Systems and methods for EEG-based iboga alkaloid dosing

Abstract

A method for treatment of a patient using an iboga alkaloid comprises recording a baseline electroencephalogram (EEG) signal from a patient, administering a first dose of an iboga alkaloid to the patient, monitoring a treatment EEG signal from the patient after administering the first dose, determining a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, and administering a second dose of the iboga alkaloid to the patient based on the determined change in the at least one spectral EEG index.

Description

SYSTEMS AND METHODS FOR EEG-BASED IBOGA ALKALOID DOSING CROSS-REFERENCE TO RELATED APPLICATIONS

[0001] This application claims priority to U.S. Application No. 63 / 760,063, titled "EEG-Based Dosing of Ibogaine", filed February 18, 2025, and U.S. Application No.63 / 804,501 titled "EEG-Based Dosing of Ibogaine", filed May 12, 2025, the disclosures of which are hereby incorporated by reference in their entirety.FIELD OF INVENTION

[0002] The present disclosure relates to systems and methods for administering iboga alkaloid compounds based on neurophysiological monitoring, and more particularly to electroencephalography-based dosing of ibogaine and ibogaine derivatives for the treatment of patients with neuropsychiatric disorders.BACKGROUND

[0003] Neuropsychiatric disorders encompass brain diseases or dysfunctions that cause a psychiatric symptom. Neuropsychiatric disorders include depression, schizophrenia, post-traumatic stress disorder, and anxiety disorders. They also include neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, Huntington's disease ataxia, Lewy body disease and others. Many of these neuropsychiatric disorders have few treatment options and there remains a need for treating the disorders and their symptoms.

[0004] Electroencephalography (EEG) is a non-invasive neurophysiological monitoring technique that measures electrical activity of the brain using electrodes placed on the scalp. The electrical signals recorded by EEG reflect the synchronized activity of populations of neurons and are typically characterized by oscillations at various frequencies. These frequency bands include delta (0.5-4 Hz), theta (4-8 Hz), alpha (8-13 Hz), beta (13-30 Hz), and gamma (30-100 Hz), each associated withdifferent brain states and cognitive processes. EEG provides high temporal resolution, enabling real-time monitoring of brain activity.SUMMARY

[0005] Systems and methods for EEG-based iboga alkaloid dosing in accordance with embodiments of the invention are illustrated. One embodiment includes a method for treatment of a patient using an iboga alkaloid, comprising recording a baseline electroencephalogram (EEG) signal from a patient, administering a first dose of an iboga alkaloid to the patient, monitoring a treatment EEG signal from the patient after administering the first dose, determining a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, and administering a second dose of the iboga alkaloid to the patient based on the determined change in the at least one spectral EEG index.

[0006] In a further embodiment, the at least one spectral EEG index includes at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, aperiodic exponent, and peak alpha frequency.

[0007] In still another embodiment, administering the second dose includes administering the second dose when the treatment EEG signal does not demonstrate at least one of increased theta power, increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal.

[0008] In another additional embodiment, the second dose is higher than the first dose.

[0009] In a still further embodiment, the iboga alkaloid includes ibogaine, an ibogaine derivative, or a pharmaceutically acceptable salt or solvate thereof.

[0010] In yet another embodiment, administering the first dose includes administering the iboga alkaloid orally at a dosage of approximately 2-3 mg / kg.

[0011] In a yet further embodiment, administering the second dose includes automatically administering the second dose using an infusion pump in response to the determined change in the at least one spectral EEG index.

[0012] In another additional embodiment, the method further includes steps for continuing to monitor the treatment EEG signal for approximately 12 hours after administering the first dose to determine whether an additional booster dose is needed.

[0013] In a further additional embodiment, a total dosage of the iboga alkaloid administered to the patient is limited to an upper cap of 14 mg / kg.

[0014] In another embodiment again, a total dosage of the iboga alkaloid administered to the patient is limited to an upper cap of 25 mg / kg.

[0015] In a further embodiment again, administering the second dose includes providing an oral form of iboga alkaloid.

