Can ibogaine repair brain damage in multiple sclerosis? New case reports spark interest

In a recent case report published in Frontiers in Immunology, scientists in Canada described how an experimental treatment using a naturally derived substance called ibogaine appeared to improve symptoms and brain health in two individuals with multiple sclerosis. These initial findings, based on brain scans and patient reports, suggest that ibogaine could potentially offer a new approach for managing this challenging neurological condition.

Multiple sclerosis is a disease that affects the brain and spinal cord, which together form the central nervous system. In multiple sclerosis, the protective covering around nerve fibers, called myelin, is damaged. This damage disrupts communication between the brain and the rest of the body. The disease can lead to a wide range of symptoms, including fatigue, mobility problems, pain, vision issues, and difficulties with balance and coordination.

Currently available treatments for multiple sclerosis often focus on managing symptoms and slowing the progression of the disease. However, these treatments do not always stop the disease from getting worse, and they can have undesirable side effects.

Ibogaine is a psychoactive substance derived from the root bark of an African shrub. It has historically been used in traditional spiritual and healing practices. In more recent times, ibogaine has gained attention for its potential therapeutic uses, particularly in treating addiction.

Researchers are exploring ibogaine’s effects on the brain, and early studies suggest it may have several actions that could be beneficial for brain health. These actions include influencing brain chemicals that are important for nerve cell communication and flexibility, supporting the growth and survival of nerve cells, reducing brain inflammation, and improving the energy production within cells. Researchers believe these combined effects could potentially help the brain repair itself and restore function in conditions where nerve cells are damaged.

The new case report details the experiences of two patients with multiple sclerosis who received ibogaine treatment, which they had initially sought for other health problems.

Patient A was a 41-year-old man who had been diagnosed with relapsing-remitting multiple sclerosis. This form of multiple sclerosis is characterized by periods when symptoms worsen, followed by periods of improvement. In addition to multiple sclerosis, Patient A also experienced post-traumatic stress disorder, major depressive disorder, and had suffered a traumatic brain injury ten years prior.

Before receiving the experimental treatment, his multiple sclerosis symptoms included increasing difficulty with movement, coordination problems, some issues with bladder control, slowed thinking, short-term memory difficulties, and intense vertigo, a sensation of spinning. He was prescribed medication for multiple sclerosis a month before the treatment, but his neurological condition continued to decline. Brain scans taken before treatment revealed a significant lesion, an area of damage, in a specific region of his brain.

Patient A underwent an ibogaine treatment program at a specialized facility in Mexico. Before the treatment, he had a thorough medical evaluation, including heart and metabolic tests. During the treatment, he received a specific dose of ibogaine in capsules over a short period. To minimize potential heart-related risks associated with ibogaine, he was given magnesium before treatment and was monitored closely by medical staff for 24 hours afterwards. Following the initial treatment, he continued a very low daily dose of ibogaine.

Remarkably, just one day after the ibogaine treatment, Patient A reported that his multiple sclerosis symptoms had lessened. Two months later, his scores on a questionnaire measuring fatigue related to multiple sclerosis had significantly improved. His bladder control issues had completely resolved. He also showed noticeable improvement in his overall physical and mental well-being. Impressively, despite previous difficulty walking, he later reported participating in a 200-mile ultramarathon. Importantly, one year after treatment, he had not experienced a return of the vertigo symptoms that had troubled him before.

Brain scans were repeated three months after the treatment. These scans showed a substantial reduction in the size of the brain lesion, shrinking by 71%. Additionally, a measurement called the Apparent Diffusion Coefficient, which provides information about tissue health, decreased within the lesion area. A decrease in this value can suggest improved nerve fiber integrity, reduced inflammation, or the repair of myelin.

Further analysis of the brain scans indicated changes in the thickness of certain areas of the brain’s outer layer, the cortex, and in deeper brain structures. Some areas showed thinning of the cortex, while others showed thickening. These changes were observed in brain regions known to be involved in emotions, thinking, and movement.

