Ketamine: Calming The Neuroinflammatory Storm
Understanding microglial biology, chronic stress, and ketamine's clinical role beyond depression
Master the neuroscience behind ketamine and microglial biology to elevate clinical decision-making across complex, treatment-resistant cases.
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Course Description
Chronic stress, adverse childhood experiences, and persistent neuroinflammation are reshaping the cases clinicians see every day. Patients arrive with layered diagnoses, histories that do not resolve with standard protocols, and a nervous system that conventional frameworks have not fully addressed.
This course reframes ketamine not as a trend but as a clinically grounded intervention rooted in microglial biology. Dr. Spencer Zimmerman, dual-licensed chiropractor and nurse practitioner with advanced functional neurology training, walks through the M1 and M2 microglial polarization states, the inflammatory cytokine cascades driving treatment resistance, and how sub-anesthetic ketamine modulates neuroplasticity, synaptogenesis, and the brain-gut axis. Clinicians leave with a mechanistic framework they can apply immediately, whether or not ketamine is within their scope of practice.
What you’ll learn:
- Identify M0, M1, and M2 microglial states and the signals driving each
- Explain how chronic stress alters hippocampal and prefrontal neurocircuitry
- Describe ketamine's anti-inflammatory effects on key cytokine cascades
- Apply ketamine's neuroplasticity mechanisms beyond depression clinically
- Evaluate patient readiness and collaborative care roles for ketamine therapy
More About This Course
Ketamine has moved from the periphery of psychiatric research into mainstream clinical conversation faster than most providers have had time to process the underlying science. Ketamine neuroinflammation, microglial activation, sub-anesthetic dosing, and neuroplasticity are now terms appearing in journals across neurology, psychiatry, and rehabilitation medicine. For clinicians working within functional neurology, understanding the biological mechanisms behind this shift is not optional. It is the difference between observing a trend and being equipped to guide patients through it intelligently.
This course builds that capability from the ground up. Dr. Spencer Zimmerman begins with the foundational biology of microglial cells, detailing the M0, M1, and M2 polarization states and the cytokine signals that drive each. From there, the course maps how chronic stress, adverse childhood experiences, and persistent neuroinflammation alter hippocampal structure, amygdala reactivity, prefrontal function, and synaptogenesis. Clinicians gain a precise mechanistic understanding of how ketamine modulates pro-inflammatory markers including interleukin-1 beta, interleukin-6, and tumor necrosis factor alpha, and how that modulation translates to antidepressant, anxiolytic, and neuroprotective outcomes. The course extends these principles into applications beyond depression, covering post-stroke recovery, traumatic brain injury, multiple sclerosis, and the brain-gut-microbiome axis. Clinical case examples and practical precaution frameworks make the content immediately applicable.
This course is designed for licensed chiropractors, chiropractic neurologists, functional neurology practitioners, and allied healthcare providers who regularly manage patients with complex neurological, mood, or stress-related presentations. It is equally valuable for clinicians whose patients are already seeking ketamine therapy and who want to serve as informed guides within that process, even without prescriptive authority.
Components
Educational Syllabus
- The Microglial Cell as a Clinical Target
- Discover how the brain's resident immune cells govern plasticity, synaptogenesis, neurogenesis, and neurodegeneration. Understanding microglial polarization states is the foundation for everything ketamine changes.
- Chronic Stress and the Inflamed Brain
- Chronic stress does more than affect mood. Trace how persistent psychosocial and physiological stressors remodel the hippocampus, amygdala, and prefrontal cortex through microglial priming and cytokine dysregulation.
- How Ketamine Calms the Neuroinflammatory Storm
- Examine the precise mechanisms by which sub-anesthetic ketamine reduces IL-1 beta, IL-6, and TNF-alpha, restores dendritic spine density, and promotes durable neuroplasticity through the HPA axis and kynurenine pathway.
- Expanding the Clinical Lens Beyond Depression
- Apply ketamine's neuroinflammatory framework to post-stroke depression, TBI recovery, multiple sclerosis, and the brain-gut axis. Learn the precautions and collaborative care strategies that produce the best patient outcomes.
Venue, Hotels & Schedule
Also includes


Ketamine: Calming The Neuroinflammatory Storm
Master the neuroscience behind ketamine and microglial biology to elevate clinical decision-making across complex, treatment-resistant cases.
$
$
(
$
The Carrick Institute team is ready to assist with enrollment, CE approval, or program planning. Email visit our CE Portal or Contact Us directly.
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