[0016] One embodiment includes a system for EEG-based iboga alkaloid dosing, comprising an EEG device configured to record EEG signals from a patient, a memory storing instructions, and a processor in communication with the EEG device and the memory, wherein the processor is configured to execute the instructions to receive a baseline EEG signal from the EEG device, receive a treatment EEG signal from the EEG device after administration of a first dose of an iboga alkaloid to the patient, determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, and generate dosing parameters for a subsequent dose of the iboga alkaloid based on the determined change in the at least one spectral EEG index.

[0017] In still yet another embodiment, the at least one spectral EEG index includes at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, and peak alpha frequency.

[0018] In a still yet further embodiment, the processor is configured to generate dosing parameters indicating administration of the subsequent dose when the treatment EEG signal does not demonstrate at least one of increased theta power,increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal.

[0019] In another additional embodiment, the subsequent dose is higher than the first dose.

[0020] In still another additional embodiment, the method further includes steps for an infusion pump in communication with the processor, wherein the infusion pump is configured to automatically administer the subsequent dose of the iboga alkaloid based on the generated dosing parameters.

[0021] In a still further additional embodiment, the processor is configured to transmit the generated dosing parameters to the infusion pump via a network.

[0022] In still another embodiment again, the EEG device includes a plurality of electrodes arranged according to a 10-10 system ora 10-20 system.

[0023] In a still further embodiment again, the processor is configured to perform spectral decomposition of the treatment EEG signal to extract normalized band power across delta, theta, alpha, beta, and gamma frequency bands.

[0024] In yet another additional embodiment, the processor is further configured to continue monitoring the treatment EEG signal for approximately 12 hours after administration of the first dose to determine whether an additional booster dose is needed.

[0025] In a yet further additional embodiment, the processor is further configured to enforce an upper limit on a total dosage of the iboga alkaloid administered to the patient.

[0026] In yet another embodiment again, the upper limit is 14 mg / kg of the patient.

[0027] In a yet further embodiment again, the upper limit is 25 mg / kg of the patient.

[0028] One embodiment includes a system for EEG-based iboga alkaloid dosing, comprising an EEG device configured to record EEG signals from a patient, an infusion pump configured to administer an iboga alkaloid to the patient, a memory storing instructions, and a processor in communication with the EEG device, theinfusion pump, and the memory, wherein the processor is configured to execute the instructions to receive a baseline EEG signal from the EEG device, receive a treatment EEG signal from the EEG device after administration of a first dose of the iboga alkaloid to the patient via the infusion pump, determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, wherein the at least one spectral EEG index includes at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, and peak alpha frequency, generate dosing parameters indicating administration of a subsequent dose of the iboga alkaloid when the treatment EEG signal does not demonstrate at least one of increased theta power, increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal, and transmit the generated dosing parameters to the infusion pump to automatically administer the subsequent dose of the iboga alkaloid.

[0029] In another additional embodiment again, the iboga alkaloid is ibogaine.

[0030] One embodiment includes a system for EEG-based iboga alkaloid dosing, comprising a controller configured to receive EEG signals of a patient from an EEG device, the EEG signals includes a baseline EEG signal and a treatment EEG signal recorded after administration of a first dose of an iboga alkaloid to the patient, determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, and generate a dosing recommendation fora subsequent dose of the iboga alkaloid based on the determined change in the at least one spectral EEG index.

[0031] Additional embodiments and features are set forth in part in the description that follows, and in part will become apparent to those skilled in the art upon examination of the specification or may be learned by the practice of the invention. A further understanding of the nature and advantages of the present invention may be realized by reference to the remaining portions of the specification and the drawings, which forms a part of this disclosure.BRIEF DESCRIPTION OF FIGURES

[0032] The description and claims will be more fully understood with reference to the following figures and data graphs, which are presented as exemplary embodiments of the invention and should not be construed as a complete recitation of the scope of the invention.

[0033] FIG. 1 is a schematic diagram of a system for EEG-based iboga alkaloid dosing in accordance with an embodiment of the invention.

[0034] FIG. 2 is a block diagram of a treatment controller in accordance with an embodiment of the invention.

[0035] FIG. 3 is a flowchart of a method for EEG-based dosing of iboga alkaloid in accordance with an embodiment of the invention.

[0036] FIG. 4 is a series of graphs depicting normalized power measurements across EEG frequency bands at different time points in accordance with an embodiment of the invention.

