Itâs not about whether I could physically work out while smoking â itâs that weed was suppressing glutamate and masking the symptoms of my underlying condition. Once I quit, the suppression lifted and the real dysfunction showed up. Thatâs a neurochemical reality.
I never claimed Lamotrigine works for everyone.. Iâve only spoken about my case. My qEEG was flagged with clear abnormalities, and Lamotrigine addresses the exact glutamatergic/sodium channel issues that showed up in my scans. Thatâs not placebo, and itâs not magnesium speculation. dismissing headaches or neuralgias as âpsychosomaticâ ignores decades of neurovascular and electrophysiological research. If you want to debate, at least keep it grounded in real data.. not guesswork
Thank you Dogworld for raising this point. I agree that modern brain mapping risks becoming a kind of digital phrenology / if we overstate what scans can reveal. Thatâs why I clarified in the discussion that my claim is narrower: a circuit signature can guide care, but it is not the whole of human experience.
In my case, brain mapping was critical for moving past a mislabel of âbipolarâ and finding the right treatment path. You are right that no two brains are the same, but this is exactly why psychiatry needs tools beyond the DSM. Advances that combine objective biomarkers with lived experience can help prevent misdiagnosis and lead to more accurate, individualized care.
Psychiatrists also need more tools to distinguish when a patientâs problems are neurological versus psychological. In my own journey, my psychiatrist even apologized, admitting that the field needs a bridge between these two worlds. Brain mapping gave me that bridge.
I didnât think clearly at all I had to go to the Emergency room twice⊠The headaches I had were on the same level as cluster headaches â which neurologists consider the most painful condition in medicine. It was like having an ice pick driven into my skull, nonstop, until Lamotrigine finally calmed the glutamate chaos.
The qEEG changed everything â it flagged excessive theta, PAC disruption, and frontalâtemporal undercoupling. Instead of a vague DSM label, I had a mechanism. That shifted me from symptom-chasing to targeted NMDA modulation: Lamotrigine + Memantine, exactly what clinical logs from Dogris, De Ridder, and others show restores thalamocortical rhythms. I donât accept that answering a PHQ-9 questionnaire should label me for life â I want objective data. For example, itâs no different than getting an X-ray to see if a bone is broken.
Yes, exactly â thatâs the same mechanism I was describing. Elevated glutamate activity with reduced inhibitory balance shows up in auditory/cortical circuits and creates the basal dysregulation my qEEG flagged. I focused on the circuit-level effects (theta overdrive, PAC loss, frontalâtemporal undercoupling) rather than the upstream contributors like MTHFR/folate metabolism, but weâre really pointing to the same chain of dysfunction â excess glutamatergic drive leading to disrupted cortical rhythms.
Every day, nonstop â until Lamotrigine finally stabilized the glutamate chaos driving the thalamocortical misfiring.
Those âice-pickâ migraines werenât random â they were the brainâs warning sign of excitotoxic overload and rhythm instability. Once the circuits were stabilized, they stopped.
No doctor ever understood my case â I was misdiagnosed for years. What changed everything was using AI to cross-reference my qEEG results with over 30 research papers and case reports from people showing the same brainwave abnormalities. Thatâs how I was able to identify the correct diagnosis and treatment path myself.
In my case, a qEEG was the turning point â it gave me the data I needed. That was the best brain scan in my situation to give me evidence of my disorder.
Thanks for sharing this. Iâve already had my folate, B12, and homocysteine levels tested â all normal â and I supplemented folate daily with no effect on symptoms. That pretty much rules out MTHFR or folate metabolism as the driver in my case.
My qEEG shows clear circuit-level abnormalities (PAC, frontalâtemporal undercoupling, theta overdrive), which line up with thalamocortical dysrhythmia literature. That points directly to NMDA/AMPA dysregulation at the circuit level, not a systemic folate issue.
