This case series (n=3) describes three people with persistent symptoms after traumatic brain injury or hypoxic brain injury who took a 6-week iboga microdosing protocol alongside psychotherapy and supportive care. All three reported marked improvement, and two said their symptoms had fully resolved at long-term follow-up, but the authors do not claim the treatment caused these changes.
Background
Traumatic brain injury (TBI) can result in prolonged post-concussive syndrome and chronic hypoxic-ischemic brain injury (HIBI) sequelae remains therapeutically challenging with the persistence of significant neurological and cognitive impairments. While conventional treatments often provide limited relief, emerging research explores alternative therapeutic interventions, including psychedelic compounds combined with therapeutic interventions.
Objectives
This naturalistic case series examines clinical observations following an integrative, participant-directed iboga-containing microdosing protocol paired with Accelerated Experiential Dynamic Psychotherapy (AEDP) in three individuals with persistent neurologic symptoms after traumatic brain injury (TBI) or hypoxic-ischemic brain injury.
Methods
Three participants completed a 6 week protocol using Tabernanthe iboga root bark biomass (participant-directed titration 0.1–1.0 g/day, 4 days-on/3 days-off). Quantitative qNMR/HPLC analysis (University of Cape Town) demonstrated approximately 3.845% ibogaine content by mass, yielding estimated ibogaine-equivalent exposure of 3.8–38.5 mg/day. All administration utilized whole root bark biomass only. Weekly AEDP psychotherapy and supportive nutraceuticals were provided concurrently.
Patient one
A 43 year-old man with TBI sustained in a motorcycle accident. Patient Two: A 40-year-old woman with chronic hypoxic brain injury sustained during an avalanche burial event. Patient Three: A 19 year old woman with TBI sustained in a motor vehicle accident.
Results
All three patients demonstrated progressive neurological recovery over the 6-week microdosing iboga protocol with two of the patients declaring complete symptom remission at a long term follow up assessment. Initial reported symptoms included a constellation of daily headaches, episodic migraines, disequilibrium, irritability, mood swings, fatigue, brain fog, sleep disruptions, and loss of interest in typical life activities. At the conclusion of the protocol, and at long term follow-up visits, patients felt able to discontinue all prescription medications for symptomatic treatment, reporting absence of severe migraine headaches, resolution of brain fog, fatigue, irritability, and stabilized mood, with the ability to return all regular activities with a renewed enthusiasm for life. All patients provided consent to share their significant clinical and therapeutic improvement journey in this publication.
Safety considerations
The microdosing protocol was carefully implemented with rigorous screening to mitigate potential cardiac and neurological risks associated with iboga administration, including medical background screening for potential drug interactions, and past medical history contraindications including heart conditions and/or the concomitant administration of selective serotonin reuptake inhibitors (SSRIs).
Conclusion
This naturalistic case series provides hypothesis-generating observations regarding possible clinical improvement following an integrative iboga-containing intervention paired with psychotherapeutic and supportive care. The findings do not establish causality or iboga-specific efficacy and should be interpreted within the context of multimodal therapeutic exposure and substantial methodological limitations. These preliminary observations suggest that an integrative iboga microdosing protocol, in association with psychotherapeutic and supportive care, may be linked to meaningful improvements in prolonged post-concussive symptoms. As a hypothesis-generating case series, these findings warrant further investigation in controlled trials to establish causality and specificity.
Papers cited by this study that are also in Blossom
Antonio, T., Childers, S. R., Rothman, R. B. et al. · PLOS ONE (2013)
Blest-Hopley, G., Pasculli, G., Ruffell, S. G. D. et al. · Frontiers in Psychiatry (2025)
Brown, T. K., Alper, K. · The American Journal of Drug and Alcohol Abuse (2017)
Cameron, L. P., Tombari, R. J., Lu, J. et al. · Nature (2020)
Traumatic brain injury and chronic hypoxic-ischaemic brain injury can leave people with persistent headaches, fatigue, cognitive problems, sleep disturbance, mood changes, and reduced function, yet standard treatments often provide only limited relief. The paper situates iboga and ibogaine within a growing interest in psychedelic-assisted approaches, but notes that the use of whole-plant iboga in sub-perceptual microdoses, particularly for post-concussive or hypoxic brain injury syndromes, had not been explored in western clinical settings. Tabaac and colleagues set out to describe clinical observations from a naturalistic case series of three people with prolonged neurological symptoms after traumatic brain injury or hypoxic-ischemic brain injury who completed an integrative iboga microdosing protocol alongside psychotherapy. The paper aims to report symptom changes over the course of treatment and follow-up, while presenting the intervention as an exploratory, clinically supervised approach rather than a controlled efficacy study.
This is a naturalistic case series of three participants with persistent post-concussive symptoms or post-hypoxic brain injury symptoms. Participants were self-referred or referred through clinicians, community networks, or peer recommendations, and were recruited passively. Eligibility required documented mild to moderate traumatic brain injury or post-hypoxic brain injury, symptoms persisting for at least 3 months despite conventional care, age 18 years or older, capacity to consent, and medical stability for outpatient integrative care. Exclusion criteria included active psychosis or severe untreated psychiatric illness, current substance dependence other than nicotine, contraindicating medications such as QT-prolonging drugs, severe cardiac disease, pregnancy, and inability to engage in psychotherapy. Before treatment, the researchers performed screening covering medical, psychiatric, substance use, and cardiac risk factors. This included review of personal and family history relevant to arrhythmia risk, baseline vital signs, medication review, and 12-lead ECG when clinically indicated. Participants were managed in the United States, in Nevada, and all therapy sessions were conducted in English. The paper states that the case series was based on de-identified clinical observations, with written informed consent for publication; formal IRB review was not required under institutional policy because no intervention was assigned prospectively by the investigators. The intervention used whole Tabernanthe iboga root bark biomass rather than synthetic ibogaine hydrochloride. Dosing was participant-directed, using approximately 0.1-1.0 g/day on a 4 days-on, 3 days-off schedule over 6 weeks. Third-party qNMR/HPLC analysis indicated approximately 3.845% ibogaine content by mass, corresponding to an estimated ibogaine-equivalent exposure of about 3.8-38.5 mg/day. Participants also received weekly virtual psychotherapy based on Accelerated Experiential Dynamic Psychotherapy (AEDP), together with supportive nutraceuticals and monitoring. Outcomes were assessed clinically over the treatment period and at follow-up visits. The paper also describes a narrative review of earlier literature, based on database searches through December 2025, but this appears to have been used to contextualise the case series rather than as a formal systematic review.
