New pathway emerges for post-concussion treatment option

Preventing cortical inflammation from doing downstream damage to sensory processing areas

The old school protocol for a head trauma was to rest and do nothing and let the healing happen (as if we had broken our arm and our skull was some kind of cast).

As many of us know all too well, our symptoms can actually worsen over time. We’re told we’ll feel better in three months, six months, a year, and at the end of that time, we actually feel worse.

Why is that? Well, it appears we now have a better handle on one of the factors.

When a head trauma causes damage to the cortex, it triggers a self-protective inflammatory response around the site of injury, and there’s a particular molecule involved in that response, known affectionately as C1q.

If this inflammation goes on for some time, molecules of C1q do downstream damage to the thalamus. Even if the thalamus wasn’t damaged in the head trauma, it can be damaged as time goes on by this mechanism of action.

In a new study, scientists found that by blocking C1q, they could prevent this damage to the thalamus (the reticular thalamus in particular) in the aftermath of a cortical brain injury.

The thalamus is responsible for wide array of things, including the integrated processing of nearly all sensory information (except your sense of smell). Vision, hearing, your sense of where your body is in space, the thalamus helps put it all together.

The thalamus is also involved in the regulation of sleep and alertness.

While a traumatic brain injury could involve direct damage to the thalamus, it’s becoming clearer that the thalamus can be damaged over time by lingering inflammation around cortical injury sites, thanks in part to the C1q molecule.

In the future, blocking this molecule could become a treatment option in the aftermath of a head trauma. Meanwhile, what can we do now?

My thoughts on how this news could help now

If your injury was some time ago, you may still have lingering inflammation around sites of cortical injury.

If your injury was recent, you (and ideally the medical professionals helping you) should look at the problem of lingering inflammation in the brain as a major concern. It seems clear that you could prevent further damage by reducing that inflammation and its downstream effects.

However, as the authors of the study note, this might not be entirely solved by taking medications that reduce general inflammation, in part because inflammation is also involved in healing (inflammation is both good and bad).

If you’re reading this in the immediate aftermath of injury, don’t take a bunch of Advil, as that can cause further bleeding. For headaches, the Mayo Clinic recommends Tylenol. Quoting:

Headaches may occur in the days or weeks after a concussion. To manage pain, ask your doctor if it's safe to take a pain reliever such as acetaminophen (Tylenol, others). Avoid other pain relievers such as ibuprofen (Advil, Motrin IB, others) and aspirin, as these medications may increase the risk of bleeding.

After those initial days and weeks, the question remains: How to best deal with any lingering inflammation?

Identifying and reducing inflammation

Bloodwork can show markers of inflammation, so looking for such markers with your doctor is one step in the process—although I would ask your doctor if those markers could be expected to show up in the same way in the case of inflammation around a cortical injury site.

There are other specific markers of brain inflammation to look for, including these, but as with so many other diagnostic tools for the brain, they will likely involve expensive brain imaging technologies that are likely unavailable to you.

If you had some level of chronic brain inflammation prior to your brain injury, that would likely make your recovery that much more difficult, especially if the conditions causing it have continued. Chronic brain inflammation is linked to a variety of neurological and psychiatric disorders.

Diet is an area that can help generally reduce chronic inflammation, especially if you are unwittingly consuming commonplace foods that you’re mildly allergic to, such as wheat. (There’s an entire book on this subject called Grain Brain, which I admittedly haven’t read, but nevertheless, I typically avoid eating both wheat and sugar.)

Stimulating the brain’s lymphatic drainage system

The health of the brain’s lymphatic drainage system is likely to be a critical factor in your recovery and healing, and this system can be stimulated and maintained by two things that are under your control.

One is the simple act of walking. Among its other benefits, walking for about 30 minutes a day (between 5,000 and 8,000 steps) helps stimulate drainage. This is why walking is a great treatment option from the post-acute phase of one’s injury all the way to one’s present day.

Guess when your brain’s lymphatic drainage system really gets pumping? That’s right, in specific stages of deep sleep. And what is disrupted by a brain injury? Sleep.

It’s easy to see how this can easily become a negative feedback loop. No sleep, no drainage. No drainage, no healing, no sleep. And the thalamus is in the center of that loop.

