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Exploding vs. imploding headache in migraine with Botox and Botox review study

 Exploding vs. imploding headache in migraine prophylaxis with Botulinum Toxin A 
In this study the responders vs non-responders was not dependent on symptoms, episodic vs chronic, aura vs no aura or other factors but there did seem to be this interesting correlation between how people described there pain. Exploding pain vs imploding pain, which leads to some speculation as to why botox might be effective in responders and not effective in non-responders.

I often speculate my brain is both exploding and imploding during a migraine such that a new black hole is about to burst forth in there... but the fact is in reality the pain I experience is very much exploding. Very much expanding beyond the realms of my scull. Except I also get a great deal of eye pain, temple pain, jaw pain, teeth pain, check pain, constant neck pain. And all the facial pain might suggest a lot of nerve pain on the surface. When I got botox it did not do a damn thing. Made my forehead numb. I could not do my infamous 'Spock' eyebrow lift. That was sad. I hated that numb feeling. But did nothing to reduce the frequency or intensity of the migraines. What it did to was give me more temple pain, that then radiated down into my jaw and teeth. That was very unpleasant by the way. To be honest I think it rather opened the pathway for the migraine to travel that way since I certainly began to get more jaw and teeth pain after that... sort of makes me reluctant to give it another go for sure. I thought to myself they would have to give me a crapload more botox to follow the pain if that is the result of it. My neuro said if I had no positive result there was in fact no reason to try again as I was not the sort to respond to it. Perhaps he was right in that. Yet while I am definitely on the exploding end of the spectrum, I do have ocular pain, yet I was definitely a non-responder as well.

The study:

"Migraine headache is routinely managed using medications that abort attacks as they occur. An alternative approach to migraine management is based on prophylactic medications that reduce attack frequency. One approach has been based on local intramuscular injections of Botulinum Toxin Type A (BTX-A). Here, we explored for neurological markers that might distinguish migraine patients who benefit from BTX-A treatment (100 units divided into 21 injections sites across pericranial and neck muscles). Responders and non-responders to BTX-A treatment were compared prospectively (n=27) and retrospectively (n=36) for a host of neurological symptoms associated with their migraine. Data pooled from all 63 patients are summarized below. The number of migraine days per month dropped from 16.0±1.7 before BTX-A to 0.8±0.3 after BTX-A (down 95.3±1.0%) in 39 responders, and remained unchanged (11.3±1.9 vs. 11.7±1.8) in 24 non-responders. The prevalence of aura, photophobia, phonophobia, osmophobia, nausea, and throbbing were similar between responders and non-responders. However, the two groups offered different accounts of their pain. Among non-responders, 92% described a buildup of pressure inside their head (exploding headache). Among responders, 74% perceived their head to be crushed, clamped or stubbed by external forces (imploding headache), and 13% attested to an eye-popping pain (ocular headache). The finding that exploding headache was impervious to extracranial BTX-A injections is consistent with the prevailing view that migraine pain is mediated by intracranial innervation. The amenability of imploding and ocular headaches to BTX-A treatment suggests that these types of migraine pain involve extracranial innervation as well."