All three participants were reported to improve during or after the iboga-containing protocol, although the pattern and durability of improvement differed across cases. The authors describe progressive neurological recovery in each person over the 6-week treatment period, with two participants later stating that their symptoms had fully remitted at long-term follow-up. In patient one, a 43-year-old man with post-concussive symptoms after a motorcycle accident, headaches, fatigue, mood lability, sleep disruption, and emotional distress gradually improved across the therapy sessions. By the end of the protocol, headaches had become much less frequent, anger outbursts had resolved, energy had improved, and he reported returning to activities such as hiking and spending time with his son. At later follow-up, he described headaches as very rare, had self-discontinued prescribed medications, and reported that sleep had normalised and emotional resilience had improved. The authors summarise his outcome as near-complete or complete functional recovery by 11 months post-injury. Patient two, a 40-year-old woman with chronic hypoxic brain injury and long-standing headaches, brain fog, fatigue, PTSD symptoms, and mood instability, reported substantial improvement during the protocol. Her headache frequency reportedly fell from several severe headaches per month to about one per month by January 2025, and her brain fog resolved. She also reported improved sleep, better emotional regulation, and the ability to discontinue antidepressant medication after 20 years without relapse. The paper notes that she briefly experienced increased headaches early in the iboga period, but these subsided over time. Although she improved markedly, the authors also note that at June 2025 follow-up some headaches and emotional dysregulation had returned, suggesting incomplete or fluctuating recovery rather than sustained remission. Patient three, a 19-year-old woman with post-concussive symptoms after a motor vehicle accident, initially reported severe headaches, cognitive slowing, confusion, visual symptoms, vertigo, nausea, vomiting, fatigue, sleep disruption, and emotional volatility. During the iboga protocol, she reported large gains in headache burden, energy, sleep, balance symptoms, and emotional regulation, including a reduction in feeling symptomatic from about 90% to 45%. By February 2025, nausea, vomiting, lightheadedness, vertigo, and right-hand numbness had resolved, and headache frequency had fallen to one self-resolving episode in the prior 4 weeks. However, at June 2025 follow-up, the paper reports recurrence of headaches, emotional dysregulation, cognitive fatigue, and sensitivity to heat, indicating that sustained remission was not achieved. Across the three cases, the authors emphasise improvements in headaches, fatigue, cognitive fog, sleep, mood regulation, and return to activities. They also note that all participants were able to reduce or stop some symptomatic medications during the course of recovery. The paper reports the use of adjunctive therapies, including AEDP, counselling, supplements, sensory deprivation tanks in some cases, and standard headache medications, which makes the independent effect of iboga difficult to separate from the overall treatment package.
The authors interpret these cases as suggesting that a structured iboga microdosing protocol, delivered with psychotherapy and supportive care, may be associated with neurological and psychological improvement in persistent post-concussive syndrome and chronic hypoxic-ischemic brain injury. They present the 4 days-on, 3 days-off regimen as a cautious approach intended to reduce adverse effects while potentially supporting neuroplasticity, meaning the brain’s capacity to adapt and reorganise. They place the findings in the context of earlier work on ibogaine and other psychedelics, arguing that iboga’s pharmacology may be relevant to recovery through effects on neurotrophic signalling, especially GDNF and BDNF, and possibly broader network-level plasticity. The discussion also compares these cases with emerging evidence for psilocybin and 5-MeO-DMT in TBI-related symptoms, and with recent human observations in veterans and other groups, which the authors present as broadly consistent with the improvements seen here. The authors are explicit about limitations. They stress the very small sample size, absence of randomisation, lack of blinding, and anecdotal nature of the report. They also note that natural recovery after concussion can continue over months to years, so some improvement may have occurred without the intervention. Because the participants also received psychotherapy, integration work, ritual elements, supplements, and in some cases standard medications or other therapies, the specific contribution of iboga cannot be isolated. They further acknowledge reliance on subjective symptom reporting, lack of systematic biomarker or neuroimaging data, and the possibility of selection bias and expectancy effects, all of which limit causal inference. In terms of implications, the authors argue that the cases justify further systematic study of iboga-containing interventions in brain injury rehabilitation. They call for larger controlled trials, standardised protocols, longitudinal follow-up, objective neuropsychological and imaging outcomes, and biomarker studies to examine whether iboga influences neuroplastic or neurotrophic pathways in humans. They also note the importance of careful screening because of known cardiac risks such as QT prolongation and arrhythmias.
The authors conclude that iboga microdosing warrants further systematic investigation as a potential adjunctive approach for traumatic brain injury and hypoxic brain injury rehabilitation. They state that the observed recoveries are promising but preliminary, and that controlled prospective studies with objective safety and efficacy measures are needed to clarify the therapeutic role, mechanism, and risk profile of iboga-containing interventions.
The participants completed a pre-screen assessment including health, mental health, and substance use. Health questions include heart condition, physical activity, cerebellar dysfunction, epilepsy, brain disease, dementia, impaired kidney or liver function. Mental health questions include acknowledgement of schizophrenia, bipolar disorder, depersonalization and/or derealization disorder, and psychosis or any acute confusional state. Substance use questions include use of any psychiatric drugs (anti-anxiety medication, antidepressants, and mood stabilizers), use of opiate drugs (heroin, opium, morphine, oxycontin, suboxone, methadone), use of benzodiazepines, and use of any drugs for sleeping or staying awake. All data collected in assessments are collected electronically and secured in a secure, password-protected database.
Participants were self-referred or referred by clinicians, community networks, or peer recommendations, seeking novel integrative options for persistent post-concussive symptoms that had not adequately responded to standard medical and rehabilitative care. Recruitment was passive and occurred through word-ofmouth, and professional referrals. Inclusion criteria included: (1) documented history of traumatic brain injury (mild to moderate severity), (2) prolonged post-concussive symptoms or post-hypoxic brain injury symptoms persisting for at least 3 months (and typically much longer) despite conventional treatments, (3) age 18 years or older, (4) capacity to provide informed consent, and (5) medical stability for outpatient integrative care. Exclusion criteria included: active psychosis or severe untreated psychiatric illness, current substance dependence (other than nicotine), contraindicating medications (e.g., QT-prolonging drugs), severe cardiac disease, pregnancy, or inability to engage in psychotherapy. All participants paid for the therapy component portion of the intervention on a sliding-scale basis, ranging from USD $1,100 to $1,500, which covered integrated psychotherapy sessions (weekly counseling, parts work, AEDP, and integration). No financial incentives or subsidies were provided, and fees were structured to ensure accessibility while supporting the therapeutic practice. Screening was comprehensive and conducted by the treating clinician (the corresponding author, a board-certified physician with expertise in psychedelic-assisted therapies), in consultation with participants' existing medical providers as needed. The process included: a detailed medical and psychiatric history review; specific cardiac risk assessment (beyond a general 'heart condition' question) encompassing personal/family history of arrhythmias, QT prolongation, syncope, or sudden cardiac death; review of current medications for potential interactions; baseline vital signs measurement; and, where clinically indicated, 12-lead ECG to evaluate QTc interval and other abnormalities. Participants with any concerning cardiac findings were referred for cardiology consultation prior to proceeding. This rigorous screening ensured participant safety given known cardiovascular risks associated with ibogaine-containing preparations. The iboga was obtained by the patients directly from the traditional healers. The therapy portion intervention was administered in the United States, in the state of Nevada. Participants were recruited from the United States. No non-US participants required translators, as all sessions were conducted in English with native fluent speakers. Ethics and Informed Consent: This case series describes naturalistic observations from individuals who independently elected to engage in an iboga-containing protocol outside formal clinical care. Data were collected and de-identified for scholarly analysis. As no intervention was assigned by investigators and no prospective human-subject experimentation occurred, formal IRB review was not required under institutional policy. All participants provided written informed consent for publication of de-identified clinical information. To ensure the highest ethical standards, the work was conducted in full accordance with the ethical principles outlined in the Declaration of Helsinki (2013 revision), with particular emphasis on: 1. Respect for persons (autonomy through voluntary participation and informed consent processes), 2. Beneficence (maximizing potential benefits while minimizing risks via careful screening and monitoring), and 3. Justice (equitable access to the integrative protocol without coercion). All participant data were de-identified prior to analysis and reporting, with stringent measures to protect privacy and confidentiality in line with HIPAA Safe Harbor guidelines. Participants provided written clinical informed consent for the integrative iboga microdosing and psychotherapeutic intervention as part of standard care in a therapeutic setting. Subsequently, for inclusion in this observational case series, separate research informed consent was obtained, allowing use of anonymized clinical data for publication. The research consent process included full disclosure of study aims, risks/benefits, confidentiality measures, and voluntary withdrawal rights.