[0037] FIG. 5 is a series of scatterplots depicting relationships between baseline EEG power and symptom reduction after ibogaine treatment in accordance with an embodiment of the invention.DETAILED DESCRIPTION

[0038] Iboga alkaloids are alkaloid constituents of the Tabernathe iboga. Ibogaine, ibogaline, ibogamine and tabernathine are representative molecules, and are psychoactive. Despite being known for over a century, the full scope of effects on the human body have remained unclear. For example, ibogaine has been reported to be effective in treating substance addiction, such as alcohol addiction and drug addiction, including opioid and stimulant drugs, but has remained a less used pharmaceutical option due to its hallucinogenic (oneirogenic) effect and potential for neurotoxic and cardiovascular side effects. Approximately 1 in 300 people may suffer from cardiacarrest when treated with ibogaine. Given the dangers of the drug, ibogaine has been classified in the United States as a Schedule I controlled substance.

[0039] Recently, Ibogaine has demonstrated additional therapeutic potential for treating neuropsychiatric disorders, including post-traumatic stress disorder (PTSD), depression, anxiety, and cognitive impairment associated with traumatic brain injury (TBI), as discussed in U.S. Patent Application No. 18 / 181 ,513 titled "COMPOSITIONS OF IBOGA ALKALOIDS AND METHODS OF TREATMENT" filed August 28, 2024, the entirety of which is hereby incorporated by reference. Appropriate dosing levels for individual patients is a particular issue for dangerous drugs, especially those with hallucinogenic effects. Under-dosing may result in reduced treatment efficacy, as the patient may not experience sufficient neurophysiological engagement to achieve therapeutic benefits. Over-dosing may increase the risk of cardiovascular side effects or other unwanted adverse events such as overextended hallucination periods. Current ibogaine dosing techniques rely on subjective reports of ibogaine-induced symptoms rather than objective biological indicators of neural engagement, which may lead to inconsistent treatment outcomes across patients.

[0040] The systems and methods described herein address these challenges by utilizing electroencephalography (EEG) monitoring to guide ibogaine dosing through real-time analysis of spectral EEG indices. EEG provides sub-millisecond temporal resolution and captures cortical oscillations that serve as markers of different brain states. Spectral decomposition of EEG signals allows extraction of measures including normalized band power across delta, theta, alpha, beta, and gamma frequency bands, as well as associated derived metrics such as theta / beta ratio and peak alpha frequency. These spectral EEG indices may serve as objective markers of ibogaine's effects on neural function.

[0041] Administration of ibogaine has been observed to modulate cortical oscillations in a characteristic pattern. Specifically, ibogaine treatment may result in increased theta power (4-8 Hz), increased alpha power (8-13 Hz), decreased betapower (13-30 Hz), decreased gamma power (30-50 Hz), increased theta / beta ratio, and decreased peak alpha frequency compared to baseline measurements. These changes reflect an overall slowing of spontaneous cortical oscillations after ibogaine treatment. By monitoring these spectral EEG indices during treatment, a clinician or automated system may determine whether a patient has achieved target drug effects and may adjust dosing accordingly.

[0042] The EEG-based dosing approach enables personalized treatment administration guided by neurophysiological indicators. Rather than relying on subjective patient reports alone, the systems and methods described herein provide objective measures of neural engagement that may be used to titrate ibogaine dosing. When monitored EEG signals do not demonstrate the characteristic spectral changes associated with ibogaine treatment, additional doses may be administered to achieve target drug effects. Conversely, when monitored EEG signals demonstrate sufficient spectral changes, further dosing may be withheld to reduce the risk of over-dosing. This approach may reduce rates of both under-dosing and over-dosing, thereby improving treatment outcomes while minimizing cardiovascular or other unwanted side effects.

[0043] Pre-treatment EEG recordings may also provide biomarkers for predicting individual treatment outcomes and determining treatment viability. Baseline measures of cortical oscillations, including peak alpha frequency and spectral power across frequency bands, have been observed to correlate with improvements in executive function, PTSD symptoms, and anxiety symptoms after ibogaine treatment. Patients demonstrating low peak alpha frequency, low alpha power, high delta power, high beta power, and high gamma power at baseline may be identified as candidates who may benefit from ibogaine treatment. The EEG-based approach thus enables both patient selection and treatment monitoring using accessible and affordable neuroimaging technology. EEG-based dosing systems are described below.