Rather than acting centrally, BTX-A may exert its prophylactic action on migraine through inhibition of peripheral sensory neurons (Aoki 2005). That BTX-A can inhibit sensory neurons is consistent with evidence that the toxin inhibits release of substance P from embryonic dorsal root ganglion neurons in vitro (Welch et al. 2000), or CGRP from trigeminal ganglion neurons in vitro (Durham and Cady 2004), or glutamate from peripheral nociceptors terminating in the dorsal horn in vivo (Cui et al. 2004). Using quantitative sensory testing, however, Blersch et al (2002) showed that subcutaneous injection of BTX-A did not change pain thresholds to local cold, heat and electrical stimulation, and concluded that BTX-A may block pain through chemodenervation or anti-inflammatory action, rather than by direct peripheral anti nociceptive effect.
Regardless of the exact peripheral mechanism of BTX-A action, at issue here is whether the peripheral action is exerted intracranially or extracranially. The finding that exploding headache was impervious to extracranial BTX-A injections is consistent with the general view that migraine pain is mediated by intracranial nociceptors innervating the meninges and sinuses of the dura. Such a concept may also be tested in the future using patients whose headache stems from a clear intracranial pathophysiology. On the other hand, the amenability of imploding and ocular headaches to BTX-A treatment suggests that these types of migraine pain also involve extracranial sensory fibers adjacent to the injection sites. Involvement of extracranial tissue in the pathophysiology of certain migraine patients has been proposed some five decades ago (Selby and Lance 1960; Wolff et al. 1953). If so, it is tempting to speculate that imploding headache involves activation of extracranial nociceptors that innervate scalp tissues, such as bone and periostium.
The dramatic difference between responders and non-responders in the incidence of migraine after BTX-A treatment suggests that previous studies that pooled data from all treated patients without such distinction (Binder et al. 2000; Dodick et al. 2005; Evers et al. 2004) may have missed the full magnitude of the prophylactic effect of the toxin at the level of the individual patient. Of the 42 subjects that participated in our prospective study, only 14 (33%) were clear-cut responders, while 13 (31%) were clear-cut non-responders. It remains to be determined what types of headache are present in patients whose attack frequency after BTX-A dropped between 33 and 80% (‘partial responders’).


Now keep in mind... 

As of April 2012 the review on Botox I read suggested I wasn't alone in 'not responding' to Botox. In fact I had assumed it was a last resort for a reason. We all were told to glowing statistics for it... but those stats were from the early trials and not the new ones or the review on all of them. Not responding or having a minimal to little response is the norm according to the latest review... with an 'average of two fewer migraines per month'. Wow. Color me impressed. I would notice that since I am daily. But in the scheme of things that is not exactly a 'WOW' factor given the cost. It is only impressive due to the lack of side effects... well there is the lack of expression. But other than that. Yet clearly some people do respond well, above average.

"In the new study, which appears this week in the Journal of the American Medical Association, researchers analyzed findings from 27 trials that compared Botox to placebo and four studies that compared it to other migraine treatments.
The analysis found that Botox injections were not effective for preventing migraines in patients who have less than 15 headaches a month. The treatment also did not appear to benefit patients with chronic tension headaches.
But Botox-treated patients with chronic migraines and daily headaches had an average of two fewer headaches per month.
Researcher Jeffrey L. Jackson, MD, of the Medical College of Wisconsin, says it is clear that much better migraine therapies are needed, especially for the most frequent sufferers.
"All of the available migraine treatments benefit some patients and not others," he tells WebMD. "Until we really understand migraines it will be hard to design treatments that work well for all patients."
He says that while the average Botox patient may not experience big improvements, results for some patients might be dramatic.

Botox Finding 'No Big Surprise'

Headache specialist Satnam Nijjar, MD, of Johns Hopkins University School of Medicine, says the research analysis will surprise few clinicians working in the field.
"This review emphasizes that most patients experience modest benefits, but we already knew that," he tells WebMD." WebMD
But then there is this...

Botox Maker Responds

In an interview with WebMD, a spokesperson for Botox manufacturer Allergan Inc. says the study reinforces its role as a treatment to prevent chronic migraines.
Crystal Muilenburg, Allergan's director of corporate communications, says some patients in company-sponsored trials experienced a 50% reduction or more in headache days per month after two cycles of Botox, and more than 2 out of 3 patients showed some improvement. WebMD

So 'some', yes some indefinite some people experience 50% reduction after two cycles and 'more than' 2 out of 3' show 'some' improvement... which I assume means 'about two less migraines a month'. Unfortunately 'some' could mean 2 people. But I assume it is more than that. I assume it might be people with imploding type migraines in fact. And that I do find interesting because it says something about the structure of migraines. And also is a great potential for the treatment in those cases... and does explain the success stories we hear for Botox as well.

However why Botox does not work in 'some' cases also makes sense given our knowledge of recent research into intracranial pathophysiology of migraines. I never did quite understand why it would work except for maybe skin nerve pain, which is an issue, especially with fibromyalgia which is an entirely different issue... but makes my scalp hurt. Nevertheless, if the pathophysiology in migraines can differ then the treatment might need to be catered to different patients.
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