Traumatic Brain Injury and Visual Processing: Exploring the Connection through a Case Study

Around the world it is increasingly being recognized and understood that traumatic brain injuries create an interplay of symptoms including neurological, psychiatric and most recently understood, cardio-vascular disease.  Traumatic brain injuries induce alterations in neurobiological processing increasing the risk for chronic dysfunction of the immune system, autonomic nervous system, systemic inflammation and disruptions in the brain-gut connection.  Along with this recognition and understanding is the emerging conception that injuries to the brain create chronic conditions, rather than being limited to the acute aftermath of the injury.  And that there are additional risk factors from brain injuries including Complex-PTSD, an increase in depression and anxiety and more serious psychiatric problems including schizophrenia and manic/depression (bipolar I & II).   In turn these factors elevate the risk for cardio-vascular disease and cognitive decline and present additional risk factors for diabetes, hypertension, hyperlipidemia, dementia and sleep disturbances [1,2].

This increasing awareness notes that traumatic brain injuries involve multiple mechanisms at play creating a wide range of symptoms are very complex.  In addition, it is important to every brain injury is also a person with their unique blend of developmental history, values, opinions, struggles and goals.  All of this represents a unique challenge to medicine.  To which I would add that a key piece of the above understanding has often been left out.  Injuries to the brain also involve, because 40-50% of the brain in taken up with this factor, damage to visual processing.

What is visual processing all about?

This is the process of converting light energy into the meaningful images that we see day in and day out. It involves several steps, facilitated by numerous brain structures and higher-level cognitive processing.    Visual inputs begin in the retina, the optic nerve and the thalamus.  These inputs then travel from the thalamus to the visual cortex, the occipital lobe, in the rear of the brain.  There the visual cortex combines the elementary building blocks of vision (such as contrast, color and movement) to produce our complete visual perception.  This process appears to be very straight forward, but in reality it is very complex and easily damaged by injuries to the brain.  Moreover, this damage can occur through a traumatic brain injury, a stroke, hemorrhage, seizures, infections, illness and disease [3]. What is missing from much of our current understanding is that traumatic brain injuries, caused by blows to the head, severely affect an individual’s vision damaging those parts of the brain involved in visual processing and perception.  These injuries do so by disrupting and interfering with the flow and processing of visual information in the brain.  Specially, brain injuries slow the acquisition and processing of visual information and impair the formation of visual memory [4].

• Further, brain injuries can cause dysfunctions in visual processing that affect
• Binocularity (binocular vision or eye teaming) describes the way in which our 2 eyes work together to integrate images seen by each eye into one image).
• Spatial Orientation.
• Posture and Balance. 
• Neurological Events (dizziness, headaches, loss of coordination and an inability to focus and/or concentrate).

What is often not recognized with injuries to the brain (and I would include here strokes, seizures, infections, illness and diseases) is that these injuries interrupt the functioning of the neurological systems that innervate extraocular muscles controlling eye movements and system that regulate focusing (clear or blurry eyes for example).

Further, many aspects of our medical system are not recognizing Post Trauma Vision Syndrome which includes problems with:

• Exotropia (eyes turned outward)
• Exophoria (the tendency for the eyes to turn out)
• Convergence Insufficiency
• Accommodative Insufficiency

Additional symptoms from trauma to the brain include:

• Double Vision
• Blurred Vision
• Perceived Movement of Print
• Asthenopia (eye strain and fatigue)
• Headaches
• Photophobia (sensitivity to light) [5]. 

The key problems here is that the injured brain is unable to adequately process visual information leading to a host of problems with daily living.  In addition, that it is important to recognize that all blows to the head, concussions and post-concussion syndrome issues warrant serious attention to the effects on the individual’s visual system. And I will go a step further by suggesting that all injuries to the brain/mind including strokes, seizures, infections, illnesses and diseases create some disturbances in visual processing. JM was referred for treatment of his anxiety co-occurring with his neuro-optometry treatment. In exploring his history, he related that he was struck by a car at around age 10 while out riding his bicycle. He was taken to the ER but nothing conclusive was found (at that time?). And he had experienced a number of small concussions as a result of his motorcycle racing hobby. Third, he related that he had been diagnosed with lazy eye syndrome (left eye) from an early age. In my experience, increases in anxiety and depression follow all injuries to the brain, because at an unconscious level the brain/mind knows that it is not functioning normally. Depression because there is a huge loss of the person’s ability to function normally in daily activities. And increases with anxiety because the brain/mind is aware that it is not able to cope with everyday reality and that reality is a big threat to them. So, the need for this referral is understandable and is needed in all cases of trauma to the brain.

