Could Ketamine Accelerate Concussion Recovery? Insights from an N=1 Case Study
A calculated risk involves making a decision to engage in a potentially uncertain or dangerous action after carefully weighing the benefits and drawbacks. It’s about assessing the likelihood of success and considering possible consequences—turning what could be a reckless gamble into a strategic choice.
I’ve been using ketamine as part of my journey to manage Persistent Post-Concussive Symptoms (PPCS) after multiple Traumatic Brain Injuries (TBIs). Five years ago, I lost my vision, hearing, ability to walk, and sense of normalcy. It’s no secret I credit microdosing psilocybin for learning to walk again after being told by multiple doctors that I wouldn’t recover. I later starting thinking, what about using psychedelic medicine as an acute intervention? After years of working with ketamine both personally and professionally, I hypothesized it was particularly promising for this purpose, despite the potential risks. Unfortunately, I got an opportunity to test that hypothesis.
I braced for the usual drawn-out decline—the coming weeks and months of pounding headaches, dizziness, and nausea. But within just 24 hours, those symptoms had almost completely faded. Instead of the slow decline I had anticipated, I felt noticeably normal. It made me wonder: Could ketamine play a more significant role in concussion recovery?
Below, I’ll share why I chose to try ketamine, the science behind its potential benefits for brain injury recovery, the risks I considered, and the possibility of future clinical trials. Please note, this is an N=1 experiment—just one person’s experience. If you’re considering a similar approach, I strongly encourage you to consult with a healthcare professional first.
Understanding Traumatic Brain Injuries
Traumatic Brain Injuries (TBIs) set off a cascade of biochemical, cellular, and metabolic processes that can linger long after the initial injury. These processes often result in debilitating symptoms, including cognitive impairment, headaches, fatigue, and emotional dysregulation—collectively known as Persistent Post-Concussive Symptoms (PPCS). Below are some of the primary mechanisms at play:
Neuroinflammation: After a concussion, microglial activation and the release of pro-inflammatory cytokines (e.g., interleukin-1β, TNF-α, interleukin-6) create widespread inflammation in the brain. This inflammation disrupts neuronal signaling, creating a toxic environment that hinders recovery.
Excitotoxicity: Excessive glutamate release during the injury overstimulates NMDA receptors, leading to calcium influx and neuronal damage. This excitotoxicity contributes to cell death and long-term cognitive and emotional challenges.
HPA Axis Dysregulation: Concussions can interfere with the hypothalamic-pituitary-adrenal (HPA) axis, which regulates the body’s stress response. Chronic dysregulation leads to imbalances in stress hormones, contributing to fatigue, emotional instability, and becoming one of the primary drivers of prolonged recovery.
Metabolic Crisis: Brain injuries often induce a metabolic mismatch, where the brain’s energy demands exceed its ability to supply glucose and oxygen, impairing its capacity to function optimally. This "metabolic crisis" not only contributes to cognitive dysfunction, such as difficulty with memory and concentration, but also exacerbates inflammation and neuronal damage, further delaying the recovery process.
Autonomic Nervous System (ANS) Dysfunction: After a brain injury, disruptions in ANS regulation can occur, leading to symptoms like dizziness, light sensitivity, and difficulty controlling heart rate and blood pressure. These dysfunctions are problematic because they interfere with the body’s ability to maintain homeostasis, making recovery more challenging and increasing vulnerability to further stress.
Gut-Brain Axis Disruption: Emerging research shows that TBIs impact the gut-brain axis, with increased intestinal permeability ("leaky gut") and microbiome imbalances exacerbating neurological outcomes. This disruption can contribute to inflammation and impair brain function, potentially prolonging symptoms and hindering recovery.
Ketamine and Its Role in Brain Health
Originally developed in the 1960s for anesthesia and pain management, ketamine has gained attention in recent decades for its neuroprotective and antidepressant effects. Ketamine has been used to treat mood disorders like depression, anxiety, PTSD, and chronic pain, but its potential in brain injury recovery is just beginning to be explored.
Ketamine influences key brain functions, especially the glutamatergic system, which is involved in learning, memory, and synaptic plasticity. One of its primary mechanisms is blocking NMDA receptors, which helps mitigate excitotoxicity—an important factor in conditions like TBI.
Ketamine also promotes neuroplasticity by stimulating the release of brain-derived neurotrophic factor (BDNF), a protein essential for the growth, repair, and strengthening of neural connections. These effects are particularly relevant in brain injury recovery, where supporting neural regeneration is crucial.
Additionally, ketamine has anti-inflammatory properties, reducing pro-inflammatory cytokines and microglial activation. This helps create a neuroprotective environment conducive to healing, both immediately after an injury and long-term.
Why Use Ketamine as an Intervention in the Acute Stage of a Brain Injury
Given its neuroprotective and anti-inflammatory properties, ketamine could offer significant benefits when administered in the acute phase of a brain injury. The primary aim in the initial hours after a TBI is to reduce inflammation, prevent excitotoxicity, and promote neural repair—all of which ketamine appears to support. Here's how ketamine could help address the six markers of PPCS mentioned above:
Neuroinflammation: Ketamine has been shown to reduce the activation of microglial cells and decrease the release of pro-inflammatory cytokines. By decreasing neuroinflammation, ketamine can help create a more favorable environment for brain recovery and healing after a concussion.