[0044] EEG-based dosing systems can utilize EEG recordings obtained during treatment to guide dosing overthe course of the treatment. In numerous embodiments, dosing is automatically administered via an infusion pump. In various embodiments, the dosing is provided to a clinician for provisioning. Referring to FIG. 1 , a system 100 configured for EEG-based ibogaine dosing is illustrated. The system 100 includes a treatment controller 110, an EEG device 120, an infusion pump 130, and a network 140. Each component is communicatively coupled to other component(s) via the network, which may include one or more various communication pathways such as local area networks, wide area networks, or the Internet.

[0045] The treatment controller may be implemented as a server, computing device, or other processing apparatus configured to process data and coordinate operations within the system. The treatment controller may receive EEG data from the EEG device via the network, analyze the received EEG data to determine any changes in dosing, and transmit dosing instructions to the infusion pump based on the analysis. In some cases, the treatment controller may execute software applications that implement algorithms for spectral decomposition of EEG signals and comparison of spectral indices against baseline measurements or predetermined thresholds.

[0046] EEG devices are configured to record electroencephalogram signals from a patient. EEG devices may apply EEG sensors to the forehead and / or scalp of the patient for monitoring cortical oscillations. In some cases, EEG devices may utilize standard EEG sensor placement according to the 10-10 system or the 10-20 system, with sensors positioned at standardized locations on the scalp. EEG devices may include a cap or headset with multiple electrodes, such as 64 Ag-AgCI channels, arranged according to the selected placement system.

[0047] In many embodiments, EEG devices are configured with a sampling rate sufficient to capture cortical oscillations across frequency bands of interest. In some cases, EEG devices may sample EEG signals at a rate of 1 kHz or higher, such as 10 kHz, to provide adequate temporal resolution for spectral analysis. EEG devices maymaintain impedance below predetermined thresholds to ensure signal quality. In some cases, impedance may be maintained below 10 kOhms in a majority of channels, such as greater than 80% of channels, and below 25 kOhms in substantially all channels, such as greater than 99% of channels. In numerous embodiments, EEG devices transmit recorded EEG signals to a treatment controller via a network for analysis.

[0048] Infusion pumps can be configured to deliver doses of ibogaine, an ibogaine derivative, or a pharmaceutically acceptable salt and / or solvate thereof to the patient. In numerous embodiments, infusion pumps receive dosing instructions from a treatment controller via a network and may administer ibogaine intravenously or through other delivery routes. In some embodiments, the infusion pump may automatically adjust dosing parameters based on instructions received from the treatment controller, enabling automated titration of ibogaine based on real-time EEG monitoring. In various embodiments, the infusion pump may display recommended dosing parameters for a clinician to review and approve before administration.

[0049] Networks facilitate communication between treatment controllers, EEG devices, and infusion pumps. Networks can include wired connections, wireless connections, or combinations thereof. In some cases, the network may include secure communication protocols to protect patient data transmitted between components of the system. The configuration of the system allows for continuous or intermittent monitoring of EEG signals from the patient and automated or guided adjustment of ibogaine dosing based on the monitored EEG data.

[0050] Turning now to FIG. 2, a block diagram for a treatment controller in accordance with an embodiment of the invention is illustrated. The treatment controller 200 can be used as the treatment controller 110 described with reference to FIG. 1. The treatment controller 200 includes a processor 210, an input / output interface 220, and a memory 230. Processors are any logic processing circuitry such as central processing units (CPUs), graphics processing units (GPUs), field-programmable gate arrays (FPGAs), application-specific integrated circuits (ASICs), and / or or any otherlogic processing circuitry capable of executing instructions and managing operations of the treatment controller. The input / output interface facilitates communication between the treatment controller and external devices, such as the EEG devices and the infusion pumps. The memory can be volatile memory, nonvolatile memory, or a combination thereof that stores data and instructions for the treatment controller.