The iboga preparation used in this protocol was a natural root bark product derived from Tabernanthe iboga, containing ibogaine and other naturally occurring alkaloids (not a synthetic ibogaine hydrochloride preparation). The material was sourced directly from a Pygmy family in the Congo who cultivate and traditionally harvest the plant in accordance with sustainable and culturally respectful practices. This sourcing approach prioritizes ethical, communitybased supply chains in the plant's region of origin, minimizing risks associated with unregulated or adulterated products commonly encountered in global markets. The supplier provided a Certificate of Analysis (COA) documenting third-party laboratory testing for alkaloid content (including quantified ibogaine percentage), purity, and absence of contaminants such as heavy metals, pesticides, microbial pathogens, and adulterants. The COA was reviewed by the treating clinician prior to use to confirm suitability for therapeutic application. Participants received the product in measured, standardized doses as part of the microdosing protocol, with all administration occurring under direct clinical supervision or guided self-administration with follow-up monitoring. Participants obtained approximately 20 g of Tabernanthe iboga root bark biomass for the 6 week protocol directly from the Sangoma healers. Dosing followed an individualized participant-directed titration framework utilizing approximately 0.1-1.0 g/day on a 4 days-on, 3 days-off schedule. Third-party qNMR and HPLC Certificate of Analysis testing demonstrated approximately 3.845% ibogaine content by mass within the root bark biomass. Participants utilized biomass/root bark only and did not utilize purified ibogaine hydrochloride or concentrated extracts. Participant characteristics, injury details, iboga dosing parameters, and overall clinical course are summarized in Table.
The weekly counseling component addressed the psychological dimensions of recovery and enhanced the therapeutic efficacy of the intervention. Weekly sessions were held via virtual connection to the therapist, while monitoring adherence to the microdosing regimen. This was conducted for the duration of the 6 week treatment paradigm. This case was supervised in accordance with direction from the Sangoma healers. Literature Review: The narrative synthesis of existing literature incorporated in this manuscript was informed by searches of major databases including PubMed/MEDLINE, Google Scholar, PsycINFO, and Scopus, conducted through December 2025. Search terms included combinations of 'ibogaine', 'iboga', 'psychedelic', 'traumatic brain injury', 'TBI', 'post-concussive syndrome', 'persistent post-concussion symptoms', 'concussion', 'neuroplasticity', 'GDNF', 'BDNF', and related terms. Inclusion focused on peer-reviewed articles, reviews, and case reports relevant to psychedelic (particularly ibogaine/iboga) mechanisms or applications in TBI, post-concussive symptoms, neuroprotection, or related neuropsychiatric conditions. Exclusion criteria eliminated non-English publications, non-peer-reviewed sources, and studies unrelated to brain injury or psychedelics. Key studies were selected based on relevance to the clinical observations in our case series, with emphasis on high-impact preclinical mechanistic work and recent observational human data (e.g., ibogaine in veterans with TBI).
A 43 year-old man was referred to the neurology clinic in April 2024 following a traumatic brain injury sustained during a motorcycle accident in February 2024. The patient experienced loss of consciousness at the time of impact, sustained helmet damage, and reported a 24 h period of anterograde amnesia. The patient's initial neuroimaging occurred approximately 1-month post-injury.
Upon initial evaluation, the patient presented with a complex post-concussive syndrome characterized by daily headaches with at least 1 day per week of continuous cephalic pain. The patient described a dull occipital headache pattern with intermittent throbbing. Associated symptoms included nausea, photophobia, right-sided ocular pressure without visual disturbance, intermittent disequilibrium, lightheadedness, and diffuse fatigue more pronounced in the upper extremities. The patient's spouse reported noticeable mood lability and affective changes. Sleep patterns were disrupted, with the patient averaging approximately 6 h of sleep nightly with maintenance insomnia. Neurological examination revealed no focal sensory deficits. Initial From a psychological perspective, the patient reported significant emotional challenges, including grief over loss of identity, severely impacted physical capability, major lifestyle shifts, and diminished access to meaningful activities. The patient experienced multiple daily anger outbursts and depression stemming from inactivity and stressed family dynamics.
An MRI brain with and without contrast performed in March 2024 revealed scattered small foci of hyperintense FLAIR/T2 signal predominantly affecting the deep white matter of both frontal lobes. A subtle area of confluent signal was observed in the juxtacortical white matter of the precentral gyrus near the vertex. These imaging features were consistent with nonspecific gliosis. Notably, there was no hemosiderin deposition detected, no encephalomalacia along the polar regions of cerebral hemispheres, and no evidence of diffuse axonal injury.
First follow-up (July 2024) At a 2 month neurology clinic follow-up visit the patient showed minimal symptomatic improvement, with heat-provoked severe headaches impacting work functionality. The patient discontinued amitriptyline due to adverse effects of irritability and excessive drowsiness and did not appreciate any benefit from magnesium L-threonate administration. Treatment was modified to include sensory deprivation tank therapy and Lion's Mane supplementation (500 mg daily), while continuing Aimovig injections monthly.
Following limited improvement with conventional interventions, the patient was introduced to an iboga microdosing protocol beginning July 2024, with weekly therapeutic sessions performed virtually, scheduled for the subsequent 6 weeks.
The therapeutic intervention combined iboga microdosing with Accelerated Experiential Dynamic Psychotherapy (AEDP), a somatic-focused approach. Weekly sessions were conducted as follows: Session 1 (July 2024) Established therapeutic rapport and introduced the iboga protocol, including ritual and spiritual connection aspects. Therapeutic intervention focused on holistic assessment of the patient's life history, interpersonal relationships, emotional management, and processing of grief related to identity changes following TBI. The patient was instructed to establish a ritualized morning routine incorporating intention setting, gratitude practice, visualization, mindfulness, and connection with iboga.
The patient reported a shift in headache location from occipital to frontal regions with reduced intensity during daytime hours. Therapeutic work explored the patient's historical difficulties with emotional expression, feelings of unworthiness, and family dynamics that affected trust development since childhood. The therapist provided guidance on observing thought patterns and behaviors that might be amplified through the iboga protocol.
The patient detailed explosive anger episodes and their impact on family dynamics. Exploration of childhood experiences revealed adverse early experiences including physical punishment, anxiety manifesting as perceptual distortions, i.e., "walls closing in", and emotional isolation. The therapeutic approach incorporated somatic therapy, focusing on physical sensations in the stomach and chest associated with sadness and confusion.
The patient reported significant improvement, noting headaches were now limited to evening hours or occasionally during sleep, with decreased intensity. Physical improvements included reduced muscle aches, decreased fatigue, and increased energy. The patient reported engaging in physical activities, e.g., hiking, and emotionally connecting activities with his son. Family relationships improved from a "grin and bear it" attitude to experiences of enjoyment and enthusiasm. The patient acknowledged improved interoceptive awareness regarding stress and anger, with enhanced self-regulation through breath work and somatic awareness.
Continued improvement was noted with fewer headaches, decreased fatigue, and sustained energy throughout the day. The patient reported expanding his activity level, including hiking, and developing insight into transgenerational patterns of emotional behavior, particularly regarding his son. Morning mindfulness practices continued with reported deeper connection to "something greater," earlier waking, increased readiness for daily activities, and deeper feelings of peace. The patient acknowledged greater understanding of the connection between childhood trauma, stress, and physical pain manifestations. AEDP therapy focused on accessing somatic affect, processing childhood pain related to parental relationships, and expanding emotional tolerance through imaginal portrayal techniques.
The patient reported occasional musculoskeletal discomfort in the right lower back and shoulder. Anger outbursts had completely resolved, compared to multiple daily episodes prior to treatment. Headaches had decreased to approximately one every 2 weeks, compared to daily occurrences pre-intervention. The patient reported acceptance of lifestyle changes and increased enjoyment in new activities with his son. The final session focused on maintaining mindfulness and somatic awareness practices.