Excitotoxicity: Ketamine’s ability to block NMDA receptors plays a key role in preventing excitotoxicity, which is a critical factor in brain injuries. By mitigating excessive glutamate release, ketamine protects neurons from the toxic effects of overstimulation and helps preserve brain function.
HPA Axis Dysregulation: The anti-inflammatory properties of ketamine extend to the regulation of the HPA axis, which is crucial for managing the body’s stress response. By reducing inflammation and normalizing stress hormones, ketamine may help restore balance to the HPA axis, alleviating symptoms like fatigue and emotional instability.
Metabolic Crisis: Ketamine has been shown to support mitochondrial function, which is key in maintaining energy balance in the brain. By improving energy metabolism, ketamine may assist in alleviating the metabolic crisis often seen after a TBI, helping the brain restore its necessary energy stores more effectively.
Autonomic Nervous System Dysfunction: Ketamine’s effects on the brain’s excitatory and inhibitory systems may also extend to regulating the ANS. This can be particularly beneficial for individuals with TBI-induced dysregulation in heart rate, blood pressure, and other autonomic functions. Ketamine’s neuroplasticity effects could help recalibrate the ANS, contributing to more stable physiological states.
Gut-Brain Axis Disruption: Emerging evidence suggests that ketamine’s neuroprotective and anti-inflammatory properties could extend to the gut-brain axis, helping to restore balance in the gut microbiome and alleviate issues like intestinal permeability ("leaky gut"). This restoration could improve overall brain health and support a more holistic recovery process.
During this vulnerable stage, the brain is working hard to restore balance and begin the repair process. Ketamine’s ability to block excitotoxicity, reduce neuroinflammation, and stimulate neuroplasticity could potentially accelerate recovery by supporting these natural healing mechanisms.
Ketamine’s effects on brain-derived neurotrophic factor (BDNF) are particularly promising. By promoting BDNF release, ketamine could aid in the strengthening and formation of new neural connections, helping to rebuild areas of the brain that were damaged during the injury.
The Risks: This Was a Controversial Choice
Using ketamine during the acute phase of a concussion is not without its risks. Historically, concerns about ketamine’s potential to increase intracranial pressure (ICP) have raised questions about its safety in brain-injured individuals. Early studies suggested that ketamine could elevate ICP, which could potentially worsen outcomes. However, more recent research shows that ketamine does not significantly raise ICP and may even lower it in some cases.
Still, the use of ketamine during the acute phase of a concussion remains largely unstudied, and there are several potential risks to consider:
Unknown Effects on Early Brain Repair: After a concussion, the brain is in a vulnerable state, with energy levels depleted. Introducing ketamine during this phase could interfere with natural repair mechanisms, particularly those related to synaptic remodeling and inflammation resolution.
Changes in Cerebral Blood Flow: Ketamine alters cerebral blood flow, which could have unpredictable effects on a concussed brain. Some studies suggest that ketamine may improve cerebral perfusion, but others indicate it could cause vasodilation, potentially worsening symptoms like brain fog and headaches in sensitive individuals.
Disruption of the Brain’s Excitatory-Inhibitory Balance: While ketamine blocks excitotoxicity, it also affects neurotransmission in complex ways. Administering ketamine too soon could disrupt the brain’s natural attempt to restore equilibrium after the injury. Ketamine’s impact on GABAergic inhibition may also interfere with sleep architecture, which is vital for recovery.
Symptom Masking vs. True Recovery: There’s also the concern that ketamine’s dissociative effects might mask concussion symptoms rather than promote true healing. If ketamine quickly relieves symptoms, it could potentially delay recovery by preventing necessary rest and the body’s own healing processes.
My Results: Showing Potential for Clinical Trials
Based on this N=1 experiment and the general lack of effective care for TBI sufferers, I believe that ketamine could play a significant role in early concussion treatment. The standard advice—rest—often feels not only incomplete but potentially damaging. After taking a small oral dose within hours of my injury, I experienced a noticeable reduction in common symptoms like headache, dizziness, and nausea, which typically persist for weeks. In the following weeks, I did not experience the typical decline I had come to expect from previous concussions. This unexpected result has led me to wonder: could ketamine be a breakthrough in concussion recovery?
While some research on ketamine’s neuroprotective properties exists, there’s a lack of large-scale clinical trials investigating its use in the acute phase of concussion recovery. Given ketamine’s unique pharmacological profile and the rapid improvement—or more notably, the absence of decline—I experienced, this could be an important area for future research.
If safe dosages and timing protocols can be established, ketamine may offer a promising tool in preventing persistent post-concussive symptoms and accelerating recovery from brain injuries.
Final Thoughts
This experiment may raise more questions than answers—such as how ketamine interacts with other brain healing mechanisms and what the long-term effects might be. Nonetheless, it has opened my eyes to the potential of ketamine as a tool for brain injury recovery. As research into ketamine’s neuroprotective effects continues to evolve, I hope to see more studies exploring its role in TBI treatment. In the meantime, I’ll continue to document my experiences and share what I learn.