[0051] Within the memory 230, a dosing control application 232 is stored. Dosing control applications contains instructions that, when executed by the processor, enable the treatment controller to analyze EEG signals and determine appropriate dosing of ibogaine based on spectral EEG indices. The processor can communicate with the memory to retrieve and execute the dosing control application, and utilizes the input / output interface to receive EEG data and transmit dosing commands to connected devices.

[0052] Turning now to FIG. 3, a process for EEG-based dosing of iboga alkaloid in accordance with an embodiment of the invention is illustrated. The process 300 provides a feedback loop that enables iterative adjustment of iboga alkaloid dosing based on real-time EEG monitoring, allowing for personalized treatment administration guided by neurophysiological indicators. The process 300 includes beginning (310) an EEG recording of the patient is initiated. The EEG device may apply EEG sensors to the forehead and / or scalp of the patient and may record EEG signals at a sampling rate sufficient to capture cortical oscillations across frequency bands of interest. The recorded EEG signals provide baseline measurements against which subsequent treatment EEG signals can be compared.

[0053] A first dose of iboga alkaloid is administered (320) to the patient. In some cases, the administration is of an initial dose of an iboga alkaloid such as (but not limited to) ibogaine delivered orally at approximately 2-3 mg / kg. In various embodiments, the initial dose may be delivered intravenously. The infusion pump may administer the initial dose based on instructions received from the treatment controller, or a clinician may administer the initial dose manually.

[0054] Following administration of the first dose, the EEG signals from the patient are analyzed to determine (330) any change in EEG indices. In numerous embodiments, the treatment controller may receive EEG signals from the EEG device and may perform spectral decomposition to extract spectral EEG indices including normalized band power across delta, theta, alpha, beta, and gamma frequency bands, as well as calculate theta / beta ratio and peak alpha frequency.

[0055] Based on the determined change in EEG indices against the baseline, dosing parameters for a subsequent dose of iboga alkaloid are modified (340). In some cases, modification of dosing parameters is based on at least one of change in theta power, change in theta / beta ratio, decreased gamma power, and change in the aperiodic exponent. When the treatment EEG signals demonstrate at least one of increased theta power, increased theta / beta ratio, decreased gamma power, or an increase in aperiodic exponent, compared to baseline, the dosing parameters may be modified to increase the subsequent dose. If EEG signals demonstrate sufficient spectral changes, the dosing parameters may be modified to reduce or withhold the subsequent dose. The subsequent modified dose is then administered (350) to the patient.

[0056] In many embodiments, an upper limit on the dosage can be enforced to prevent accidental overdosing. For example, in numerous embodiments, the total ibogaine dosage may be limited up to 14 mg / kg. In some embodiments, the upper cap may be at or above 25 mg / kg based on the particular patient. The infusion pump may automatically administer the subsequent dose based on the modified dosing parameters, or the treatment controller may display recommended dosing parameters for a clinician to review and approve before administration.

[0057] After administration of the second dose, if treatment is concluded, the process 300 ends. If treatment is not concluded, the process 300 returns to determine further changes in EEG indices, allowing for continued monitoring and adjustment of dosing parameters as needed. In some cases, the process continues monitoring EEGspectral indices approximately 12 hours after initial administration to guide whether an additional booster dose is needed. The 12-hour booster monitoring timepoint allows the treatment controller to assess whether the patient has achieved and maintained target drug effects or whether additional ibogaine administration may be beneficial.

[0058] Referring to FIG. 4, a series of line graphs illustrating normalized power measurements across different EEG frequency bands at three time points is depicted. The graphs are organized in a grid format with two rows representing a frontal region of interest (ROI) and a posterior ROI, and four columns representing the theta, alpha, beta, and gamma frequency bands. Each graph displays normalized power as a percentage on the vertical axis and three measurement time points on the horizontal axis: baseline, post-ibogaine, and 1-month follow-up. Error bars representing standard error of the mean are shown at each data point.

[0059] The pattern of spectral changes depicted in FIG. 4 demonstrates the characteristic modulation of cortical oscillations following ibogaine treatment. The increase in slower oscillations (theta and alpha bands) and decrease in faster oscillations (beta and gamma bands) post-ibogaine reflects an overall slowing of spontaneous cortical activity. These spectral EEG indices may serve as objective markers of ibogaine's effects on neural function and may be utilized by the treatment controller to guide dosing decisions during the EEG-based dosing process described with reference to FIG. 3.