After initiation of the iboga microdosing protocol, the neurological clinic follow-up visit in mid-August confirmed gradual recovery with improved muscle strength and energy levels. Headaches persisted albeit with notably reduced intensity and frequency. The patient continued Aimovig injections for headache prevention alongside complementary alternative interventions aforementioned.
At a 9-month neurology clinic post-injury follow-up, the patient reported profound and significant clinical improvement with substantially reduced muscle fatigue and headaches characterizing symptoms as "very rare and very subtle." The patient selfdiscontinued all prescribed medications by this time.
At an 11 month post-injury follow up assessment, status post 5 months since completion of the microdosing iboga protocol, the patient reported mild headaches occurring only once every couple of months, with occasional mild fogginess in the occipital region occurring a few times per week. Sleep had normalized with resolution of maintenance insomnia. The patient described his emotional state as "better than ever, and better than before the accident," with improved resilience and emotional regulation. Physical symptoms had largely resolved with absence of muscle fatigue, increased motivation, and excitement about returning to pre-injury activities.
The patient's recovery trajectory demonstrated significant resolution of post-concussive symptoms over an 11-month period following a traumatic brain injury (TBI) sustained in a motorcycle accident. The integration of conventional neurological care with a 6 week iboga microdosing protocol and Accelerated Experiential Dynamic Psychotherapy (AEDP) therapy effectively addressed both the neurophysiological and psychological sequelae of TBI. Notable improvements were observed across multiple domains, with the patient reporting a quality of life surpassing his preinjury baseline.
A 40 year-old female with a prior medical history of ankylosing spondylitis and depression presented to the neurology clinic with persistent headaches following a hypoxic brain injury sustained during an avalanche in 2016/2017. No direct cranial impact occurred and no helmet damage was observed. The patient was buried beneath snow for approximately 10-15 min, consciousness progressively declined during prolonged hypoxic exposure, respiratory depression was observed upon rescue, and neurocognitive symptoms persisted chronically for approximately 7 years prior to protocol initiation.
The patient initially presented with multiple neurological sequelae following her hypoxic brain injury, including slowness of thought, memory changes, and migraine headaches. While these symptoms showed some improvement over time, she continued to experience significant impairment in her daily functioning. Two years prior to the most recent evaluation, the patient selfinitiated psychedelic therapy with LSD and psilocybin, reporting "massive improvement" in her symptoms. Despite this, she continued to suffer from severe headaches approximately once per month at initial presentation. These headaches were characterized as right-sided, accompanied by photophobia, phonophobia, and nausea, lasting from several hours to an entire day. Her initial self-management strategy involved a combination of acetaminophen, ibuprofen, and diphenhydramine, which typically provided relief after several hours. The patient also reported persistent "brain fog" with particular difficulty in word finding, which worsened with alcohol consumption. Her sleep was described as difficult, complicated by post-traumatic stress disorder (PTSD) and nightmares, though she noted some improvement with ongoing talk therapy.
During the follow-up visit in August 2024, the patient reported that ubrogepant (Ubrelvy) had been effective when tried as a sample, but insurance approval was pending. Her migraine frequency had increased to five episodes over the previous 2 months, compared to her baseline of once monthly. She had initiated supplements including N-acetylcysteine (NAC), Lion's Mane mushroom, and magnesium L-threonate, with subsequent improvement in sleep quality. Her cognitive fog remained unchanged. She had successfully completed a slow taper off bupropion (Wellbutrin) without adverse effects. At her November 2024 follow-up, the patient reported effective abortive treatment of headaches with either ubrogepant (Ubrelvy) or rimegepant (Nurtec), though insurance coverage remained problematic. She disclosed recent unemployment. Her mood was described as stable with anxiety but without depression, and her sleep quality remained variable. By January 2025, the patient had obtained new insurance coverage and a prescription for ubrogepant had been sent the previous month, though she had not yet filled it. Her headache frequency had decreased to 3-4 episodes per month, with none in the 3 weeks prior to the visit. Notably, she reported resolution of her brain fog.
In January 2025, vital signs were within normal limits: BP 108/ 60 mmHg, pulse 68/min, respiratory rate 16/min, and oxygen saturation 95%. The patient was alert and in no acute distress.
The patient was alert and in no acute distress. Neurological examination revealed a patient who was alert and oriented to person, place, and time with intact command following. Her speech was normal without dysarthria, and she demonstrated preserved naming and repetition abilities. Cranial nerve assessment showed pupils that were equal, round, and reactive to light bilaterally with full visual fields. Extraocular movements were intact, and she exhibited symmetric facial sensation and movement. Hearing was equal bilaterally to finger rub testing, and her palate elevated symmetrically. Shoulder shrug was full, and her tongue was midline. Motor examination demonstrated 5/5 strength throughout all extremities both proximally and distally with normal tone and no abnormal movements. Sensory examination did not identify any deficits. Deep tendon reflexes were 2+ and symmetric throughout. Coordination testing revealed no ataxia, and the patient ambulated independently without assistance.
No laboratory results were available for review. Neuroimaging was intentionally deferred, as noted in the assessment and plan.
Initial management included recommendations for sumatriptan (Imitrex) for severe breakthrough headaches, with a plan to transition to rizatriptan (Maxalt) if necessary. A sample of rimegepant (Nurtec) was provided. For cognitive symptoms, N-acetylcysteine and Lion's Mane supplements were recommended, along with information on sensory deprivation tanks. For insomnia, magnesium L-threonate and/or CBD gummies were suggested, with counseling on sleep hygiene. Continuation of psychological services was recommended for PTSD management. A treatment addendum in July 2024, noted a recommendation for ubrogepant (Ubrelvy), as the patient experienced four or more migraine days monthly and had failed trials of at least two triptans (sumatriptan and rizatriptan). By August 2024, improved sleep was reported with magnesium L-threonate supplementation. Ubrogepant remained the recommended abortive treatment for headaches, with additional samples provided. A sample of rimegepant was also provided as an alternative if insurance approval for ubrogepant was denied. Preventive injection therapy was deferred at that time. The November 2024 assessment noted good response to both ubrogepant and rimegepant for headache management, with continued use of magnesium L-threonate for sleep. The patient was encouraged to implement meditation practices and ensure adequate hydration to address anxiety exacerbated by recent job loss. At the January 2025 follow-up, samples of ubrogepant were provided while awaiting prescription fulfillment. The clinician documented complete resolution of both brain fog and headaches. Continued hydration and Lion's Mane supplementation were encouraged.
Following limited improvement with conventional interventions, the patient was introduced to an iboga microdosing protocol beginning 18 October 2024, with weekly therapeutic sessions performed virtually, scheduled for the subsequent 6 weeks.
The therapeutic intervention combined iboga microdosing with Accelerated Experiential Dynamic Psychotherapy (AEDP), a somatic-focused approach. Weekly sessions were conducted as follows: Session 1 (October 2024) Established therapeutic rapport and introduced the iboga protocol, including ritual and spiritual connection aspects. Therapeutic intervention focused on holistic assessment of the patient's life history, interpersonal relationships, emotional management, and processing of grief related to identity changes following TBI. The patient reported severe PTSD following the TBI with nightmares 1-3 times a month and emotional dysregulation. Experiences chronic fatigue, cognitive fog, and slowness in thought processing. Clarity and alertness are rare, usually only occurring 1-2 days/month. The patient reported strong physical health with an active lifestyle and improved alcohol moderation. Migraines occurred monthly, requiring sensory deprivation, with additional headache days. General emotional instability while navigating complex grief over her mother's decline and high stress at work. Ttrauma history includes childhood abuse and sexual assault, severe anorexia leading to inpatient treatment at age 20. The behavior has resolved though intrusive thoughts occasionally surface. Has previously received EMDR therapy.