I want to provide a wider context here for understanding traumatic brain injuries and their effect on visual processing as it relates to JM’s case.  I note, again, that visual processing, which is involved in using 40-50% of brain structure and functioning, is too often left out of our understanding of the impact of injuries to the brain/mind.  Traumatic Brain Injuries occur when physical forces (sports, car crashes, falls and other blows to the head) impact the head with sufficient intensity to cause damage to the brain/mind.  I use the term brain/mind here because the human mind is the subjective experience of the brain and therefore every injury to the brain (including strokes, seizures, infections, illnesses and diseases) affects every aspect of a person.  A traumatic brain injury is often understood as either mild, moderate, or severe.  However, in my experience, all blows to the head have long-term consequences and resting the brain/mind for several weeks and taking it easy for a month (standard protocol) does not begin to address what is happening in the brain.  Trauma to the brain creates a neurodegenerative disease that I have described elsewhere as 4 Interlocking Architectures [6]. This neurodegenerative disease process includes visual processing difficulties, cognitive decline, headaches, chronic fatigue, chronic pain, problems with memory, focus, concentration and sleep disturbances.  In the majority of cases that have come through my office, however, the connection between trauma to the brain/mind and their present symptoms is missing.  Granted, brain injuries are subtle and difficult to diagnose, but I see this pattern of lack of recognition and connection nearly every week in my practice.  It is a startling recognition. 

A recent article in Science Translational Medicine [7] suggested that 90% of traumatic brain injury cases go undiagnosed, increasing the risk of: 

• Neurological disorders
• Dementia
• Depression
• Parkinson ’s disease
• Damage to the individual’s Visual Processing System 

Further, there appears to be little recognition of the destructive processes resulting from trauma to the brain/mind occurring at the cellular and molecular levels that lead to inflammation, oxidative stress, calcium dysregulation, apoptosis (programed cell death), vascular damage, ischemia and loss of the blood-barrier integrity (compromised) that all contribute to the destruction of brain tissue [2]. Increasingly, research in neuroscience is pointing to the long-lasting effects of these processes on cognition, balance, pain, social and emotional experiences, sleep and vision.  This is indeed a wide range of symptoms all caused by trauma to the brain/mind. 

Overall, visual processing involves the brain’s ability to use and interpret visual information from the world around the person.   It does this by converting light into meaningful images.  And re-constructing a 3-dimensinal world from a 2-dimentinal projection of that world.  As stated above, 40-50% of our brain capacity is involved in one form or another with visual processing.  As an example of the importance of vision in our daily lives, learning in our schools is typically directed to visual processing approximately 75% of the time.  

Given this wider context and background regarding the long-term effects of damage to the brain/mind and its effects on visual processing, what was happening to JM when he entered neuro-optometry and neuro-psychoanalytic treatment?  First, let’s look at that part of the nervous system (CNS) that allows organisms to see: the eye to the brain Figure 1.  

• The Optic Nerve
• The Optic Chiasm
• The Optic Tract
• LGN (lateral geniculate nucleus)
• Optic Radiation
• The Visual Cortex
• The Visual Association Cortex

Figure 1: The Neurodegenerative Course of a Traumatic Brain Injury. 

Second, where exactly is the damage (and what kind of damage) that JM incurred as a result of a series of concussions and sub-concussive blows to the head?  For many years, beginning in childhood JM was told that he had a wandering left eye, but that nothing could really be done about this.  By the time he began neuro-optometry treatment it was clear that he was struggling with double vision and convergence insufficiency.  This made it impossible for him to drive his car anywhere (especially on the freeway because his damaged visual system couldn’t track motion very well). Nor could he negotiate walking the isles of a place like Home Depot because the visual stimulation of being there was overwhelming to his visual system. Overall, JM presented in his original neuro-optometry treatment with misregistering with his vision, double vision, difficulties processing what he was seeing while in motion (driving a car) and increasing anxiety (for which he was referred for treatment of). In the beginning, JM’s neuro-optometry treatment was working well for him, he was able to get back in his car on a limited basis and able to better tolerate walking the isles at Home Depot, until he suffered a visual breakdown and all his progress was lost for the moment.  After all JM’s progress it was difficult to understand why the breakdown? I have an explanation which involves how neuro-optometry and neuro-psychoanalysis need to work together in the treatment of these kinds of injuries. 