Patient B was a 44-year-old woman who had been diagnosed with secondary progressive multiple sclerosis in 2018. This form of multiple sclerosis typically follows an initial relapsing-remitting course and is marked by a steady worsening of symptoms over time. Patient B also had complex post-traumatic stress disorder from childhood trauma and had recently experienced a divorce. When she arrived for treatment, her symptoms included severe muscle stiffness, muscle wasting in her limbs, difficulties with bladder and bowel control, and infrequent but intense episodes of vertigo. She needed a wheelchair for most activities, though she could transfer herself with support. Due to exercise intolerance, she could only tolerate very short physiotherapy sessions.

Patient B had been using various medications, including cannabis, to manage her multiple sclerosis symptoms. She had also tried ketamine infusions for chronic pain, but stopped treatment a year prior. Similar to Patient A, Patient B underwent a thorough medical evaluation and received ibogaine treatment at the same facility. She received a lower dose of ibogaine than Patient A due to an increase in muscle stiffness she experienced at the start of treatment. She also continued a very low daily dose of ibogaine after the initial treatment.

Following treatment, Patient B reported a decrease in muscle stiffness. Her score on a scale measuring walking ability improved from being confined to a wheelchair to being able to walk a few steps with support. This improvement was sustained two months later. She was also able to increase her physiotherapy sessions from 10 minutes to a full hour and reported ongoing gradual improvement two years later. Questionnaires revealed improvements in her chronic pain, fatigue, bladder control, and bowel control. She also showed improvements in her physical and mental well-being scores.

Brain scans were repeated ten months after Patient B’s treatment. Similar to Patient A, the brain scans showed changes in cortical thickness and in deeper brain structures. Some areas of the cortex showed thinning, while others showed thickening. The Apparent Diffusion Coefficient measurements also changed in various brain regions, with both increases and decreases observed. These changes were found in areas associated with movement, sensation, emotions, and thinking. Clustering analysis of cortical thickness changes revealed coordinated patterns of change in brain networks related to motor function, thinking, and emotion regulation.

These case reports offer initial encouraging evidence that ibogaine treatment may be associated with both clinical improvements and changes in brain structure and function in individuals with multiple sclerosis. The observed reduction in lesion size and changes in Apparent Diffusion Coefficient in Patient A suggest the possibility of myelin repair and reduced inflammation.

The patterns of cortical and subcortical changes in both patients point to ibogaine’s potential to promote brain plasticity, the brain’s ability to reorganize itself by forming new neural connections throughout life. These findings raise the possibility that ibogaine could help to modulate brain circuits involved in multiple sclerosis symptoms, potentially improving motor function, reducing pain, and enhancing emotional well-being.

But it is important to understand that case reports like these have inherent limitations. They describe the experiences of only two individuals and cannot definitively prove that ibogaine caused the observed improvements. It is possible that other factors contributed to the positive outcomes, or that the improvements were coincidental. Case reports are primarily useful for generating hypotheses and highlighting potential areas for further investigation, rather than establishing cause-and-effect relationships or providing definitive conclusions about treatment effectiveness.

Ibogaine can also have some significant side effects. One of the main concerns is its effect on the heart, as it can disrupt the normal rhythm and potentially cause serious problems. People taking ibogaine may also experience nausea, vomiting, and difficulties with muscle coordination. Additionally, because ibogaine is a psychoactive substance, it can cause intense and sometimes challenging psychological experiences.

To determine whether ibogaine is a safe and effective treatment for multiple sclerosis, substantial additional research is needed. Future research should include well-designed, controlled clinical trials with larger groups of participants. These studies should compare the outcomes of individuals receiving ibogaine to those receiving a placebo or standard treatments. Such research would help to confirm these initial findings, clarify the potential benefits and risks of ibogaine treatment for multiple sclerosis, and explore the mechanisms by which ibogaine may exert its effects on the brain in this condition.

The report, “Significant lesion reduction and neural structural changes following ibogaine treatments for multiple sclerosis,” was authored by David Qixiang Chen, José Adalberto Inzunza Domínguez, Juan Manuel Valle Uzeta, Abhiram P. Pushparaj, and Jonathan E. Dickinson.