Once beginning iboga treatment, the patient experienced headaches resembling a "vice" on her head with mild noise and light sensitivity. Dreams also became more vivid. The patient reported feeling more connected to her body than before. She engaged in grounding exercises to increase bodily awareness. The patient recalled an unexpected memory from childhood accessing sadness and treatment focused on shame, anger, grief, instability, fear, and loss. Significant emotional release followed. Session 3-6 (November 2024) Treatment used AEDP Psychotherapy to explore traumatic childhood memories across various ages continued in all the following weeks. In particular memories between ages 10-15 that the patient shared had never been revealed including incidents with her alcoholic mother, incarceration of a parent, physical abuse from father, and neglect of basic needs like food and shelter. Iboga created notable access to memories that had not been accessed in decades and processing of emotions like fear, guilt and shame. Significant work done to regulate the overwhelm of emotions, the ability to remain present and connected to the body while experiencing emotion, and narrative re-experiencing of new experiences like safety, trust, co-regulation with another, affirmation, confidence, and care. Follow Up (January 2025): The patient reported progressive improvement in headaches, emotional regulation, fatigue, and cognitive symptoms following the integrative protocol. The patient reported a significant reduction in frequency of headaches from 3-6 severe headaches monthly to one per month and patient self-reporting iboga greatly improving brain health. Initially iboga led to an increase in headache occurrence then symptoms subsided over time. In terms of mood, the subject reported a substantial and sustained improvement after iboga, enabling her to discontinue antidepressant medication after 20 years without relapse. She noted enhanced emotional regulation and a new ability to recognize and interrupt depressive spirals. Psychologically, she described reaching a place of acceptance with past trauma and felt more emotionally resilient. Overall, she characterized the change as transformative and described the sensation of "living back in her own brain." In regards to the reported history of psychedelic use prior to the iboga microdosing protocol, the patient did not use LSD nor psilocybin during the active iboga-containing treatment interval. Rather, prior intermittent psychedelic exposures occurred years before protocol initiation. Specifically, psilocybin use began in March 2021 and LSD use began in May 2021, whereas the ibogacontaining protocol was initiated in October 2024. LSD exposure occurred intermittently, approximately four times annually, outside the active treatment interval and was not co-administered during the protocol.
The patient's recovery trajectory demonstrated progressive resolution of post-hypoxic injury sequelae symptoms over a 6 month period following the initiation of the iboga microdosing protocol. The integration of conventional neurological care with an iboga microdosing protocol and Accelerated Experiential Dynamic Psychotherapy (AEDP) therapy appeared to address both the neurophysiological and psychological sequelae of chronic hypoxic-ischemic brain injury (HIBI). Notable improvements were observed across multiple domains: 1. Physical Symptoms: The patient experienced a near-complete resolution of headaches, with frequency decreasing from 3-6 severe episodes monthly to one per month by the January 2025 follow-up. Initially, the iboga microdosing protocol led to a temporary increase in headache occurrence, described as a "vice" on her head with mild noise and light sensitivity, but these symptoms subsided over the course of treatment. Chronic fatigue, a significant issue at baseline, was markedly reduced, allowing the patient to resume an active lifestyle. Sleep quality improved with the use of magnesium L-threonate supplementation, and nightmares associated with post-traumatic stress disorder (PTSD) decreased in frequency from 1-3 times monthly to rare occurrences. The patient's overall physical health remained strong, supported by improved alcohol moderation and enhanced bodily awareness developed through grounding exercises during therapy. 2. Cognitive Symptoms: Cognitive functioning showed substantial improvement, with complete resolution of persistent brain fog, which had been the most debilitating symptom at presentation. The patient reported enhanced memory recall, reading comprehension, and clarity of thought, achieving cognitive alertness on a near-daily basis compared to only 1-2 days per month initially. While the iboga protocol contributed significantly to these improvements, the patient noted a marked cognitive enhancement following selfdirected LSD use, which she described as restoring cognitive integration through visual patterning experiences. By the end of the treatment period, the patient reported a return to full cognitive functioning, enabling her to engage in complex tasks without the slowness of thought or word-finding difficulties that characterized her initial presentation. 3. Emotional/Psychological Symptoms: The patient achieved significant emotional stability, culminating in the cessation of antidepressant medication after 20 years of use without relapse. Emotional dysregulation, driven by PTSD and complex grief related to her mother's decline, improved substantially, with the patient developing the ability to recognize and interrupt depressive spirals. AEDP therapy facilitated the processing of traumatic childhood memories, including abuse, neglect, and parental incarceration, allowing the patient to access and regulate emotions such as fear, guilt, and shame. By the end of treatment, she reported enhanced emotional resilience and a newfound sense of acceptance regarding past trauma. The patient described a transformative psychological shift, characterized by increased confidence, trust, and the ability to co-regulate emotions with others, marking a significant departure from her baseline emotional instability. 4. Functional Outcomes: The patient's functional recovery was transformative, enabling a return to meaningful activities and improved quality of life. She resumed an active lifestyle, including physical activities previously limited by fatigue and headaches. Social and interpersonal functioning improved as she navigated complex grief and workplace stress with greater emotional regulation. The patient reported enhanced self-care capacity, including the ability to set boundaries and prioritize her needs. Despite recent unemployment, she maintained a stable mood and optimism, reflecting improved coping strategies. The discontinuation of antidepressants and reduced reliance on abortive headache medications (e.g., ubrogepant and rimegepant) underscored her development of sustainable self-management techniques. Overall, the patient described the treatment as a profound return to living "back in her own brain," reflecting a significant restoration of identity and purpose.
A 19 year-old female with no significant past medical history presented to the neurology clinic following consultation for traumatic brain injury (TBI) sustained in a motor vehicle accident (MVA).
The patient was initially evaluated in the emergency department in November 2024, after being involved in an MVA where her vehicle was T-boned at an intersection by another vehicle traveling at approximately 50 mph. She was a restrained driver and denied airbag deployment. At the time of the emergency department presentation, she reported headache located on the superior aspect of her head, mid-back pain, and left-sided chest wall pain. She specifically denied loss of consciousness, nausea, vomiting, dizziness, blurry vision, neck pain, further chest pain, lower back pain, abdominal pain, urinary complaints, or bowel/bladder incontinence. During her initial neurology clinic visit in December 2024, approximately 2 weeks post-injury, the patient's clinical presentation had evolved significantly. She reported blurred vision, chronic fatigue, and cognitive difficulties described as "feeling drunk 90% of the time" with confusion. She also noted personality changes including irritability, emotional volatility, and being "less reserved than usual" with "no filter." The patient described headaches occurring 2-3 times per week, located frontally, throbbing in quality, severe in intensity, and lasting up to 2 days. Acetaminophen provided no relief. She reported nausea and vomiting, alongside both intermittent lightheadedness and vertigo. The patient also described dropping objects and experiencing intermittent numbness in her right hand. Her sleep patterns were significantly disrupted, requiring 4-6 h naps daily in addition to sleeping 12 h nightly. She acknowledged significant screen time exposure and reported that a 90 min session at a sensory deprivation facility (Healing One) the previous week had provided temporary benefit, described as "clarity of thought for 2 h"
At her follow-up visit on 22 January 2025, approximately 2 months post-injury, the patient reported medication intolerances. Sumatriptan (Imitrex) caused increased lethargy and worsened hand numbness without alleviating her headaches. Rizatriptan (Maxalt), initiated on 19 December 2024, produced extreme fatigue and lethargy with worsening headache symptoms. Ubrogepant (Ubrelvy), prescribed in January 2025, provided no benefit. Her headache frequency had increased to 2-4 episodes weekly, with a continuous headache for the 4 days preceding her visit. She continued to experience excessive sleep requirements and reported poor memory, noting an episode where she "got lost" at school. The patient described anxiety and depression related to her diagnosis. A trial of a sensory deprivation tank had provoked anxiety. She inquired about iboga as a potential treatment, noting her father's positive experience with this substance for TBI. By her February 2025 follow-up, approximately 3 months postinjury, the patient reported self-sourcing iboga and following a microdosing protocol similar to her father's. She was in week 4 of a planned 6 week protocol. At this visit, she reported a continuous headache for the previous 3-4 days, located at the crown and worsening with postural changes such as bending down. The headache was described as pressure-like in quality and moderate in intensity. Rimegepant (Nurtec) had provided no relief, while ubrogepant had offered some improvement. The patient reported significant symptom improvement across multiple domains. Her fatigue and confusion had substantially improved, now describing herself as 45% symptomatic compared to 90% in December 2024. Emotional lability and volatility had improved by approximately 70%, an assessment her accompanying father agreed with emphatically. Nausea and vomiting had completely resolved. Sleep requirements had decreased to 9-10 h nightly with rare naps (approximately twice weekly, lasting 4-6 h). Lightheadedness, vertigo, and right-hand numbness had all resolved. Headache frequency had decreased substantially, with only one self-resolving episode in the preceding 4 weeks. A second experience with a sensory deprivation tank had been beneficial without provoking anxiety. The patient also reported pursuing talk therapy.
