Using "pain sketches" to optimize migraine surgery outcomes

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“Can you draw me a picture of your headache?” may sound like an unusual question—but drawings of headache pain provide plastic surgeons with valuable information on which patients are more or less likely to benefit from surgery to alleviate migraine headaches.

Patients with more “typical” patterns on pain sketches have larger reductions in headache scores after migraine “trigger site” surgery, suggests a new study by Lisa Gfrerer, MD Ph.D. and William Gerald Austen, Jr., MD, and colleagues of Harvard Medical School. The study appears in the October issue of Plastic and Reconstructive Surgery, the official medical journal of the American Society of Plastic Surgeons (ASPS).

Migraine surgery has become an established treatment alternative for some patients with intractable migraine headaches. Developed by plastic surgeons who noticed that some migraine patients had fewer headaches after cosmetic forehead-lift, migraine surgery targets specific trigger sites linked to certain headache patterns. More than 5,200 patients underwent migraine peripheral trigger site surgery in 2019, according to ASPS statistics.

However, it can be difficult to predict which patients will get good results from migraine surgery. Drs. Gfrerer, Austen and colleagues have noticed that there are “pathognomic” pain patterns for each trigger site. “In our experience, a valuable method to visualize pain/trigger sites is to ask patients to draw their pain,” the researchers write. In the new study, they analyzed how well the patterns on these pain drawings predict the outcomes of migraine surgery.

The study included 106 patients who made pain sketches as part of their evaluation for migraine surgery. The sketches were reviewed by experienced researchers who were unaware of the patients’ headache symptoms or other characteristics, and classified into three groups:

  • Typical – showing pain originating from and spreading along the expected path of a specific nerve (59 percent of sketches)
  • Intermediate – showing pain along the path of the nerve, but with an atypical spread (radiation) of pain (29 percent)
  • Atypical – pain originating and radiating outside of the expected nerve distribution (12 percent)

One year after surgery, outcomes were assessed using a standard score, the Migraine Headache Index (MHI). Patients with typical or intermediate patterns on their pain drawings had similarly good outcomes: MHI scores improved by 73 and 78 percent, respectively.

However, for patients with atypical pain sketches the results were not as good: only 30 percent improvement in MHI score. Just one-fifth of patients in the atypical group had more than 30 percent improvement after migraine surgery.

The researchers emphasize that pain drawings should be just one part of the standard patient assessment. Migraine patients with atypical pain drawings may still have “compelling reasons” for surgery but should understand that they have lower chances of a positive outcome.

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Potential target identified for migraine therapy

Migraines affect millions of people worldwide, often lasting days and severely disrupting lives. More than simply super-intense headaches, some migraines actually result from pathological excitation of neurons in the brain. A new study in mice led by Kohichi Tanaka at Tokyo Medical and Dental University (TMDU) shows that susceptibility to migraines could be related to a molecular transporter that normally works to prevent excessive excitation of neurons.

Neurons in the brain communicate with each other by passing along molecules called neurotransmitters. After a neurotransmitter takes care of business, it is transported away from the synapse—the space between two neurons—so that it cannot be used over and over again. This process is called reuptake, and is one of many ways in which over-excitation of neurons in the brain is prevented. Migraines are related to a condition called cortical depression, in which a large wave of hyperactivity spreads across the brain, followed by a wave of inhibition, or depressed brain activity. Tanaka and his team hypothesized that susceptibility to cortical spreading depression is related to disrupted transport of glutamate, the most common excitatory neurotransmitter.

In turns out that mammals have four molecules that transport glutamate, and three of them are in the cerebral cortex. To determine which of these, if any, is related to cortical spreading depression, the researchers created three strains of knockout mice, each of which lacked one of the three cortical glutamate-transporter genes. They found that when mice lacked the GLT-1 transporter, cortical spreading depression occurred more frequently and spread more quickly than in control mice or in the other knockout mice.

“We know that 90% of glutamate is transported by GLT-1 back into astrocytes, not neurons,” says Tanaka. “Our findings thus highlight another important function of glial cells in the brain as they support neuronal function.”

To confirm their findings, the team then measured the amount of glutamate outside of cells using a platinum-iridium electrode coated with glutamate oxidase. When glutamate oxidase interacts with glutamate, it creates a negative current that can be detected by the electrode very quickly, allowing almost real-time measurements of glutamate concentration in the region.

“A fast biosensor is critical,” explains Tanaka, “because cortical spreading depression only lasts about 5 minutes, and the changes in glutamate concentration could never be found using conventional methods that take minutes to hours of sampling.” When testing the three knockout mice, only the GLT-1 knockout mice produced current that differed from that of the control mice. This means that the greater and faster accumulation of glutamate outside of neurons resulted from impaired uptake by astrocytes.

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