Health
Overview
Decades of repetitive head hits, concussions and traumatic brain injury. The last injury, 2012. At this time, I had to stop all activities. One reason, post concussive symptoms. These became an issue during late teenage years. Then they increased in severity, with additional symptoms appearing throughout my twenties and thirties.
During these years, TBI and Mental Health specialists were seen around the country. They prescribed therapies, medications, exercises and rehabilitation programs. There was also weight training 5-7 days per week along with 1-3 hours of cardio per day. In addition to eating clean and incorporating supplementation. Further, an average of 4+ hours a day was devoted to the study of TBI, health, psychology, fitness, etc. [Reference Appendix A-B]
These efforts helped manage the post concussive symptoms. However, the majority remain. Additional and more severe symptoms continue to appear.
2023 - 2024 created more concern. I was admitted to the ICU (5/23). Put on a ventilator. Many doctors were consulted. No answers provided. They know something is wrong. Yet they weren’t able to provide diagnosis. Throughout the following year relevant bloodwork, scans, tests, etc. have also been completed. All indicate good health.
At this point, the primary concern is the symptoms experienced and how they’ve progressed over time. It’s not finding answers for the May 2023 hospitalization. It’d be nice to know why. But doctors have not been able to figure it out. There’s also the possibility of this being a one-time incident. There’s the possibility of my body / brain shutting down due to the drugs they put in the IV and the way medical professionals managed the situation. There’s the possibility it could be associated with past hits to the head, concussions and traumatic brain injury. There’s the possibility it could be all the above.
Regardless, the health challenges remain. They continue to intensify. I’ve been dealing with post concussive symptoms for sixteen years now. Symptoms continue to get more problematic.
Most recently, pace of walk (slowed shuffling sometimes wide gait) along with speech difficulties (slowed, slurred, stuttered, inability to talk, etc.). Just as concerning, the personality. It started changing in my early thirties (and continues to do so). Not in good ways. There’s deep depression. Severe mood swings. Loss of interest. I’ve become far more emotional while at the same time being apathetic. I’m less patient. I then get easily triggered. All of which leads to an uncontrollable temper with explosive outbursts. These are some of the reasons why I continue to become more distant and recluse. I’m hypersensitive to everything. These sensitivities drain my energy. They make the post concussive symptoms worse. So, I try to limit exposure to outside forces to maintain some sense of balance and steady behavior. It just feels like I’m losing control of my thoughts and behaviors. I no longer trust myself in how I respond. So, I isolate and limit exposure.
I’ve suspected most of this to be TBI related. Possible Chronic Traumatic Encephalopathy (CTE) – Traumatic Encephalopathy Syndrome (TES). Of all the potential diagnoses that would provide clarity on the health situation, CTE has always aligned most.
History of repetitive and severe head trauma (cause of the disease).
Symptoms and their progression align.
Markers (MRI/DTI, SPECT, Cognitive, Studies) align.
All other issues and diseases have been ruled out.
[Reference Appendix C]
In the meantime, we continue to do more bloodwork, scans, etc. We continue to consult with doctors. All of whom continue to be confused. They aren’t able to provide answers. We’ve consulted with seventeen (not including ICU, six being Neurologists) in twelve months.
I’m seeking probable diagnosis for a reason. Regardless of if it’s CTE or something else. I say “probable” because an official diagnosis of CTE is not possible. It can only be made through post‐mortem neuropathological examination. Nor is there a cure. However, that doesn’t mean that we can’t work towards pursuit of them.
One reason for taking this approach is that it provides a clear objective.
It’s also important to note that uncertainty of diagnosis (when symptoms are debilitating and have a significant impact on executing the basics of everyday life) creates hopelessness. This is not a good feeling. Nor does it lead to positive behaviors and results.
Thus the reason for generating a clear objective. It creates hope. Just as importantly, it creates purpose. Both of which are required to build resilience in order to work through the adversity being faced.
Appendix A – Symptoms, Diagnoses & Therapies
Appendix B – Pharmaceuticals & Supplements
Pharmaceuticals
Focalin (10-40mg) in twenties. Went off in late twenties for 18 months. Didn’t want to be reliant on Pharmaceuticals. Struggled. Went back on (10-30mg).
Lorazepam (don’t remember dosage) in early twenties. Stopped taking after a year.