JM’s initial progress failed because he didn’t have enough Energy within his nerve cells to support his increased progress. In addition, patients who are struggling with an injury to the brain (including strokes, seizures, infections, illnesses and diseases and PTSD are always experiencing an increase in anxiety, because at an unconscious level the brain/mind recognizes that it is injured and not functioning in the interest of its survival (the brain’s main function).  Both anxiety and depression are huge energy drains on the brain. The combination of limited Energy in the brain to support the new visual processing gains and a drain on the brain’s Energy from anxiety and depression caused his back sliding. 

JM’s symptoms are typical following a traumatic brain injury (motorcycle accident) including visual fatigue, mental fatigue and low physical Energy in general. This constantly interfered with his daily activities. General mental fatigue occurs following a brain injury because the brain/mind is not functioning efficiently and must expend additional Energy to perform those activities that previously did not deplete his Energy reserves. A damaged brain/mind becomes easily overloaded at a very low threshold and is very slow to recover (especially without treatment). For example, when memory tasks are involved, the traumatized brain exhibits increased activity progressively over time in the bilateral dorsolateral prefrontal cortex and the inferior parietal brain regions as a compensatory mechanism to meet the demands on it. This then results in the chronic fatigue so common with brain injured patients. Looking further, trauma induced changes in regional cerebral blood flow also help us understand the fatigue issues these patients struggle with daily [8]. 

Here is a further note that helps us understand the results of chronic fatigue in the brain following brain trauma. A study by Ramage et. al. [8] demonstrated a pattern of functional connectivity that reflected communication between different regions of the brain. The study was looking at the differences between control subjects and mTBI subjects performing behavioral tasks. And showed the heightened connectivity of all the networks in the brain for the TBI subjects. The authors reflected that it was inefficiency of the activity in the neural networks that accounted for the increased fatigue patients in the study were experiencing. In other words, the brain was working overtime to compensate for damage to the neural networks, but never doing its work successfully. In the meantime, JM was moving forward with his neuro-optometry appointments and beginning to make progress again. His visual processing was again improving. However, while his progress was slow, gradual and improving, there still appeared to be a gap in his moving forward. This is where his healing can move forward faster and more efficiently by addressing the production of energy within the mitochondria of the nerve cells. In reviewing the literature and research on TBI problems there is little mention of the damage to visual processing in the brain outside of the field of neuro-optometry.  And not a lot of information regarding damage to the mitochondria, the energy factories, in nerve cells that accounts for the chronic fatigue most TBI patients experience [9]. 

It was my hypothesis that for JM to fully recover from his visual processing issues, his brain needed to be able to support his vision. And his anxiety/depression issues also needed to be addressed so he could move forward with his recovery. How could this be accomplished?

Current research is pointing out that the major cause of traumatic brain injury damage is the secondary injury damage caused by damage to the mitochondrial portion of a nerve cell (the little energy factories inside the cell). In turn, damage to the mitochondria in the nerve cells leads to impaired brain/mind functioning. These impairments include increases in reactive oxygen species production (ROS), a decrease in bioenergetics and apoptosis (programed cell death). And these brain cellular alterations impair neurological functioning across the entire spectrum of the brain [10]. The mitochondria in nerve cells are essential to the functioning of the cells. They serve to sustain energy, redox homeostasis and are also harbingers of cell death.  A dysregulated mitochondrial network can cascade through the brain until these cells lose their ability to function and become irreparably doomed cells.  And recent research is telling us that abnormal mitochondrial functioning can occur very early after a TBI has occurred [11]. Mitochondria are fundamental for metabolic homeostasis in all multicellular eukaryotes. In the nervous system, mitochondrial generated ATP (adenosine triphosphate) is required to establish the appropriate electrochemical gradients and reliable synaptic transmissions. Several mitochondrial defects have already been identified in central nervous system disorders. Cell membrane leakage and electrolyte imbalances, pro-apoptotic pathway activation and mitophagy are among the mechanisms implicated in the pathogenesis of neurodegenerative diseases including Alzheimer’s Disease, Parkinson’s Disease, Huntington’s Disease and Ischemic Stroke. (Interestingly, Ischemic Stroke is one of the leading causes of morbidity and is the second leading cause of death worldwide.) [12]. When I address Architecture #2 in my model of the neurodegenerative disease process that always follows trauma to the brain, these are the kinds of details that occur within this architecture. [6]).

