Study Shows How Stroke Pain Spread
Date: 17th June 2026 | By: Dr Lourdes Gaspar
A recent study from Kyoto University explains why some stroke patients develop mirror-image pain, where pain is felt on both sides of the body instead of just one. Normally, after a stroke, pain occurs on the side of the body opposite to the brain injury. However, in rare cases, pain spreads to both sides, creating a symmetrical or “mirror-like” pattern. Researchers wanted to understand how and why this happens.
The study focuses on a molecule called lysophosphatidic acid (LPA). LPA is a lipid (fat-like molecule) that forms from cell membranes and plays important roles in the body, including inflammation, blood vessel function, and cell movement. After tissue damage—such as a stroke—levels of LPA increase. Scientists already suspected that LPA might worsen chronic pain, but how it causes pain to spread across both sides of the body was unclear.
To investigate, researchers used a mouse model designed to mimic stroke conditions. They applied advanced techniques such as imaging mass spectrometry, which allows scientists to see where specific molecules are located in brain tissue, and immunostaining, which highlights the activity of certain cells. These methods helped them track changes in the brain after injury.
The researchers discovered a chain of events that explains how mirror-image pain develops:
- Initial injury: A stroke damages one side of the brain.
- Increase in LPA: The injury triggers a rise in LPA levels in the affected area.
- Activation of microglia: Microglia (immune cells in the brain) become active in response to LPA. These cells are responsible for inflammation and immune defense in the brain.
- Spread of inflammation: The inflammation spreads from one side of the brain to the other through the corpus callosum, a structure that connects the left and right brain hemispheres.
- Rise of pain-related molecules: Another molecule called PGE2, which is linked to pain and inflammation, increases.
- Bilateral pain: As a result, pain is felt on both sides of the body.
This step-by-step process shows how signals from a single injury can cross over to the other side of the brain, leading to widespread pain.
One of the most important achievements of the study is that researchers were able to visualize these molecular changes directly. They created maps showing where LPA and PGE2 appeared in the brain, as well as where microglia were activated. This helped confirm their findings and provided a clearer understanding of how these factors work together.
The results suggest that LPA and microglia play key roles in spreading pain signals after a stroke. Because of this, targeting LPA production or controlling microglial activity could become new ways to treat or prevent post-stroke pain. Instead of only treating symptoms, these approaches could address the underlying cause of the problem.
Finally, the researchers believe their findings may apply beyond stroke. Similar processes might be involved in other types of chronic pain or brain inflammation. Future studies will explore whether blocking LPA or reducing microglial activation could help patients with different neurological conditions.
In simple terms, this study shows that mirror-image pain is not random—it follows a clear biological pathway involving LPA, immune cells, and inflammation spreading within the brain.