In February 2025, vital signs showed blood pressure 136/ 66 mmHg, pulse 90/min, respiratory rate 18/min, and oxygen saturation 98%. The patient's height was 170.2 cm (5′7.01″) and weight 54.4 kg (120 lb). General examination revealed a patient who was awake and in no acute distress. Cardiovascular examination demonstrated regular rate and rhythm. Neurological examination showed a patient who was awake, alert, and oriented to person, place, and time with intact command following. Her speech was normal without dysarthria, and she demonstrated preserved naming and repetition abilities. Cranial nerve assessment revealed pupils that were equal, round, and reactive to light bilaterally with full visual fields. Extraocular movements were intact with normal convergence and normal saccades. She exhibited symmetric facial sensation and movement. Hearing was equal bilaterally to finger rub testing, and her palate elevated symmetrically. Shoulder shrug was full, and her tongue was midline. Motor examination demonstrated 5/5 strength throughout all extremities both proximally and distally with normal tone and no abnormal movements. Sensory examination did not reveal any deficits. Deep tendon reflexes were 2+ and symmetric throughout. Coordination testing showed no bilateral ataxia on finger chase testing, and the patient ambulated independently without assistance.
A qualitative urine pregnancy test performed in May 2024 (prior to the accident) was negative. Computed tomography (CT) of the head performed in December 2024, revealed no acute intracranial abnormality. Magnetic resonance imaging (MRI) of the brain obtained in January 2025, demonstrated no acute intracranial process, with incidental finding of mild maxillary sinus mucosal thickening.
Initial management included recommendations for an MRI brain (which was subsequently performed), sensory deprivation tank sessions, screen time minimization, alcohol avoidance, N-acetylcysteine (NAC) supplementation, adequate hydration, and conservative management. Sumatriptan was recommended for severe headaches, alongside meditation practice and a diet high in antioxidants. At the January 2025 follow-up, given the patient's intolerance to multiple abortive medications and worsening headache frequency and intensity, management was adjusted. The treatment plan included transitioning from ubrogepant to rimegepant for breakthrough headaches, with samples provided. A sample of fremanezumab (Ajovy) was also provided for prevention. A methylprednisolone dose pack was recommended to abort the current cycle of status migrainosus. The clinician provided academic information from medical literature regarding iboga following the patient's inquiry, while clarifying inability to prescribe this Schedule I substance. By the February 2025 visit, the patient had self-initiated iboga microdosing with substantial symptomatic improvement. The clinician documented inability to formally recommend this therapeutic but offered to provide academic information from the medical literature. A single 30 mg intramuscular dose of ketorolac (Toradol) was administered during the visit to address status migrainosus.
The therapeutic intervention combined iboga microdosing with Accelerated Experiential Dynamic Psychotherapy (AEDP). Weekly sessions were conducted as follows:
Established therapeutic rapport and introduced the medicine protocol. Therapeutic intervention focused on holistic assessment of the patient's life history, interpersonal relationships and emotional management following TBI. The patient reported a significant increase in migraine frequency following the motor vehicle accident. Prior to the accident, she experienced occasional stress-induced headaches but no major neurological concerns. Post-accident, migraines escalated to multiple occurrences per week, described as debilitating and leading to extensive sleep and exhaustion. The patient also noted confusion, disorientation and memory loss. Inter-relationally, the patient described difficulties with processing social interactions, leading to feelings of awkwardness. The patient also reported increased isolation since the accident and difficulty relating to others. Lifestyle transition from an active, social lifestyle to one with increased restrictions led to a sense of disconnection. Treatment included somatic and parts work which opened into a space of recognizing emotional suppression and culminated in episodes of crying and emotional release linked to frustration and exhaustion. Surfaced acknowledging of anger regarding the disruption to her life and loss of control. Additional therapeutic treatment through AEDP Psychotherapy to create safety with a regulated presence of another to allow and process emotions rather than suppress them.
Patient revealed notable shifts in emotional regulation and somatic awareness describing a shift from reactivity to calmness. Reported improvement of energy levels and increased awareness of body, sensations and needs. Cognitive effects were mixed, with reported instances of disorientation and becoming lost in a familiar space. Therapeutic treatment included explorations around fear of unpredictable parental emotions, the death of her grandmother, and the absence of emotional expression. Therapeutic breakthrough with the patient coming to terms with expressing the anger and fear at the impact of the accident on her life, the loss of control, and the fear of not improving. The patient reported a profound sense of peacefulness.
The patient reported overwhelming academic and professional responsibilities in the aftermath of the accident. Treatment focused on exploring the somatic sensations of anxiety, nausea and abdominal tension which surfaced the processing of mothers multiple cancer diagnoses and grandmothers passing. The session focused on increasing tolerance for emotional distress and the patient recognized emotional suppression as a longstanding coping mechanism, originating in childhood as a response to overwhelming circumstances. The patient noted a remarkable shift in change of emotional response from distress to curiosity, presence and peace in a distressing situation. Progress in her ability to remain with emotions rather than avoid them, marking an emerging sense of agency in emotional regulation.
Notable improvements in migraine symptoms from previous severity levels of self reported 9-10 down to 5-6, enabling functional activities like hiking that were previously impossible. Therapeutic work centered on somatic awareness and brought forward minimized traumatic memory when the patient was drugged without consent ("roofied"), resulting in a 4 h memory gap, 15 h of severe vomiting and hospital submission. Treatment focused on accessing overwhelm, fear, anger, confusion, and aloneness. Through guided imagery and somatic processing released adaptive action tendencies and restored nervous system regulation.
Session five documented a notable shift in the patients saying, "I feel like a return to myself pre-accident." The patient noted new and improved memory functions. Treatment focused on actual processing of the accident and the recognition of significant attachment injury with family members and the long-lasting impact on family relationships. Treatment focused on surfacing deep emotions of anger, resentment, sadness, grief, and aloneness.