JM’s healing treatment through neuro-optometry was once again back on track and working well. But this was not the complete treatment that was needed. If his brain does not yet have its full Energy capacity (or almost full), then his healing will take much longer, or perhaps not occur at all. It is necessary that JM’s brain/mind be healed enough to support his visual processing. And a major piece of healing from brain injuries entails the repair of damage to the mitochondria of his nerve cells so that his brain/mind has the Energy to move forward. Over the past 8 years that I have been working with TBI patients, I have developed a protocol for their treatment. Each each of the 5 Protocols are unique for each individual patient and involves 5 lines/structures of treatment. 

1. The use of supplements for the brain (rather than drugs). With JM’s case Niacinamide Plus and other individualized brain supplements helped to restore the functioning of his mitochondria in the nerve cells. 
2. Stimulants for the Brain (I prefer soft, healing music with noise cancelling headphones several times a day). 
3. Total immersion in the healing process with a daily schedule/structure that is followed as much as possible. 
4. The use of “flow experiences,” which reduce demands on the brain and allow for further healing. 
5. Neuro-Psychoanalytic sessions 1-3 times per week to process the work on the injury. 

Finally, I note that there is an increasing realization and understanding that traumatic brain injuries are associated with long term risk factors for cardiometabolic, neurological and psychiatric comorbidities [13]. To these comorbidities I would add problems with visual processing as outlined above. In my experience, because of the pervasive nature of structures in the brain that support vision, all trauma to the head effects visual processing on some level. And I also note the study that concluded that: “Comorbidities after TBI were associated with higher mortality. These findings suggest a need for proactive screening of chronic systemic diseases after brain injury of any severity [13]’’.

1. Yasgur BS (2024) Traumatic Brain Injury and CVD: What’s The Link in Medscape, Monday, April, 8th, 2024.
2. Rauchman SH, Zubair A, Zubair A, Rauchman D, Pinkhasov A, et al. (2023) Traumatic Brain Injury: Mechanisms, Manifestation, and Visual Sequelae. Front Neurosci 17: 1090672.
3. Vision Problems and Traumatic Brain Injury in MSKTC (Model Systems Knowledge Translation Center), msktc.org/tbi/factsheets/vision-problems-and-traumatic-brain-injury.
4. Sen N (2017) An Insight into The Vision Impairment Following a Traumatic Brain Injury. Neurochem Int 111: 103-107.
5. Richman EA (2024) Traumatic Brain Injury: What Every Ophthalmologist Should Know”. Richman in Eye Net Magazine.
6. Reynolds LJ (2023) The Complex Architecture and Healing of Traumatic Brain Injuries: Listening To The Brain. Cambridge Scholars Publishing.
7. Lindsay Brownell (2024) Shining a Light on The Hidden Damage of Mild Brain Injuries” in Science Translational Medicine.
8. Fischer TD, Hylin MJ, Zhao J, Moore AN, Waxham MN, et al. (2016) Altered Mitochondrial Dynamics and TBI Pathophysiology”. Front Neurol 10: 1-11.
9. Ramage AE, Tate FD, New AB, Lewis JD, Robin DA (2019) Effort and Fatigue-Related Functional Connectivity in Mild Traumatic Brain Injury.” Front Neurol 9: 1165.
10. Hiebert JB, Shen Q, Thimmesch AR, Pierce JD (2015) TBI and Mitochondrial Dysfunction. Am J Med 350: 132-138.
11. Robertson CL, Saraswati M, Fiskum G (2007) Mitochondrial Dysfunction Early After Traumatic Brain Injury in Immature Rats. Neuro Chem 101: 1248-1257.  
12. Norat P, Soldozy S, Sokolowski JD, Gorick CM, Kumar JS, et al. (2020) Mitochondrial Dysfunction in Neurological Disorders: Exploring Mitochondrial Transplantation. NPJ Regen Med 5: 22.
13. Izzy S, Chen PM, Tahir Z, Grashow R, Radmanesh F, et al. (2022) Association of Traumatic Brain Injury With the Risk of Developing Chronic Cardiovascular, Endocrine, Neurological and Psychiatric Disorders. JAMA Netw Open 5: e229478.