Thank you for sharingâthatâs exactly the problem. Psychiatry keeps chasing surface symptoms while ignoring root dysfunction. My qEEG showed circuit-level abnormalities backed by neuroscience, yet doctors only saw âdepression.â Just like your brother, the system misreads the signals. Until psychiatry looks deeper, patients will keep falling through the cracks
Psychiatrists arenât trained to interpret qEEG patterns or thalamocortical dysfunction. Their training is built on DSM checklists and symptom clusters, which is why so many people like me get mislabeled or given the wrong drugs. My case is not about vague categories â itâs about measurable abnormalities (PAC deficits, frontalâtemporal disconnection, theta overdrive) that neuroscientists like LlinĂĄs, De Ridder, and Vanneste have already demonstrated and treated successfully. To say we should just âask a psychiatristâ is missing the point: the profession isnât equipped to handle circuit-level evidence. Thatâs why research and clinical neurophysiology, not symptom lists, are what actually drive recovery. evidence.
I would love for psychiatry to understand thisâŠbut right now, they donât
Iâm not replacing the DSM.. Iâm saying circuit-level dysfunction creates the very profiles psychiatry later labels as disorders.
Excessive glutamate excitotoxicity is already documented as the mechanism driving thalamocortical dysrhythmia (TCD).
My qEEG showed that exact pattern.
This isnât just correlation â LlinĂĄs, Jeanmonod, and De Ridder demonstrated that NMDA/AMPA imbalance destabilizes thalamocortical rhythms, and that interventions like Lamotrigine + Memantine restore them.
Saying nothing can alter qEEG wave patternsâ ignores decades of published data and clinical practice.
That claim isnât just wrong⊠it dismisses proven neurophysiology.
I didnât replace one narrow chemical theory with another. What I documented was objective qEEG evidence: cortical undercoupling, theta dominance, and PAC deficits⊠the same abnormalities described by LlinĂĄs, Vanneste, and De Ridder in thalamocortical dysrhythmia. Thatâs not speculation, itâs measurable physiology. Psychiatry has been content with vague metaphors like âserotonin imbalance,â while ignoring circuit-level dysfunctions that can actually be recorded. To call that narrow-minded misses the point: evidence expands the frame, it doesnât shrink it. If we want psychiatry to move forward, we have to acknowledge the brainâs rhythms as real contributors to lived experience.. not dismiss them because theyâre harder to confront. Dismissing evidence because it complicates the story isnât wisdomâŠitâs avoidance.
Itâs not about whether I could physically work out while smoking â itâs that weed was suppressing glutamate and masking the symptoms of my underlying condition. Once I quit, the suppression lifted and the real dysfunction showed up. Thatâs a neurochemical reality.
Report comment
I never claimed Lamotrigine works for everyone.. Iâve only spoken about my case. My qEEG was flagged with clear abnormalities, and Lamotrigine addresses the exact glutamatergic/sodium channel issues that showed up in my scans. Thatâs not placebo, and itâs not magnesium speculation. dismissing headaches or neuralgias as âpsychosomaticâ ignores decades of neurovascular and electrophysiological research. If you want to debate, at least keep it grounded in real data.. not guesswork
Report comment
Just wanted to stop and live a better life going to the gym everyday. I never knew the consequences of what was hiding underneath.
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Thank you Dogworld for raising this point. I agree that modern brain mapping risks becoming a kind of digital phrenology / if we overstate what scans can reveal. Thatâs why I clarified in the discussion that my claim is narrower: a circuit signature can guide care, but it is not the whole of human experience.
In my case, brain mapping was critical for moving past a mislabel of âbipolarâ and finding the right treatment path. You are right that no two brains are the same, but this is exactly why psychiatry needs tools beyond the DSM. Advances that combine objective biomarkers with lived experience can help prevent misdiagnosis and lead to more accurate, individualized care.
Psychiatrists also need more tools to distinguish when a patientâs problems are neurological versus psychological. In my own journey, my psychiatrist even apologized, admitting that the field needs a bridge between these two worlds. Brain mapping gave me that bridge.
Report comment
I didnât think clearly at all I had to go to the Emergency room twice⊠The headaches I had were on the same level as cluster headaches â which neurologists consider the most painful condition in medicine. It was like having an ice pick driven into my skull, nonstop, until Lamotrigine finally calmed the glutamate chaos.
Report comment
The qEEG changed everything â it flagged excessive theta, PAC disruption, and frontalâtemporal undercoupling. Instead of a vague DSM label, I had a mechanism. That shifted me from symptom-chasing to targeted NMDA modulation: Lamotrigine + Memantine, exactly what clinical logs from Dogris, De Ridder, and others show restores thalamocortical rhythms. I donât accept that answering a PHQ-9 questionnaire should label me for life â I want objective data. For example, itâs no different than getting an X-ray to see if a bone is broken.