Wellbutrin (don’t remember dosage) in late twenties for depression. Stopped taking after 6 months.
Modafinil (200mg) in early thirties due to excessive fatigue / sleepiness. Still taking.
Lamictal (don’t remember dosage) in mid-thirties for bipolar. Stopped taking after a few months.
Naltrexone (1.5mg) in mid-thirties. Stopped taking after a few weeks.
Xelstrym (9-13.5mg) in mid-thirties. Potential replacement for Focalin. Need to further assess.
Topomax (don’t remember dosage) was recommended in mid-thirties by PA / Neurologist. Did not take. Risk profile was too severe. Also had concerns regarding the medical professionals assessment of condition and immediacy of putting me on this medication without identifying cause.
Prednisone (60mg) in mid-thirties. Neurologist thought this might resolve the symptoms experienced. It gave me more energy. Circulation seemed to improve. However, there was insomnia most nights, stomach issues and it did not improve the primary symptoms of concern (speaking, walking and TBI). Stopped taking after 4 weeks.
Nicotinamide Adenine Dinucleotide (NAD+), Glutathione and IV vitamins for ten sessions. No noticeable impact.
Psychiatrists have also recommended various SSRIs over the years. Tried a couple (can’t remember the names with exception to the ones detailed above) despite being hesitant. Some had adverse effects. Others did not prove to be beneficial. Likely won’t take them in the future based on research, experience and risk profile.
Supplements
Vitamin D
Fish Oils
DHEA
Pregnenolone
Vinia
Liver+
Nattokinase
Creatine
Psilocybin: I’ve been studying medicines with potential to heal TBI for years. Hesitant to take them. Never done “drugs”. However, due to research, case studies, time and the increasing severity of symptoms (despite efforts to improve), I made the decision to assess. Started with 50-250mg (two days on one day off). No noticeable difference. Stopped taking after four weeks. Then went off for a few months off. Continued research. Found another medicine with potential. Tested dosage range (250-700mg). For the most part, I continue following the recommended usage guidelines. There are times where I test three days on one to two days off. There are times where I go off the medicine for a few weeks as well. This medicine / approach appears to have a positive impact. One example, I used to cry uncontrollably (for no reason at all). This has become less frequent. Another example, aggression, explosive outbursts, temper and paranoia seem to lessen in frequency and severity. I’ve also done extensive bloodwork / testing while using the medicine. Clean. Overall, Psilocybin has been a positive.
Current Dosage: 50-700mg Psilocybin / 350-700mg Lions Mane / 500mg Syrian Rue
Appendix C – Chronic Traumatic Encephalopathy (CTE) / Traumatic Encephalopathy Syndrome (TES)
I’ve shared thoughts about CTE – TES being a potential / probable cause for several years.
The symptoms and their progression have always aligned. This intuition of diagnosis has only strengthened considering that the testing completed has ruled out all other issues / diseases.
Here are 7 Case Studies that support the potential / probable diagnosis.
Case Study 1 - Chronic Traumatic Encephalopathy: A Review by Michael Saulle and Brian D. Greenwald
Most content in this study is technical. The analysis below is focused on a simplified review of symptoms associated with CTE and how it progresses.
Highlighted and underlined blue text are symptoms experienced.
As reported by McKee, the first symptoms of CTE were noted at ages ranging from 25 to 76 years. McKee also reported that at the time of retirement one-third of these athletes were symptomatic with another half becoming symptomatic within 4 years of leaving sports [5]. In 14 cases (30%), mood disturbances were reported while movement abnormalities like Parkinsonism, ataxia, antalgic gait, and dysarthric speech were reported in 41% of subjects [5]. The course of symptom progression seems to follow a somewhat continuous path beginning with cognitive and emotional decline leading to eventual motor deterioration [5].
Initially, patients begin to have poor concentration, attention, and memory along with disorientation, dizziness, and headaches. They typically progress to experience irritability, outbursts of violent or aggressive behavior, confusion, and speech abnormalities. During this stage of the disease, there is a high frequency of suicide, drug overdose, and mood disorders, mainly major depressive disorder [5]. A study by Omalu and colleagues describes a similar clinical profile with a latent asymptomatic period between play and symptom onset. He reports worsening of cognitive and social functioning leading to poor money management, bankruptcy, social phobias, paranoid ideation, insomnia, poor relationships, divorce, emotional/physical abuse, and substance abuse [18]. Family and friends of the affected individuals reported many of these symptoms to researchers through standard forensic interviews [18].