[0060] Referring to FIG. 5, a series of scatterplots depicting relationships between baseline normalized power measurements and percentage reduction in PTSD symptoms and anxiety symptoms one month after ibogaine treatment is illustrated. The top row of scatterplots shows correlations between baseline normalized power and PTSD symptom reduction for delta, alpha, and gamma frequency bands. The bottom row of scatterplots shows correlations between baseline normalized power and anxiety symptom reduction for alpha, beta, and gamma frequency bands. Eachscatterplot displays individual data points as open circles, a regression line, and a shaded region representing the 95% confidence interval around the regression line.

[0061] The scatterplots in FIG. 5 demonstrate that baseline spectral power measurements may serve as predictive biomarkers for treatment outcomes following ibogaine administration. The delta and gamma plots in the top row and the beta and gamma plots in the bottom row show negative correlations, indicating that higher baseline power in these frequency bands is associated with greater symptom improvement. The alpha plots in both rows show positive correlations, indicating that lower baseline alpha power is associated with greater symptom improvement. The baseline power values reflect average power from channels that showed statistically significant correlations after false discovery rate correction.

[0062] With continued reference to FIG. 5, the treatment controller may utilize baseline EEG measures to predict treatment outcomes for individual patients. Baseline EEG measures that may be used as predictive biomarkers include low peak alpha frequency, low alpha power, high delta power, high beta power, and high gamma power. Patients demonstrating these baseline spectral characteristics may be identified as candidates who may experience greater reductions in PTSD and anxiety symptoms following ibogaine treatment. The treatment controller may compare baseline spectral power measurements against predetermined thresholds to generate predictions of treatment response.

[0063] The predictive biomarkers depicted in FIG. 5 may be used by the treatment controller to determine treatment viability prior to ibogaine administration. When a baseline EEG recording from a patient demonstrates low peak alpha frequency, low alpha power, high delta power, high beta power, and high gamma power compared to predetermined thresholds, the treatment controller may provide an indicator of treatment viability. The predetermined thresholds may be established based on population-level data correlating baseline spectral measures with treatment outcomes. In some cases, the treatment controller may generate a treatment viability score basedon multiple baseline spectral measures, with higher scores indicating greater predicted treatment response.

[0064] Although specifics are discussed above, many different systems and methods can be implemented in accordance with many different embodiments of the invention. Additionally, while ibogaine is discussed as a particular iboga alkaloid used for treatment herein, any number of different iboga alkaloids can be used as appropriate to the requirements of specific applications of the invention. It is therefore to be understood that the present invention may be practiced in ways other than specifically described, without departing from the scope and spirit of the present invention. Thus, embodiments of the present invention should be considered in all respects as illustrative and not restrictive. Accordingly, the scope of the invention should be determined not by the embodiments illustrated, but by the appended claims and their equivalents.

Claims

CLAIMS1. A method for treatment of a patient using an iboga alkaloid, comprising:recording a baseline electroencephalogram (EEG) signal from a patient; administering a first dose of an iboga alkaloid to the patient;monitoring a treatment EEG signal from the patient after administering the first dose;determining a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal; andadministering a second dose of the iboga alkaloid to the patient based on the determined change in the at least one spectral EEG index.

2. The method of claim 1, wherein the at least one spectral EEG index comprises at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, aperiodic exponent, and peak alpha frequency.

3. The method of claim 2, wherein administering the second dose comprises administering the second dose when the treatment EEG signal does not demonstrate at least one of increased theta power, increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal.

4. The method of claim 3, wherein administering the second dose comprises increasing a dosage compared to the first dose.

5. The method of claim 1, wherein the iboga alkaloid comprises ibogaine, an ibogaine derivative, or a pharmaceutically acceptable salt or solvate thereof.

6. The method of claim 1 , wherein administering the first dose comprises administering the iboga alkaloid orally at a dosage of approximately 2-3 mg / kg.

7. The method of claim 1, wherein administering the second dose comprises automatically administering the second dose using an infusion pump in response to the determined change in the at least one spectral EEG index.

