The Cerebral Cortex – Dr. Todd Schwedt

Fascinating article…by Nancy Bonk on Health Central

“Another study used a white moving dot pattern on a black background to visually stimulate the subjects, showing the Migraine group had a stronger activation in the middle temporal complex (motion sensitive region) compared to the non-Migraine group. These studies support the idea that Migraineurs have enhanced reaction to light and motion stimuli in addition to having thicker cortex in the visual motion processing centers of the brain compared to non-Migraineurs.”

Yep… that relation I can understand since I am really hypersensitive to both light and motion. Both of which persistent beyond the migraine but are obviously worse with one.

“Dr. Schwedt rounded out his session discussing how a Migraineur “co-processes” different stimuli and that Migraine itself is multisensory integration that has “gone wrong.” He went on to explain what multisensory integration is:
“sensory-specific brain responses and perceptual judgments of incoming sensory stimuli which concern one sense may be modulated by relations with other senses.”

This means, our brains can take in many sensory stimuli (visual, olfactory, auditory and somatosensory) at the same time and process them simultaneously – we don’t process one type of stimuli at a time. He thinks this is important because Migraineurs with osmophobia seem to have a higher attack frequency and are found to be photophobic. If Migraineurs are hypersensitive to light they may also be sensitive to odors and have a hyper reactive trigeminal system. One study that measured pain thresholds in a group of Migraineurs who were not experiencing a Migraine and were exposed to bright light, became more sensitive after exposure when their pain thresholds were re-measured. This did not happen in the control group.”

Again, isn’t that interesting to note? How the stimulus gets tangled up? Makes a lot of sense doesn’t it? Certainly, it seems that our senses are hyper-aware during a migraine. That super sense of smell, photophobia, super hearing… too much of everything. And I am definitely photophobic and have been for decades. And odors… Anyway, it is quite intriguing. This was a few years back. I am re-printing it from my brainless blogger blog.

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Throbbing: rhythm of the brain

migraine

With a migraine the word Throbbing is definitely a word that is commonly used. And more. But there is throbbing. It feels like our brain is pulsing with our hearts. Like every blood vessel in our brains is throbbing in pain.

But apparently, Throbbing pain has nothing to do with blood flow. And everything to do with the brain.

Throbbing pain is actually connected to the pulsing rhythms of Alpha brain waves. That is right, we are throbbing to the rhythm of our brain.

In the study, researchers examined a patient who suffered from a throbbing sensation that remained even after her chronic migraine headaches had been resolved.

The researchers simultaneously observed the patient’s feelings of throbbing pain as well as her arterial pulse and found that they were unrelated to one another, suggesting that the pulsing of blood from the heartbeat was not connected to the throbbing quality of pain.

Through the use of an electroencephalogram, however, they discovered that the throbbing quality was linked to a type of brain activity — alpha waves.

“We understand very little about alpha waves, but they appear to have an important role in attention and how we experience the world,” Ahn said. “In addition, by analogy to how a radio works, alpha waves may also act as a carrier signal that allows different parts of the brain to communicate with itself.”

Scientists still aren’t sure how just alpha waves cause throbbing pain. But the current research suggests that the experience of throbbing pain is tied to how the brain works and not to the pulsations of blood at the location of pain. PsychCentral

Intriguing. One study doesn’t make fact, but if true then it makes you realize how little we understand some pain, doesn’t it?

 

White Matter Lesions and migraines

So I recently discovered I have these migraine brain lesions. Not because I was told, but because I read the letter he sent to my doctor where he said “scan from July 2009 had minimal scattered lesions.”

I suspected as such when my pain doc said he could ‘see’ I had migraines after reviewing my files and that old MRI. I knew you cannot see anything of the sort, other than damage due to stroke, therefore I very likely had some lesions showing at that time.

The research is as interesting as it is confounding. What is going on? Why is it going on? Is there any long term damage from the accumulation of these lesions? Are there any other structural changes going on with the brain we are unaware of? (such as with other forms of chronic pain some atrophy can be seen in certain areas). It puzzles me. Nevertheless is is damage for the migraines. And that is disturbing in itself.

This research in 2011:

 the dBrain white matter hyperintensities are more prevalent in migraine patients than in the general population, but the pathogenesis and the risk factors of these hyperintensities are not fully elucidated. The authors analyzed the routine clinical data of 186 migraine patients who were referred to the Outpatient Headache Department of the Department of Neurology, Medical School, University of Pécs, Hungary between 2007 and 2009: 58 patients with white matter hyperintensities and 128 patients without white matter hyperintensities on 3 T MRI. Significant associations between the presence of white matter hyperintensities and longer disease duration (14.4 vs. 19.9 years, p = 0.004), higher headache frequency (4.1 vs. 5.5 attacks/month, p = 0.017), hyperhomocysteinemia (incidence of hyperintensity is 9/9 = 100%, p = 0.009) and thyroid gland dysfunction (incidence of hyperintensity is 8/14 = 57.1%, p = 0.038) were found. These data support the theory that both the disease duration and the attack frequency have a key role in the formation of migraine-related brain white matter hyperintensities, but the effects of comorbid diseases may also contribute to the development of the hyperintensities.NCBI

At the bottom you can note that study determined disease duration and attack frequency were factors.

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