As the disease progresses in severity, there is a greater loss of motor functioning. Some patients may develop Parkinsonian symptoms of tremors, masked facies, wide propulsive gait, poor speech, ocular abnormalities, vertigo, bradykinesia, deafness, and a small group developing dementia. Currently, the number of cases with confirmed dementia remains small. As more postmortem exams are done in the at-risk group, it is expected more cases will be diagnosed. Some individuals with CTE have committed suicide, overdosed on drugs, or died from accidents preventing progression of the disease [5, 20].
As highlighted above, I experience most of the symptoms. The symptoms have also progressed in the same ways. Case in point:
Starts with poor concentration, attention, and memory along with disorientation, dizziness, and headaches.
Experienced throughout 20’s. Put on ADHD medication to help with executive function. CPT3 (Section 2 – Case Study 5) confirms diagnosis. Saw TBI specialists to assist with the symptoms that come with head trauma.
Progresses to irritability, outbursts of violent or aggressive behavior, confusion, and speech abnormalities. During this stage of the disease, there is a high frequency of suicide, drug overdose, and mood disorders, mainly major depressive disorder [5].
Depression, irritability, outbursts and aggressive behavior became more of an issue in early 30’s. Depression and Bipolar were diagnosed by several doctors. SPECT and qEEG (Section 2 – Case Study 4 and 5) confirms diagnosis. Speech has now become a significant issue.
Which then leads to a greater loss of motor functioning. Some patients may develop Parkinsonian symptoms of tremors, masked facieses, wide propulsive gait, poor speech, ocular abnormalities, vertigo, bradykinesia, deafness, and a small group developing dementia.
Gait, speech (apraxia/dysarthria), ocular, vertigo (might be severe dizziness), bradykinesia, parkinsonism, etc. are all symptoms that have become more severe and problematic.
This study details CTE symptoms and their progression that tracks in a near identical way to what I have been experiencing. See Appendix A and B for more detail and evidence.
Case Study 2 – Dr Robert Cantu on Managing and Treating Suspected CTE
Dr. Cantu is the Medical Director and Director of Clinical Research at the Cantu Concussion Center at Emerson Hospital. He is also the Founding Member and Chairman Medical Advisory Board of the Concussion Legacy Foundation.
In this video he features a Symptom Checklist (10:20) used to identify the signs of CTE. This has been completed with my ratings below.
Case Study 3 – MRI & The Neuropathology of Chronic Traumatic Encephalopathy
Completed MRI on July 15, 2023.
The Neuropathology of Chronic Traumatic Encephalopathy
Author: Dr. Ann McKee
There’s a connection between what was found in the MRI and what Dr. Ann McKee sees in people who have CTE (studied and diagnosed after death). Key phrases to note for alignment include Frontal Lobe, Corpus Callosum and White Matter. In review, cross reference the "Conclusion" of the MRI above with the highlighted / underlined text below.
I have the history of repetitive and severe head trauma (which is the cause of the disease). My symptoms and their progression align. In addition, we continue to see doctors and do bloodwork, tests, scans, etc. All of which are ruling out issues / diseases that were in consideration.
Now there’s a connection between the results of my MRI and what leading CTE experts see in people who have the disease.
Further, this video explains how CTE causes tau proteins to accumulate and form abnormal clusters or aggregates. It’s thought that they can disrupt cellular communication and their presence is associated with the degeneration and death of neurons. Degeneration and loss of neurons is noted in the Conclusion of my MRI. There also may be a connection with the disruption of cellular communication and my struggles with speech and walking. See Case Study 4 for additional evidence.
Case Study 4 – Corpus Callosum: Broca & Motor Cortex
Case Study 3 shows my MRI Scan. Specifically, the damage and neuronal loss in the Corpus Callosum.
As noted in the screenshot below, this part of the brain interconnects with the Broca (responsible for speech) and Motor Cortex (responsible for movement).
Below are videos / notes that explain this in more depth.
2-Minute Neuroscience: Broca’s Area
Broca resides in left cerebral hemisphere.
Interconnected with the corpus callosum.
MRI / SPECT shows damage here.
Broca is responsible for speech production.
