Neuroinflammation: When the Brain’s Immune Response Runs Long

What Is Neuroinflammation?

Neuroinflammation refers to an inflammatory response within the central nervous system (CNS), the brain and spinal cord; characterized by activation of brain-resident immune cells (e.g., microglia, astrocytes), release of cytokines, chemokines, reactive oxygen species, and disruption of the blood–brain barrier (BBB).

While acute inflammation is protective (to clear debris, respond to injury, fight pathogens), chronic or dysregulated neuroinflammation becomes damaging, leading to neuronal dysfunction, synaptic pruning, glial scarring, and sometimes neurodegeneration.

Mechanistically, when triggers (trauma, toxins, infection) persist or the regulation is faulty, microglia (the brain’s innate immune cells) may shift into a prolonged pro-inflammatory phenotype, producing excessive cytokines (e.g. IL-1β, IL-6, TNF-α) and reactive oxygen/nitrogen species.  These mediators further damage neurons, impair mitochondrial function, and disrupt homeostasis.

Also, when the blood–brain barrier becomes leaky (due to systemic inflammation, toxins, or injury), peripheral immune cells (T cells, macrophages) can cross into the CNS and amplify inflammation.

How Neuroinflammation Emerges Across Conditions

Neuroinflammation doesn’t come from one cause, it’s a final common pathway in many brain-stress and injury conditions. Below are common drivers:

• Traumatic Brain Injury (TBI) / Concussion: mechanical disruption damages neurons and vasculature, releasing DAMPs (damage-associated molecular patterns) that activate microglia and inflammasomes (like NLRP3). 

• Post-Traumatic Stress Disorder (PTSD) / Psychological Trauma: chronic stress triggers systemic inflammatory signaling, HPA axis dysregulation, and glial priming. 

• Psychiatric Disorders: depression, bipolar disorder, and schizophrenia often show elevated peripheral and central inflammatory markers. The “neuroinflammation hypothesis of depression” posits that cytokines may drive changes in neurotransmitter systems, neuroplasticity, and mood regulation. 

• Toxins / Environmental Exposures: heavy metals, mold mycotoxins, and pesticides can trigger oxidative stress, glial activation, and BBB disruption. 

• Chronic Illness & Systemic Inflammation: conditions like autoimmune disease, metabolic syndrome, chronic infections (e.g. Lyme) can drive systemic inflammation, which “leaks” into the CNS via the organ-brain axis. 

• Neurodevelopmental Conditions (ASD, etc.): some research implicates immune activation, microglial dysregulation, and higher baseline neuroinflammation in subsets of autism spectrum disorder. These shifts may impact synaptic pruning, connectivity, and plasticity. (While direct, controlled human evidence is still evolving, many functional neurologists track inflammatory markers in these populations.)

• Residual Infections: persistent pathogens (e.g. Lyme, viruses) may maintain a low-level inflammatory state in the CNS if not adequately cleared.

Importantly, neuroinflammation is not limited to these; many other insults (ischemia, metabolic stress, aging, vascular disease) feed into similar pathways.

Why Neuroinflammation Matters: Effects on Mood, Cognition & Brain Function

When neuroinflammation persists, the following often emerge:

• Cognitive symptoms: brain fog, slowed processing, memory lapses, executive dysfunction

• Mood & emotional dysregulation: anxiety, irritability, depression, mood swings

• Neurotransmitter disruption: Cytokines can alter tryptophan metabolism (shifting toward kynurenine pathways), reduce serotonin, impair dopamine and glutamate balance

• Neuronal injury / synaptic loss: Chronic inflammation triggers synapse retraction, excitotoxicity, apoptosis

• Mitochondrial dysfunction: ROS, cytokines, and nitric oxide impair mitochondrial energy production, reducing cellular resilience

• Glial and astrocyte dysfunction: affecting support for neurons, ion balance, nutrient transport, and clearing of metabolic waste

These cascading effects link inflammation to mental health, neurodegenerative disease, and chronic neurologic dysfunction.