Significant neuropsychological and interpersonal developments. Cognitive changes included happiness, a sense of euphoria, and enhanced perspective-taking abilities and increased awareness of others' experiences. Academic functioning showed improvement with faster information absorption. Concurrently, the client experienced mild cognitive disruptions including conversational memory lapses and increased clumsiness. The session revealed significant progress in emotional processing capacity with the patient's initiating relational repair conversations with parents. Most remarkable was improved affect regulation with anger-with self-regulated processes of acknowledgment, expression, natural deescalation, and resolution-a process previously inaccessible. Patient expressed optimism regarding future plans, perceiving them as an avenue for personal exploration and growth and gratitude for being a "completely different person."
Overall, recent months showed high levels of physical energy and participation in life including hiking, swimming, and rock climbing. Recent weeks have seen an increase in frequency of headaches to 2-3 times per week, typically beginning with light pressure and lasting for a day. The past month was also characterized with more emotional dysregulation, mood swings, indecision, and anxiety. The patient is also experiencing feeling sensitive to environmental changes like heat, being drained by schoolwork and inability to retain information. The patient expressed interest in participating in another microdosing protocol with iboga.
The patient's recovery trajectory demonstrated partial symptomatic improvement over a 3 month period following injury; however, sustained remission was not achieved. Follow-up assessment in June 2025 documented recurrence of headaches, emotional dysregulation, cognitive fatigue, and environmental sensitivity, suggesting incomplete recovery and possible relapse of symptoms consistent with the known natural history of post-concussive syndromes. The patient's trajectory may partially reflect the expected natural recovery curve observed in mild traumatic brain injury. Physical symptoms showed remarkable resolution throughout the treatment course. The patient experienced complete resolution of nausea, vomiting, lightheadedness, and vertigo that had significantly impacted her daily functioning at initial presentation. Headache frequency dramatically decreased from 2-4 episodes weekly to just one self-resolving episode over a 4 week period. The right-hand numbness and coordination issues that initially caused her to drop objects completely resolved. Sleep patterns normalized substantially; initially requiring 12 h nightly plus 4-6 h daily naps, the patient's requirements decreased to 9-10 h nightly with only occasional naps. Energy levels improved considerably with substantially reduced fatigue. Additionally, the patient developed enhanced somatic awareness of body sensations and needs, which appeared to contribute to her improved selfregulation. 1. Cognitive symptoms demonstrated significant improvement from baseline. The patient's initial presentation of confusion, described as "feeling drunk 90% of the time," improved to just 45% symptomatic by the end of the treatment period. Memory function improved substantially, with the patient reporting a sense of "return to myself pre-accident." Information processing and academic functioning enhanced beyond the temporary relief previously experienced with sensory deprivation therapy. The patient demonstrated faster information absorption and improved learning capacity, along with regained ability to navigate familiar environments. Some mild cognitive disruptions persisted, including occasional conversational memory lapses, representing an area for continued therapeutic focus.
This case series presents a compelling narrative of neurological recovery using a novel iboga microdosing protocol for two patients experiencing prolonged post-concussive syndrome following traumatic brain injury, and one patient with chronic hypoxicischemic brain injury (HIBI) refractory to conventional measures. The patients' progressive improvements over a 9 month period, status post the microdosing protocol, underscores the potential therapeutic value of this innovative approach. The iboga microdosing intervention, characterized by a carefully structured regimen of sub-perceptual ibogaine doses, demonstrates promising neurological rehabilitation potential. The dosing protocol of 4 days on and 3 days off over a 6-week duration minimized potential adverse effects, while potentially leveraging the compound's neuroplasticityenhancing properties.
The complex pharmacological profile of iboga suggests multiple mechanisms contributing to neurological recovery. Studies have demonstrated its ability to modulate growth factors like GDNF and BDNF in brain regions involved in dopaminergic circuits, which may be particularly relevant in TBI rehabilitation. The compound's interaction with neuroplasticity pathways could potentially facilitate neural repair and functional restoration. Future work might include EEG recordings to examine signature 'psychedelic' related brain activity changes, such as the 'entropic brain effect'. Traumatic brain injury (TBI) and hypoxic brain injury (HBI) involve distinct yet partially overlapping pathophysiologic mechanisms that may differentially influence neurocognitive outcomes and recovery trajectories. TBI is characterized primarily by biomechanical injury processes including axonal shear stress, focal contusion, microvascular disruption, bloodbrain barrier dysfunction, and neuroinflammatory cascades resulting from direct mechanical force. In contrast, hypoxic injury involves diffuse cerebral oxygen deprivation leading to metabolic failure, mitochondrial dysfunction, glutamate-mediated excitotoxicity, oxidative stress, and widespread neuronal vulnerability in regions with high metabolic demand. Hippocampal structures, particularly the CA1 region, demonstrate heightened susceptibility to hypoxic injury and may contribute prominently to persistent impairments in memory consolidation, concentration, and cognitive processing speed. Cortical association networks and watershed regions may likewise exhibit selective vulnerability following prolonged hypoxic exposure. Although the injury mechanisms differ substantially, both TBI and hypoxic injury may converge upon downstream neuroinflammatory and neuroplasticity-related pathways, including dysregulation of brain-derived neurotrophic factor (BDNF) and glial cell line-derived neurotrophic factor (GDNF) signaling. Consequently, while mechanistic extrapolation from TBI and addiction-focused ibogaine literature to chronic hypoxic injury remains highly preliminary, neurotrophic and network-level plasticity pathways may represent biologically plausible areas for future investigation across both injury contexts. The clinical progression for all three reported patients is notable. Initial presentations of daily headaches, disequilibrium, and fatigue gradually resolved, with the final follow-up revealing substantially and profound reduction in symptomatology. This trajectory aligns with emerging research exploring psychedelic interventions for neurological recovery, particularly in veteran populations.
While the case series highlights promising outcomes, it's crucial to acknowledge the potential risks associated with ibogaine. Previous research has documented concerns about cardiac effects, including QT interval prolongation and potential arrhythmias. The careful screening procedure employed in this study, which excluded patients with cardiac conditions and other contraindications, represents a critical risk mitigation strategy. The microdosing protocol was implemented acknowledging medical background screening for potential drug interactions, and past medical history contraindications including heart conditions and/or the concomitant administration of selective serotonin reuptake inhibitors (SSRIs). The involvement of indigenous healers for ongoing monitoring and support adds an important layer of holistic care and potentially contributes to the intervention's efficacy. This approach resonates with emerging ethical principles in psychedelic research that emphasize traditional knowledge and comprehensive patient support.
Complementing the potential neuroplastic and antiinflammatory effects observed in our iboga microdosing cases, recent reviews highlight the promise of other serotonergic psychedelics, such as psilocybin and 5-methoxy-N,Ndimethyltryptamine (5-MeO-DMT), in alleviating TBI-related impairments through enhanced neuroplasticity, reduced neuroinflammation, and neurotrophic actions (e.g., via TrkB receptor targeting by psilocybin and sigma-1 receptor modulation by 5-MeO-DMT), underscoring the broader therapeutic potential of this class for post-concussive recovery. Recent observational evidence from veterans with a history of traumatic brain injury participating in psilocybin retreats further supports the potential of serotonergic psychedelics for this population, demonstrating substantial reductions in PTSD (50% decrease in PCL-5 scores), depression (65% decrease in PHQ-9 scores), and anxiety symptoms, alongside normalized spontaneous EEG activity (e.g., reduced delta and theta power in frontal/temporal regions indicating improved emotional processing and cognitive control, with enhanced alpha/beta coherence suggesting better neural connectivity)-outcomes that parallel the symptomatic and functional improvements reported in our iboga microdosing cases and highlight shared therapeutic pathways in prolonged postconcussive recovery. Building on these serotonergic parallels, recent neurophysiological evidence from veterans with traumatic brain injury treated with magnesium-ibogaine demonstrates a singlesession 'slowing' of cortical oscillations-characterized by increased power in slower theta-alpha bands, decreased betagamma power, an elevated theta/beta ratio correlating with improved cognitive inhibition, and persistently reduced neural complexity (lower spatiotemporal signal entropy)-which associates with sustained enhancements in executive function, PTSD, and anxiety symptoms; these objective EEG changes provide mechanistic insight into ibogaine's potential to reorganize disrupted brain networks in TBI, offering convergent support for the symptomatic improvements observed in our iboga microdosing protocol and highlighting avenues for future biomarker integration in prolonged post-concussive research.
