Medicines Used for Migraines & Depression

Are Medicines Needed? 

Migraines and depression are considered to be neurological diseases though some treat them as mental illnesses with the associated stigma [1, 2]. Both migraines and depression are energy crisis and can be stopped by voltage applied to specific brain regions in trouble[3-6, 9]. The cause is seen in scanners [1, 10]: dormant regions that have no observable electrical activity. When electrical stimulation is applied to a dormant brain region, it regains its function. Crucially for migraines, it has been demonstrated that a dormant area is shocked by a wave of electricity generated by the brain itself. This is called cortical spreading depression, which energizes the area to create action potential again [11-14]. This wave of energy reaches the meninges where pain sensory neurons are located [14] so migraine pain is caused by this wave of energy.

Similarly to how a cardiac arrest does not always get the heart to continue beating again, the electric shock of generated by the brain may not awaken the dormant regions either. Energy for proper functioning of both heart or brain must be created from something. To continue voltage generation after the shock, minerals have to be ready and waiting.

One can only drive a car on fumes for so long. Interestingly we understand this very well when it comes to our cars but we forget it when it comes to our body. Energy for our body is generated from what we eat and drink. The energy is carried to the cells by electrolytes. Electrolytes are water mixed with vital nutrients. Electrolytes take up 55%-70% of our body per gender and age with salt about 9 grams per liter. Brain regions that lack important nutrients will not function.

We understand that brain regions starved from energy are not able to generate action potential and cause abnormal synaptic transmissions [15, 16] (synaptic transmission is how neurons communicate). Yet rather than restocking the brain with nutrients, currently we use a medicinal route of some form of serotonin medicine, such as triptans or serotonin reuptake inhibitors (SSRIs or SNRIs). Unlucky migraineurs and depression patients (as well as fibromyalgia, bipolar, chronic fatigue and a host of other conditions) also receive voltage dependent calcium channel blocker medicines, one of which I tore apart in my last article. Given that these medications are so often prescribed, one would think that they actually work. But do they?

These medications don’t actually work for depression in over 70% of the time. And for migraines? Well, that is another story as I am about to discuss.  It is also important to note that where energy is needed, medicines that block energy actually work against recovery and dull the brain, using symptom management instead of prevention or treatment.

Why Triptans and SSRIs/SNRIs are Hit or Miss for Migraines

Serotonin for migraines sometimes works and sometimes it does not. Regardless if it works or not, it comes with tremendous side effects, often causing depression, violence, and fatalities. The Stanton Migraine ProtocolTM has treated thousands of migraineurs over the years and the statistics show that 80% initially take some serotonin preventive, usually an SSRI or SNRI, and also need abortives, such as triptans, and even after that they still have migraines! Not only does this show that serotonin does not work but also that there is a very dangerous practice of “more is better,” which may be followed by fatal consequences, such as serotonin syndrome.

Medicines given to migraineurs, by blocking all possible energizing channels, block the inflow of nutrients and the outflow of toxins.

Does Serotonin Make Any Sense At All for Migranes?

A brain region that is not able to generate action potential, as shown, serotonin is not the energizer. It is possible that the particular region that cannot generate energy happens to be responsible for serotonin production, in which case adding serotonin will indeed take the pain away. Taking serotonin is a band-aid and will not treat the cause of not having enough energy.

During deep brain stimulation of conscious humans, they were able to explain what they felt and how their depression lifted during the procedure [4-6, 17]. Since migraine shows the exact same patter and deep brain stimulation also works for them, though they were never made to talk and explain their stories while under procedure, they did improve and their pain went away.  It all sounds so simple since we know what generates action potential in the brain: salt.

So why do patients keep on getting serotonin medications knowing that serotonin has absolutely nothing to do with migraines? This is a great question that I would like to ask many physicians! Habits are hard to break but eventually they must!

There is a small chance that triptans or SSRIs may work for your migraines (30% or less) but it is 100%  certain that adverse effects will cause enough problems that will prevent your brain from working properly. In the long run, these drugs cause permanent damage–I have seen that happen.

Instead of popping the  next pill, learn what migraines are and learn how simple it is to prevent them. Since migraines and depression have the same cause as seen in the scanners, why not try the same solution for depression as well?

Join the movement for healthy life without medicines. Contact us for the solution!