8. The method of claim 1, further comprising continuing to monitor the treatment EEG signal for approximately 12 hours after administering the first dose to determine whether an additional booster dose is needed.

9. The method of claim 1 , wherein a total dosage of the iboga alkaloid administered to the patient is limited to an upper cap of 14 mg / kg.

10. The method of claim 1, wherein a total dosage of the iboga alkaloid administered to the patient is limited to an upper cap of 25 mg / kg.

11. The method of claim 1, wherein administering the second dose comprises providing an oral form of iboga alkaloid.

12. A system for EEG-based iboga alkaloid dosing, comprising:an EEG device configured to record EEG signals from a patient;a memory storing instructions; anda processor in communication with the EEG device and the memory, wherein the processor is configured to execute the instructions to:receive a baseline EEG signal from the EEG device;receive a treatment EEG signal from the EEG device after administration of a first dose of an iboga alkaloid to the patient;determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal; andgenerate dosing parameters for a subsequent dose of the iboga alkaloid based on the determined change in the at least one spectral EEG index.

13. The system of claim 12, wherein the at least one spectral EEG index comprises at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, and peak alpha frequency.

14. The system of claim 13, wherein the processor is configured to generate dosing parameters indicating administration of the subsequent dose when the treatment EEG signal does not demonstrate at least one of increased theta power, increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal.

15. The system of claim 14, wherein the generated dosing parameters further indicate an increase in dosage.

16. The system of claim 12, further comprising an infusion pump in communication with the processor, wherein the infusion pump is configured to automatically administer the subsequent dose of the iboga alkaloid based on the generated dosing parameters.

17. The system of claim 16, wherein the processor is configured to transmit the generated dosing parameters to the infusion pump via a network.

18. The system of claim 12, wherein the EEG device comprises a plurality of electrodes arranged according to a 10-10 system ora 10-20 system.

19. The system of claim 12, wherein the processor is configured to perform spectral decomposition of the treatment EEG signal to extract normalized band power across delta, theta, alpha, beta, and gamma frequency bands.

20. The system of claim 12, wherein the processor is further configured to continue monitoring the treatment EEG signal for approximately 12 hours after administration of the first dose to determine whether an additional booster dose is needed.

21. The system of claim 12, wherein the processor is further configured to enforce an upper limit on a total dosage of the iboga alkaloid administered to the patient.

22. The system of claim 21 , wherein the upper limit is 14 mg / kg of the patient.

23. The system of claim 21 , wherein the upper limit is 25 mg / kg of the patient.

24. A system for EEG-based iboga alkaloid dosing, comprising:an EEG device configured to record EEG signals from a patient;an infusion pump configured to administer an iboga alkaloid to the patient; a memory storing instructions; anda processor in communication with the EEG device, the infusion pump, and the memory, wherein the processor is configured to execute the instructions to:receive a baseline EEG signal from the EEG device;receive a treatment EEG signal from the EEG device after administration of a first dose of the iboga alkaloid to the patient via the infusion pump;determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal, wherein the at least one spectral EEG index comprises at least one of theta power, alpha power, beta power, gamma power, theta / beta ratio, and peak alpha frequency;generate dosing parameters indicating administration of a subsequent dose of the iboga alkaloid when the treatment EEG signal does not demonstrate at least one of increased theta power, increased alpha power, decreased beta power, decreased gamma power, increased theta / beta ratio, increased aperiodic exponent, and decreased peak alpha frequency compared to the baseline EEG signal; and transmit the generated dosing parameters to the infusion pump to automatically administer the subsequent dose of the iboga alkaloid.

25. The system of claim 24, wherein the iboga alkaloid is ibogaine.

26. A system for EEG-based iboga alkaloid dosing, comprising:a controller configured to:receive EEG signals of a patient from an EEG device, the EEG signals comprising a baseline EEG signal and a treatment EEG signal recorded after administration of a first dose of an iboga alkaloid to the patient;determine a change in at least one spectral EEG index by comparing the treatment EEG signal to the baseline EEG signal; andgenerate a dosing recommendation for a subsequent dose of the iboga alkaloid based on the determined change in the at least one spectral EEG index.

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