Negative impact on language communication.
Experiencing.
No impact on language comprehension.
Not experiencing.
16:17 describes Dysarthria.
17:36 describes Broca Aphasia.
Both align with my symptoms / scans.
2-Minute Neuroscience: Motor Cortex
Interconnected with the corpus callosum.
Motor Cortex is responsible for voluntary movement.
Experiencing.
The study referenced in Case Study 3 shows connection between the results of my MRI and what leading CTE experts see in people who have the disease. Now there’s evidence of the connection between the Corpus Callosum and Broca / Motor Cortex explaining why there are issues with my speech and walking.
Note: See Case Study 7 for additional evidence that align with these issues.
Case Study 5 – Activation Impairments: Dorsolateral Prefrontal Cortex
Completed SPECT Scan on June 15, 2023.
The Neuropathology of Chronic Traumatic Encephalopathy
Author: Dr. Ann McKee
There’s another connection between what was found in the SPECT Scan and what Dr. Ann McKee sees in people who have CTE (studied and diagnosed after death). Key term to note for alignment is Dorsolateral Prefrontal Cortex. Specifically regarding “activation impairments”. The doctor references this in our consultation video (16:59). In review, cross reference the image / notes of the SPECT Scan above with the highlighted / underlined text below.
So, all symptoms being experienced are associated with CTE (Case Study 1 and 2). There is also identical progression (Case Study 1). Now we have a second marker in a scan that shows connection to what leading CTE experts see in people who have the disease.
Next is Case Study 6. It features five more markers in scans / tests that show connection to the symptoms of CTE.
Case Study 6 – Behavioral / Mood Disorders: Conners Continuous Performance Test (CPT 3), SPECT Scan and Neurologics qEEG
The study referenced in Case Study 1 details the symptoms associated with CTE and how it progresses. One component of the symptoms is Behavioral / Mood Disorders.
I have met with several Psychiatrist over the years. Diagnoses include ADHD, Anxiety, Depression and Bipolar (Appendix A and B). I have also completed several tests / scans. All of which confirm these diagnoses. The three included in this Case Study 6 are Conners Continuous Performance Test (CPT 3), SPECT Scan and Neurologics qEEG.
Conners Continuous Performance Test (CPT 3)
The doctor notes that all results (nine out of nine) fell outside the normal range in our consultation video (2:40). Indicating a very high likelihood of attention disorder.
SPECT Scan – Basal Ganglia
Healthy brain shows Blue with a small amount of Red / White (in the Cerebellum). My scan is Red / White throughout. High inflammation. The Diamond Plus Pattern is also present. Indicating trauma and mood disorders. More detail is provided in the consultation video (20:45).
The doctor notes issues with the Basal Ganglia in our consultation video (24:13). He spoke to how increased activity in this area elevates anxiety, panic, restlessness, irritability, fear and tics.
Additional research notes that dysfunction of the basal ganglia can lead to a wide range of neurological conditions. This includes disorders of behavior control and movement along with cognitive deficits that are like those that result from damage to the prefrontal cortex.
All of which are experienced. All of which are associated with CTE.
SPECT Scan – Anterior Cingulate Gyrus (ACG)
The doctor notes issues with the Anterior Cingulate Gyrus (ACG) in our consultation video (25:34). He spoke to how increased activity in this area results in stuck thinking patterns of looping, worrying, obsessing, etc.
Additional research notes that ACG is the subject of many cognitive and neurocognitive studies. It has been associated with anxiety, depression and bipolar. The ACG also affects your ability to respond to certain stimuli. This could lead to aggressive behavior, shyness and decreases in emotional expression.
All of which are experienced. All of which are associated with CTE.
Note: The ACG is the frontal part of the cingulate cortex that resembles a "collar" surrounding the frontal part of the corpus callosum. The MRI (Section 2 – Case Study 3) shows damage in this area of the brain.
SPECT Scan – Thalamus
The doctor notes issues with the Thalamus in our consultation video (26:18). He spoke to this being the mood center of the brain. When it heats up the most common association is depression.
Additional research notes that the Thalamus primary function is to direct motor and sensory signals to the cerebral cortex. Symptoms that may be associated with damage to the thalamus include amnesia, aphasia, difficulties with attention, impaired movement, impaired posture, chronic pain, sleepiness, loss of alertness / activation, impaired processing of sensory information and apathy.
