by 5-60 minutes.  Auras can include visual disturbances such as photo sensitivity or scotomas or, in less frequent cases, somatosensory, auditory or gustatory hallucinations.(3)

The pathophysiology of migraine headaches is not clearly understood.  Initially migraine headaches were thought to be of vascular origin.  Recent evidence suggests the possibility of neurogenic causes.  Whether these neurogenic causes are related to vascular change is still under investigation.

There is no single standard of care for patients presenting with migraine symptoms, and treating acute migraine is challenging because of substantial non-response rates among medication users and difficulty in predicting individual’s responses to a specific agent or dose.  Abortive therapy is typically suggested as early as possible after the onset of symptoms. Effective first-line therapies for mild to moderate migraine are nonprescription nonsteroidal anti- inflammatory drugs and combination analgesics containing acetaminophen, aspirin, and caffeine.

Triptans, (a class of serotonin receptor agonists) are first-line therapies for moderate to severe migraine, or mild to moderate migraine that has not responded to adequate doses of simple analgesics. However, triptans have to be avoided in patients with vascular disease, uncontrolled hypertension, or hemiplegic migraine. There are restrictions as to how many triptans can be taken within a specific time period. Triptan overuse has also been implicated in increased frequency and severity of headache in some patients, a phenomenon termed medication overuse headache (which can be remediated only by discontinuation of any analgesia during migraine attacks for a period of up to three months). Additionally, triptan administration has been seen to elicit a behavioural syndrome of enhanced sensitivity to surrogate triggers of migraine that is maintained for weeks following discontinuation of drug, a phenomenon termed ‘triptan-induced latent sensitization.(4)

The first combination product of a 5-HT1 receptor agonist and an NSAID, Treximet, was approved by the US Food and Drug Administration in April 2008. Efficacy was demonstrated in 2 randomized, double-blind, multicenter, parallel-group trials comparing the combination product to placebo and each individual active component (ie, sumatriptan and naproxen sodium). The percentage of patients remaining pain free without use of other medications through 24 hours post-dose was significantly greater (p<0.01) among patients receiving a single dose of Treximet (25% and 23%) compared with placebo (8% and 7%) or either sumatriptan (16% and 14%) or naproxen sodium (10%) alone.(5) However, the percentage of pain free patients is still quite low.

Agents that interact with the GABAergic system seem to have a positive effect in reducing migraine attacks. Divalproex sodium (Depakote) and topiramate (Topamax) are most commonly used and are FDA-approved for migraine prophylaxis. Both drugs have class I evidence supporting their effectiveness in decreasing the frequency of migraine attacks. Other anticonvulsants with weaker evidence for effectiveness include gabapentin, lamotrigine, carbamazepine, and zonisamide.  Intravenous antiemetics, with or without intravenous dihydroergotamine, are effective therapies in an emergency department setting. Dexamethasone may be a useful adjunct to standard therapy in preventing short-term headache recurrence.  Intranasal lidocaine may also have a role in relief of acute migraine.  Isometheptene-containing compounds and intranasal dihydroergotamine are also reasonable therapeutic options.

Injections of botulinum toxin (BOTOX®) around the scalp, neck, and shoulders have been used as a treatment in some patients who are intolerant of, or refractory to, other pharmacologic interventions.(6)

Surgery has also become a potential therapy for patients suffering from migraines.  Surgical release of the greater occipital nerve has been demonstrated to be clinically effective in eliminating or reducing chronic migraine symptoms for some patients, but migraine symptoms persist in others after this procedure.(7)  Recent studies of implantable occipital nerve stimulation devices have shown promising but mixed results.  Other permanent implants directing electrical stimulation to facial and cranial nerves have been tried as well.  Several studies, both retrospective and prospective, have been reported showing migraine frequency and severity relief from implanted vagal nerve stimulators typically used for epilepsy patients.

Despite significant advancements in the medical management of this challenging disorder, clinical data have revealed a proportion of patients who do not adequately respond to pharmacological or surgical intervention and remain symptomatic. Approximately 40% of all attacks do not respond to current available therapies.(8)

Sources
  • 1) “Management of Cluster Headache – February 15, 2005 – American Family Physician”. Aafp.org. 2005-02-15. Retrieved 2012-09-14.
  • 2) http://www.who.int/healthinfo/statistics/bod_migraine.pdf
  • 3) IHS. The International Classification of Headache Disorders (2004). Cephalalgia Vol 24. Blackwell/Sage. Retrieved 6/27
  • 4) De Felice M., Triptan-induced enhancement of neuronal nitric oxide synthase in trigeminal ganglion dural afferents underlies increased responsiveness to potential migraine triggers. Brain (2010 Aug) 133(Pt 8):2475-88
  • 5) Brandes JL, Kudrow D, Stark SR, O’Carroll CP, Adelman JU, O’Donnell FJ, et al. Sumatriptan-naproxen for acute treatment of migraine: a randomized trial. JAMA. Apr 4 2007;297(13):1443-54.
  • 6) Gilmore B, Treatment of acute migraine headache. Am Fam Physician (2011 Feb 1) 83(3):271-80
  • 7) Janis JE Neurovascular compression of the greater occipital nerve: implications for migraine headaches. Plast Reconstr Surg (2010 Dec) 126(6):1996-2001
  • 8) Edwards KR, Norton J, Behnke M. Comparison of intravenous valproate versus intramuscular dihydroergotamine and metoclopramide for acute treatment of migraine headache. Headache. Nov-Dec 2001;41(10):976-80