Restoring the Brain’s Tempo
An endgame hypothesis for sensory-autonomic integration?
This is a bit longer than usual, but I’m tying strands together for something of an “endgame hypothesis” that I find pretty fascinating. I’ve been massaging this idea for quite some time now. It’s time to test it.
Last week, I walked into a new Vancouver clinic and got something I’ve been waiting two years for— a practitioner who looked at my EEG data and said “yes, we can work with this.” (!)
The previous clinician had vanished, but not before helping me sharpen a hypothesis that might address both sensory and autonomic chaos at their shared root. Before I commit my schedule to it, I want to lay out the reasoning like a persistent scientist who finally gets to test a big idea.
A Pattern Without a Plan
A couple of years ago, an academic did me a favour and performed an EEG on me. It showed “hypersynchrony” — regions of my brain working too much in step, particularly in networks involved in sensory integration. These networks happen to overlap with autonomic networks (breathing, heart rate, and other processes that should operate in the background).
The EEG doesn’t reveal damage like lesions on an MRI; rather it reveals the electrical patterns in real time. The reading was acknowledged politely, raising some clear questions, and then set aside. He said “maybe it will resolve on its own.” I liked the unfounded reassurance.
While I waited for spontaneous resolution, I learned everything I could about “hypersynchrony” and called every practitioner in the country to consider a treatment based on that pattern. From my read, inhibition of the right temporoparietal junction (rTPJ) would be a low-stakes test. The TPJ is where the ‘outside’ (sensory input) meets the ‘inside’ (autonomic state).
The hypothesis simply hummed along in the background while medications blunt the edges.
Why the Brain Chooses Volume Over Timing
In a healthy brain, networks synchronize briefly to integrate information, then quickly desynchronize to preserve flexibility. But when synchrony becomes excessive (ie. too stable, too global) the system gets stuck. Everything becomes loud, visual contrast increases, and senses become painfully high. Some brains might overcompensate with vestibular and spatial signals. Essentially, bodily states of arousal get stuck without inhibition.1 Without coordination, everything stays on lockdown even if you otherwise feel fine.
That hypersynchrony has a medical term: “thalamocortical dysrhythmia” —persistent low-frequency cortical coherence. In this model, the thalamus, just above the brainstem, amplifies sensory throughput and uses volume as a substitute for timing. The rTPJ appears to be one of the best ways to influence the thalamus because it participates in both timing and salience, and relays those timing signals back toward thalamic circuits. Without correct network control, the thalamus has an incompetent gatekeeper.
Hypersynchrony makes some sense from a survival perspective. When the neocortex is unreliable, the safest assumption for an ancient nervous system is not subtlety but LOUDNESS. It may be “better” to hear and see too much than to miss something that might matter.
What is adaptive in acute injury becomes unbearable as time goes on. The wrong regions get locked into the wrong rhythm for far too long and the result is not alertness, but overwhelm and noise.
GABA as main ingredient
Form and substance both matter here: targeting the right region can also shift neurotransmitter function.
From the beginning of this “experiment,” I’ve known that GABA is a key ingredient somehow. I started by trying to improve “GABA quantity,” to improve inhibition (like my early use of wine, which immediately improved symptoms). But the main issue in this model is not just “quantity of compound” — though it helps a bit — it’s actually the time-release function.
In other words, it’s not that the brain lacks enough GABA, it’s that inhibition is arriving at the wrong time. GABA-interneurons don’t just suppress activity, they shape when activity happens. When that timing breaks down, inhibition arrives late or out of phase. What I’m saying is that even if brain structures can function “normally,” the brain keeps the volume turned up because it GABA can’t do the timing work.
This is another reason for an rTPJ target. The effect wouldn’t just add inhibition globally, but it would re-train GABA timing, which allows circuits to balance excitation and inhibition dynamically again.
Drive-Thru Neurology
Long before we tried to measure anything, I underwent standard rTMS over the left dorsolateral prefrontal cortex (DLPFC), which is the default target for mood and attention, or more generally, when practitioners just want to do something.
I refer to standard rTMS protocols as a kind of drive-thru — you pull up, they ask if you want the mood and attention meal, and you get exactly what everyone else gets. It’s efficient, it helps many people at least a little bit, and the doc doesn’t have to think too hard. But many people don’t need combo meals. The strategy doesn’t treat thalamacortical dysrhythmia, or re-train GABA interneurons.
My requests have been met with closed doors and dead ends, until last week.
Precision Targets
The custom EEG last week was decidedly not a combo meal.
It’s called personalized rTMS (PrTMS). It was more granular and more regionally specific. It’s designed to improve how different regions interact as a network rather than simply clearing a diagnostic threshold for depression or attention.
[interestingly, the clinician thought the EEG looked closer to “long COVID” than iatrogenic injury, which suggests these presentations might share common neurological destabilization pathways. We’ll visit that later…]
Regardless, the rTPJ also regulates some of the central autonomic network, linking directly to the insula, hypothalamus, and brainstem, which are regions that regulate vascular tone, heart rate variability, and all the processes that normally happen without thinking (note: my HR and vascular tone have been ludicrous since this started). Restoring cortical timing also requires concurrent work on cellular metabolism and vagal tone.
Anyway, spectroscopy studies show that rhythmic rTMS increases measurable GABA in targeted regions, and that TPJ stimulation can normalize GABA–glutamate ratios in the auditory cortex for tinnitus and sound sensitivity. Changes in alpha power (the rhythm most closely tied to good interneuron timing) can persist after treatment for weeks, suggesting that the system can in fact be recalibrated.
If this framing is right, the solution would be to restore timing in certain regions. When inhibitory circuits fire coherently again, cortical noise drops, thalamic gating settles, and autonomic systems finally receive the signal that it’s safe to stand down.
One malfunctioning network node might be the primary lever for the tinnitus, light sensitivity, and to some degree, autonomic strain; though this would be a multi-target treatment to entrain the whole network all at once. If hypersynchrony can be cracked, the brain might finally stand down, at least a little, at least for awhile.
Endgame hypothesis?
The hypothesis is modest and, most importantly, testable. The clinic in Vancouver has both the data and the willingness to try, but I won’t give it a shot until I have enough openness in my schedule.
I’m not (yet) claiming that network retraining is a miracle cure and my n=1 experience doesn’t prove anything about anyone else. But this is as close to a testable meta-hypothesis that I’ve had for some of the mysteries that remain. I also have a clinic willing to test it, and data that makes the whole thing look plausible.
If this works, it won’t be a cinematic breakthrough but boy would it be gratifying. After years of advocating, researching, and being told to accept the ‘combo meal’ or leave, I’m finally looking at a map that actually matches the territory. Soon, we see if the persistence pays off.
This hypersynchrony pattern seems to appear across seemingly unrelated diagnoses: concussion syndromes, persistent withdrawal, HPPD, visual snow. Each involves the brain getting mechanically stuck in disinhibition with thalamic over-firing. Testing whether these share a common treatable mechanism would require resources beyond an n=1 experiment, but the convergence is striking to me.