Most of which are experienced. Most of which are associated with CTE.
Neurologics qEEG
Neurologics provides qEEG testing and a Neuroengineering® Program to support those with Concussion and Brain Injury.
A summary of the results is shown above.
What’s important to note in this scan / test is that scores of 90 or higher are required for proper function. My results show five out of six scores being significantly below the 90-level mark.
Similar to the MRI, CPT3 and SPECT Scan, this qEEG identifies symptoms associated with repetitive and severe head trauma. All of which align with CTE.
Case Study 7 – CTE: Age & Stage
One Neurologist said I was too young for CTE. This is incorrect.
Studies show people in their twenties and thirties who have the disease.
This video provides a brief overview of the study. Note the primary symptom highlighted at 3:24… "Advanced signs, speech difficulty, difficulty talking, those types of things, it's really too late by the time that happens..."
Here's another video that speaks to a couple athletes in the study who committed suicide.
As noted, speech is a sign of advanced CTE. This study provides a brief breakdown of the 4 Stages in CTE. Stage 3 and 4 are highlighted below.
Stage 3 indicates a reduction in brain weight with mild cerebral atrophy, ventricular dilation, septal abnormalities, depigmentation of the locus coeruleus and substantia nigra, thinning of the corpus callosum, and atrophy of the mammillary bodies, thalamus, and hypothalamus. Finally, stage 4 is characterized by significant reduction in brain weight due to widespread cerebral cortical atrophy of the medial temporal lobe, thalamus, hypothalamus, and mammillary bodies. Complete depigmentation of the locus coeruleus and substantia nigra is evident along with the marked axonal loss of subcortical white matter.
Key phrases to note are "thinning of the corpus callosum" and "axonal loss of subcortical white matter." Both of which were noted in my MRI (Case Study 3). Both of which were also referenced in The Neuropathology of Chronic Traumatic Encephalopathy study where it showed those with CTE having the same issues.
When hearing the doctor say I was too young for CTE, I came to the realization that most Neurologists and medical professionals may not have the knowledge / experience to effectively assess then make a potential diagnosis. Therefore, I’ve taken the initiative to research and find answers myself.
Note: The first study mentioned (in this Case Study) aligns with the issues presented in Case Study 4. Specifically, the neuropathologic abnormalities associated with CTE, Ventricular Enlargement and Cavum Septum Pellucidum. Ventricular Enlargement is associated with slow gait. Cavum Septum Pellucidum is bounded anteriorly by the genu of the Corpus Callosum (Case Study 3). There also may be connection to the Perivascular Pigment–Laden Macrophages seen in the frontal white matter being significantly greater in those who had CTE and the abnormal single voxel MR spectroscopy in the left frontal white lobe matter that was seen in my MRI.
CONCLUSION
Official diagnosis of CTE can only be made through post‐mortem neuropathological examination.
This appears to be one reason why neurologists aren’t able to effectively assess it. There’s also no cure. It’s a progressive disease. The symptoms get more severe with time.
Of all the potential diagnoses that would provide clarity on the health situation, CTE has always aligned most. Further, all tests, scans, spinals, bloodwork, assessments, etc. that have been completed (exceptions being MRI / DTI, Amen and Neurologics) indicate that I’m healthy. In other words, all other issues / diseases have been ruled out.
Meanwhile, Doctors continue to be confused. They can’t provide answers.
What also must be taken into consideration is all the work put into Concussion / TBI Therapies throughout my twenties and thirties. As mentioned, these efforts have helped manage the symptoms. However, with time, symptoms are increasing in severity. They’re getting more problematic. More challenging to manage.
Considering their progression and severity along with the efforts given to improve, Chronic Traumatic Encephalopathy (a degenerative disease), needs to start being considered as a potential / probable cause.
I mentioned this during a video consultation with the doctor (42:36) on July 13, 2023. Since that time, every scan, test, bloodwork panel, etc. requested by doctors has been completed. All of which, has ruled out every issue / disease doctors said could be causing the symptoms.
There’s one exception though. CTE. This report provides the evidence….
History of repetitive and severe head trauma (cause of the disease).
Symptoms and their progression align.
Markers in scans and tests align with those who had the disease.
All other issues / diseases have been ruled out.
All of which lead to a potential / probable diagnosis of CTE.