Sources

  1. Gasparini, C.F., H.G. Sutherland, and L.R. Griffiths, Studies on the Pathophysiology and Genetic Basis of Migraine.Current Genomics, 2013. 14(5): p. 300-315.
  2. Young, W.B., et al., The Stigma of Migraine. PLoS ONE, 2013. 8(1): p. e54074.
  3. Holtzheimer, P.E., et al., Subcallosal Cingulate Deep Brain Stimulation for Treatment-Resistant Unipolar and Bipolar Depression. Jama Psychiatry, 2012: p. 150-158.
  4. Lozano, A.M., et al., A multicenter pilot study of subcallosal cingulate area deep brain stimulation for treatment-resistant depression. J Neurosurg, 2012: p. 315-322.
  5. Mayberg, H.S., et al., Deep brain stimulation for treatment-resistant depression, in Neuron. 2005. p. 651-60.
  6. Taghva, A.S., D.A. Malone, and A.R. Rezai, Deep brain stimulation for treatment-resistant depression. World Neurosurg., 2013: p. 826-831.
  7. Aurora, S.K., et al., Transcranial magnetic stimulation confirms hyperexcitability of occipital cortex in migraine, inNeurology. 1998. p. 1111-4.
  8. DaSilva, A.F., et al., tDCS-Induced Analgesia and Electrical Fields in Pain-Related Neural Networks in Chronic Migraine. Headache: The Journal of Head and Face Pain, 2012. 52(8): p. 1283-1295.
  9. Tepper, S.J., et al., Acute Treatment of Intractable Migraine With Sphenopalatine Ganglion Electrical Stimulation.Headache: The Journal of Head and Face Pain, 2009. 49(7): p. 983-989.
  10. Hadjikhani, N., et al., Mechanisms of migraine aura revealed by functional MRI in human visual cortex.Proceedings of the National Academy of Sciences, 2001. 98(8): p. 4687-4692.
  11. Charles, A.C. and S.M. Baca, Cortical spreading depression and migraine. Nat Rev Neurol, 2013: p. 637-44.
  12. James, M.F., et al., Cortical spreading depression and migraine: new insights from imaging? TRENDS In Neuroscience, 2001: p. 226-271.
  13. Lauritzen, et al., Clinical relevance of cortical spreading depression in neurological disorders: migraine, malignant stroke, subarachnoid and intracranial hemorrhage, and traumatic brain injury, in J Cereb Blood Flow Metab. 2011. p. 17-35.
  14. Bolay, H., et al., Intrinsic brain activity triggers trigeminal meningeal afferents in a migraine model. Nat Med, 2002. 8(2): p. 136-142.
  15. Pietrobon, D., Insights into migraine mechanisms and Ca(V)2.1 calcium channel function from mouse models of familial hemiplegic migraine. The Journal of Physiology, 2010. 588(Pt 11): p. 1871-1878.
  16. Vecchia, D., et al., Abnormal cortical synaptic transmission in CaV2.1 knockin mice with the S218L missense mutation which causes a severe familial hemiplegic migraine syndrome in humans. Front. Cell. Neurosci., 2015: p. epub ahead of print.
  17. Lozano, M. and N. Lipsman, Probing and regulating dysfunctional circuits using deep brain stimulation, inNeuron. 2013. p. 406-24.

Your comments are welcome!

Angela

About Angela A Stanton, Ph.D.

Angela A Stanton, PhD, is a Neuroeconomist focusing on chronic pain, electrolyte homeostasis, and genetics. She lives in Southern California. Her current research is focused on migraine cause, prevention and treatment without the use of medicines. As a forever migraineur from childhood, her discovery was helped by experimenting on herself. She found the cause of migraine to be at the ionic level, associated with disruption of the electrolyte homeostasis, resulting from genetic variations of all voltage gated channels that modulate electrolytes and voltage in the brain, insulin and glucose transporters, and several other related variants, such as the MTHFR variants of the B vitamin methylation process and many others. Migraineurs are glucose sensitive and should avoid eating carbs as much as possible. As a result of the success of the first edition of her book and new research and findings after treating over 4000 migraineurs world wide, all ages and both genders, she is now finishing the 2nd edition. The 2nd edition is the “holy grail” of migraines, incorporating all there is to know and also hypotheses. It includes an academic research section with suggestions for further research. The book is full of citations to authenticate the statements she makes to be followed up by those interested and to spark further research interest. It is a "Complete Guide". Due out in the summer of 2017. Dr. Stanton received her BSc at UCLA in Mathematics, MBA at UCR, MS in Management Science and Engineering at Stanford University, PhD in NeuroEconomics at Claremont Graduate University, and fMRI certification at Harvard University Medical School at the Martinos Center for Neuroimaging for experimenting with neurotransmitters on human volunteers. For relaxation Dr. Stanton paints and photographs. Follow her on Twitter at: @MigraineBook
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2 Responses to Medicines Used for Migraines & Depression

  1. Interesting. On my blog I recently also wrote about migraine and cortical spreading depression, but I focused in on brain hypoxia. You focus on the energy and electrolyte balance. Something new for me to investigate.

    Liked by 1 person

    • Thanks for visiting and commenting DL with respect to cortical depression and cortical spreading depression as part of hypoxia (or caused by hypoxia) but oxygen does not start voltage in the brain. Cortical depression is a region of no electrical activity and there is only one element that creates voltage in the brain: salt. Cortical spreading depression is a voltage shock moving from one end (the healthy part) of the brain to another (where cortical depression is) to shock it into action potential. Same as the heart: oxygen will not make it beat again. Voltage shock is needed after a heart attack. The brain’s principle of basic function is the same. The brain functions by voltage and the cortical depressed regions are not able to generate enough electricity for an action potential. In the scanner they show as a black region of no activity. Cortical spreading depression is visualized by the migraineur as aura. Not everyone has aura since to see aura the region where cortical spreading depression starts must be in the occipital lobe. This is why aura migraine is an anatomical difference in migraines and not a function of difference in terms of its severity. Only this part is not yet understood by many. I have written about this extensively.

      Have a great day,
      Angela

      Like

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