Report comment
Yes, exactly â thatâs the same mechanism I was describing. Elevated glutamate activity with reduced inhibitory balance shows up in auditory/cortical circuits and creates the basal dysregulation my qEEG flagged. I focused on the circuit-level effects (theta overdrive, PAC loss, frontalâtemporal undercoupling) rather than the upstream contributors like MTHFR/folate metabolism, but weâre really pointing to the same chain of dysfunction â excess glutamatergic drive leading to disrupted cortical rhythms.
Report comment
Every day, nonstop â until Lamotrigine finally stabilized the glutamate chaos driving the thalamocortical misfiring.
Those âice-pickâ migraines werenât random â they were the brainâs warning sign of excitotoxic overload and rhythm instability. Once the circuits were stabilized, they stopped.
Report comment
No doctor ever understood my case â I was misdiagnosed for years. What changed everything was using AI to cross-reference my qEEG results with over 30 research papers and case reports from people showing the same brainwave abnormalities. Thatâs how I was able to identify the correct diagnosis and treatment path myself.
In my case, a qEEG was the turning point â it gave me the data I needed. That was the best brain scan in my situation to give me evidence of my disorder.
Report comment
Thanks for sharing this. Iâve already had my folate, B12, and homocysteine levels tested â all normal â and I supplemented folate daily with no effect on symptoms. That pretty much rules out MTHFR or folate metabolism as the driver in my case.
My qEEG shows clear circuit-level abnormalities (PAC, frontalâtemporal undercoupling, theta overdrive), which line up with thalamocortical dysrhythmia literature. That points directly to NMDA/AMPA dysregulation at the circuit level, not a systemic folate issue.
Report comment
Thank you for sharingâthatâs exactly the problem. Psychiatry keeps chasing surface symptoms while ignoring root dysfunction. My qEEG showed circuit-level abnormalities backed by neuroscience, yet doctors only saw âdepression.â Just like your brother, the system misreads the signals. Until psychiatry looks deeper, patients will keep falling through the cracks
Report comment
Psychiatrists arenât trained to interpret qEEG patterns or thalamocortical dysfunction. Their training is built on DSM checklists and symptom clusters, which is why so many people like me get mislabeled or given the wrong drugs. My case is not about vague categories â itâs about measurable abnormalities (PAC deficits, frontalâtemporal disconnection, theta overdrive) that neuroscientists like LlinĂĄs, De Ridder, and Vanneste have already demonstrated and treated successfully. To say we should just âask a psychiatristâ is missing the point: the profession isnât equipped to handle circuit-level evidence. Thatâs why research and clinical neurophysiology, not symptom lists, are what actually drive recovery. evidence.
I would love for psychiatry to understand thisâŠbut right now, they donât
Report comment
Iâm not replacing the DSM.. Iâm saying circuit-level dysfunction creates the very profiles psychiatry later labels as disorders.
Excessive glutamate excitotoxicity is already documented as the mechanism driving thalamocortical dysrhythmia (TCD).
My qEEG showed that exact pattern.
This isnât just correlation â LlinĂĄs, Jeanmonod, and De Ridder demonstrated that NMDA/AMPA imbalance destabilizes thalamocortical rhythms, and that interventions like Lamotrigine + Memantine restore them.
Saying nothing can alter qEEG wave patternsâ ignores decades of published data and clinical practice.
That claim isnât just wrong⊠it dismisses proven neurophysiology.
Report comment
I didnât replace one narrow chemical theory with another. What I documented was objective qEEG evidence: cortical undercoupling, theta dominance, and PAC deficits⊠the same abnormalities described by LlinĂĄs, Vanneste, and De Ridder in thalamocortical dysrhythmia. Thatâs not speculation, itâs measurable physiology. Psychiatry has been content with vague metaphors like âserotonin imbalance,â while ignoring circuit-level dysfunctions that can actually be recorded. To call that narrow-minded misses the point: evidence expands the frame, it doesnât shrink it. If we want psychiatry to move forward, we have to acknowledge the brainâs rhythms as real contributors to lived experience.. not dismiss them because theyâre harder to confront. Dismissing evidence because it complicates the story isnât wisdomâŠitâs avoidance.
Report comment