This is one reason why restoring your sleep is critical. Start by working with the circadian rhythm and leaning on supplements and maybe even devices.

Stimulating and retraining the thalamus

Whether an injury was recent or not, the issue of how to help the thalamus heal emerges as a central question, especially in light of this new study.

One treatment option that involves helping (stimulating or retraining) the thalamus is syntonic light therapy. Another emerging treatment, which I’ve heard about but never tried, involves the use of translingual neurostimulation (TLNS) and/or the PoNS device, which at least one study showed as effective (in combination with physical therapy) for TBI patients with balance disorders. Cold laser therapy could also help reduce inflammation (especially if you sustained soft tissue damage in the sub-occipital area around the atlas).

My intuition is that the Wim Hof Method can also help, especially if you look at the points of emphasis I outlined in this post about it, including the use of pressure, which Wim kindly instructs us to bring to the center of our heads—which happens to be where the thalamus is. Slight inversion during the exercise may also help enhance the effect of the pressure and aid perfusion.

Beyond these ideas, any therapies that help with sensory integration, including physical and occupational therapy, will help the thalamus work toward reacquiring abilities lost in injury. This training will almost certainly involve doing things that trigger your symptoms.

If it’s the reticular thalamus that we’re rehabilitating, then that training would also need to include elements of suppression of incoming sensory information (including balance and vision).

Possible key to sensory overload

The relationship between the cortex and thalamus is fascinating. Nearly all of our sensory information passes through the thalamus (in that sense, I suppose you could think of it as a graphics chip), but the cortex dynamically uses the thalamus to “throttle” the information throughputs—to take in or suppress (ignore) incoming sensory information.

If we were to simply let all the information presented to us flood in, we would feel overwhelmed. And that’s precisely what many with post-concussion syndrome feel in loud or multi-sensory environments. A grocery store aisle. A comic book store. A loud restaurant. A dinner table with multiple conversations.

According to this study, the part of the thalamus that is especially damaged by this process , the reticular thalamus, is a key component in the suppression of sensory information. So it makes perfect sense that this damage could be at the very center of the sensory overload that so many people with TBI suffer from.

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Results of the study

Here’s an abbreviation of the study results from the journal Science.

Traumatic brain injury affects millions of people every year and is a major cause of disability worldwide. Most of the maladaptive outcomes develop months or years later and are thought to be caused by secondary injuries that are indirect and long-term effects after the initial impact… secondary and chronic neuroinflammation and neurodegeneration are caused by the C1q molecule... C1q is responsible for chronic inflammation and secondary neuronal loss.

Understanding where, when, and how secondary injuries develop is crucial for preventing or treating disability after TBI.

Although the cortex is the primary site of injury, the thalamus experiences secondary injury after a TBI, presumably because of its intimate long-range reciprocal connections with the cerebral cortex. These secondary injuries manifest as structural changes that have been implicated in a number of long-term TBI-related health outcomes and as chronic neurodegeneration and inflammation.

Most attempts to improve post-TBI cognitive outcomes with broad anti-inflammatory agents have failed, perhaps because inflammation leads to both damage and repair of neuronal circuits.

Mild TBI cases are ~10 times more common than severe TBI cases and can still lead to chronic health issues such as impaired cognition and sleep. By using a TBI model that only directly affects the cortex, we can also attribute effects on subcortical structures to chronic injury processes rather than the initial impact, which provides a greater window of opportunity for treatment.

Increased C1q… correlated with disruption of sleep spindles… hallmarks of early stages of sleep… Blocking C1q counteracted all of these outcomes.

The immune molecule C1q marks the secondary injury and is a disease modifier that could be targeted, at the proper time and location, to prevent secondary neuronal loss.

The corticothalamic circuit could thus be a new target for treating TBI-related disabilities.


Brainwave is an informational resource for people whose symptoms haven’t resolved after a concussion or mTBI. I endeavor to present this information in a clear and concise way, spelling out what’s backed by science and what remains unknown. Nothing here is meant as a substitute for professional medical advice, diagnosis, or treatment. I am not a physician or a healthcare practitioner of any kind; I’ve simply had a lot of sports-related concussions and had to learn this stuff the hard way. If you found this information helpful or know someone who might benefit from it, please share and subscribe to Brainwave.