While this is a single case series of the patients demonstrating profound benefit, the work contributes to a growing body of research exploring alternative therapeutic approaches for TBI. The multimodal approach, which included supplementation and alternative therapies alongside iboga microdosing, suggests the potential value of integrated rehabilitation strategies. Future research should focus on 1. Expanding cohort sizes to validate these preliminary findings. 2. Developing standardized protocols for iboga microdosing in neurological rehabilitation. 3. Comprehensive long-term follow-up to assess sustained neurological improvements. 4. Detailed neuroimaging and neuropsychological assessments to quantify recovery mechanisms.
The primary limitation of this case series is its small sample size, lack of randomization or blinding, and anecdotal nature. While offering valuable insights, broader clinical validation is necessary. Additionally, the potential placebo effect and the patient's concurrent therapeutic interventions cannot be definitively isolated. The observed neurological and functional improvements in these cases with prolonged post-concussive syndrome raise the possibility that iboga microdosing may exert therapeutic effects through promotion of neuroplasticity and neural repair. Preclinical studies in rodents have demonstrated that ibogaine administration upregulates glial cell line-derived neurotrophic factor (GDNF) selectively in dopaminergic regions such as the ventral tegmental area (VTA) and substantia nigra, as well as brain-derived neurotrophic factor (BDNF) across mesocorticolimbic circuits including the nucleus accumbens, prefrontal cortex, and substantia nigra. These neurotrophic changes support dopaminergic neuron survival, enhance synaptic plasticity, and may facilitate restoration of disrupted reward and motivational pathways-mechanisms potentially relevant to the persistent cognitive, emotional, and somatic symptoms following traumatic brain injury. Future research should investigate whether iboga microdosing modulates GDNF and BDNF levels in humans with traumatic brain injury and prolonged post-concussive syndrome, and whether such changes correlate with neural repair (e.g., via neuroimaging markers of white matter integrity or functional connectivity) and functional restoration. Controlled trials incorporating biomarkers of neurotrophic activity, advanced neuroimaging (e.g., diffusion tensor imaging, resting-state fMRI), and longitudinal assessments could elucidate these mechanisms and build on the promising multimodal, holistic approach described here, including integration of ceremonial frameworks, parts work, and Accelerated Experiential Dynamic Psychotherapy (AEDP). As with all case series, particularly in the emerging domain of psychedelic interventions for traumatic brain injury and prolonged post-concussive symptoms, several interpretive boundaries must be acknowledged to contextualize these preliminary observations. First, natural recovery trajectories in persistent post-concussive symptoms can extend over months to years, with a subset of individuals experiencing gradual improvement even without novel interventions; consensus guidelines indicate that while most concussion symptoms resolve within weeks to 3 months, 10%-30% develop persisting symptoms beyond this period, and spontaneous resolution or adaptation remains possible in prolonged cases. The improvements observed here could thus partly reflect ongoing natural recovery processes, though the chronicity and severity of symptoms prior to initiation of the iboga microdosing protocol (persisting for months to years despite prior care) suggest contributions beyond typical resolution. Second, participants received concurrent multidisciplinary support, including weekly counseling, therapeutic alliancebuilding, parts work, Accelerated Experiential Dynamic Psychotherapy (AEDP), and integration of ceremonial/ritual elements from Sangoma healers. These holistic components, while integral to the protocol, introduce challenges in isolating the specific causal role of iboga microdosing from nonspecific therapeutic factors or the synergistic effects of combined modalities. Third, assessments relied primarily on clinical observations, standardized patient-reported symptom scales (e.g., Rivermead Post-Concussion Symptoms Questionnaire), and functional outcomes, which are inherently subjective and susceptible to reporting biases. Objective biomarkers (e.g., advanced neuroimaging or neurotrophic factor levels) were not systematically incorporated, limiting mechanistic inference. Finally, as in much early psychedelic research, selection bias (e.g., motivated individuals seeking novel treatments) and expectancy effects may have influenced outcomes. Positive expectations surrounding psychedelics, amplified by media attention and the therapeutic reputation of iboga, can contribute to perceived benefits independent of or synergistic with pharmacological actions, a phenomenon well-documented in psychedelic trials where unblinding and expectancy often enhance apparent efficacy. These considerations represent shared constraints in hypothesis-generating case series and observational studies in this nascent field, rather than unique shortcomings of the present work. They underscore the preliminary nature of the findings and highlight the critical need for controlled, prospective trials to disentangle specific drug effects from contextual and recoveryrelated factors.
As research in this field continues to expand, it becomes increasingly important for primary care clinicians to understand the therapeutic potential and clinical considerations of ibogainebased interventions. The observed neurological recovery suggests iboga microdosing warrants further systematic investigation as a potential therapeutic approach for TBI rehabilitation. The patient's progressive symptom resolution, coupled with the intervention's apparent safety when carefully implemented, presents an intriguing avenue for future neurological research. The promising outcomes of iboga microdosing in this case series, alongside emerging research on psilocybin's potential in TBI recovery, underscore the need for further exploration of psychedelic compounds as novel therapeutic options.suggest that psychedelics inclusive of psilocybin may enhance neural repair, providing a comparative context for iboga's observed effects and warrants rigorous clinical trials. Recent observational findings from the Global Psychedelic Survey suggested that individuals with traumatic brain injury histories reported perceived improvements across cognitive, emotional, and somatic symptom domains following psychedelic use, further reflecting growing interest in exploratory psychedelicassisted neurorehabilitation paradigms. Controlled prospective investigations incorporating standardized neuropsychiatric outcomes, objective biomarkers, and longitudinal safety monitoring will be necessary to clarify the therapeutic potential, mechanistic basis, and safety profile of iboga-containing interventions in persistent post-concussive and hypoxic brain injury syndromes.
Unlike purified ibogaine hydrochloride, whole Tabernanthe iboga root bark biomass contains a complex mixture of naturally occurring indole alkaloids, including ibogaine, noribogaine, tabernanthine, ibogaline, voacangine, and related compounds that may collectively contribute to the pharmacologic and experiential profile of iboga preparations. While ibogaine remains the most extensively studied constituent, emerging ethnopharmacologic and pharmacologic literature has increasingly emphasized that whole-plant iboga preparations may not be mechanistically equivalent to isolated ibogaine exposure. The presence of multiple alkaloids with partially overlapping serotonergic, glutamatergic, opioid, sigmareceptor, and neurotrophic signaling properties raises the possibility of an "entourage effect," whereby synergistic or modulatory interactions among alkaloid constituents may influence tolerability, duration of effect, subjective phenomenology, and potential neuroplastic outcomes. Noribogaine, in particular, demonstrates distinct pharmacokinetic and receptor-binding characteristics relative to ibogaine, including prolonged serotonergic and opioidmodulatory activity that may contribute to sustained neurobehavioral effects. Consequently, mechanistic extrapolation from purified ibogaine literature to whole root bark biomass preparations should be interpreted cautiously, and future studies directly comparing isolated ibogaine to whole-alkaloid iboga preparations may be important for clarifying differential therapeutic and safety profiles.
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