How Neuromodulation Helps: rTMS, MeRT & Inflammation Control

In addition to removing upstream triggers, neuromodulation offers a powerful tool to quell neuroinflammation and promote healing:

• rTMS (repetitive Transcranial Magnetic Stimulation): Studies show rTMS can shift microglia toward anti-inflammatory states, reduce pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), suppress apoptosis, and promote neurogenesis. 

• Animal and clinical models suggest rTMS also reduces mitochondrial damage and glial activation after remote brain injury. 

• Additional evidence indicates that rTMS modulates expression of inflammatory genes in astrocytes and microglia, and may dampen pathways like NF-κB, STAT, and other intracellular inflammatory signaling. 

• MeRT (Magnetic e-Resonance Therapy) builds on the same principle, using EEG-guided neuromodulation to correct dysfunctional brain wave patterns, promoting regulation rather than hyperexcitability. While direct mechanistic studies on MeRT and neuroinflammation are fewer, the logic is that by restoring balanced brain rhythms, you reduce excitotoxic stress, neural overactivation, and maladaptive glial activation. As rTMS is a close cousin in mechanism, much of the neuroinflammatory benefit is likely shared.

• By reducing local neuroinflammation, neuromodulation enhances brain plasticity and supports recovery pathways that are otherwise impeded by chronic immune activation.

Functional Health & Root-Cause Strategy: Addressing What Drives Inflammation

Neuromodulation is powerful but most effective when paired with functional health strategies that tackle root drivers. We use a multi-pronged approach:

1. Toxin reduction / detox support — mold/mycotoxin protocols, heavy metal clearance, liver detox pathways

2. Immune balance & microbial health — gut repair, managing dysbiosis, controlling latent infections

3. Metabolic & mitochondrial support — optimizing methylation, B vitamins, antioxidants, mitochondrial cofactors

4. Hormone & neurotransmitter balance — ensuring thyroid, adrenal, sex hormone equilibrium, serotonin/dopamine support

5. Lifestyle foundations — sleep, stress regulation, movement, light exposure

Combined, these reduce the “fuel” feeding neuroinflammation and create a more receptive internal environment for neuronal healing.

SPIN / OT & the Mind–Body Component

At Brain Treatment Center NoVa, our SPIN OT program is uniquely designed to complement neuromodulation in healing neuroinflammation:

• We incorporate somatic regulation, myofascial release, movement therapy, and sensory integration to help the nervous system down-regulate and re-establish healthy autonomic balance.

• These modalities help relieve neurogenic tension, reduce peripheral stress signals transmitted to the brain, and support better circulation, lymphatic flow, and neural connectivity.

• By engaging both the brain (via MeRT, rTMS) and body (via OT/SPIN), we aim to reduce persistent inflammatory feedback loops and support whole-person neural healing.

Conclusion & Next Steps

Neuroinflammation is not just a symptom; it’s a key pathological driver across many neurological, psychiatric, and chronic illness conditions. But it doesn’t have to be permanent.

By combining neuromodulation (rTMS, MeRT) with functional root-cause work and somatic body-based therapies (SPIN/OT), it’s possible to quiet the inflammation, restore neural balance, and promote lasting recovery.

I encourage you to explore this further, request a qEEG mapping, and consider whether a combined neuromodulation + functional health approach is right for your brain healing journey. Call us today to get started. We can't wait to help! 703-857-2560

References

Cherry, J. D., Olschowka, J. A., & O’Banion, M. K. (2014). Neuroinflammation and M2 microglia: The good, the bad, and the inflamed. Journal of Neuroinflammation, 11(1), 98. https://doi.org/10.1186/1742-2094-11-98

Frank, M. G., Fonken, L. K., Watkins, L. R., & Maier, S. F. (2019). Microglia: Neuroimmune-sensors of stress. Seminars in Cell & Developmental Biology, 94, 176–185.

Block, M. L., & Hong, J. S. (2005). Microglia and inflammation-mediated neurodegeneration: Multiple triggers with a common mechanism. Progress in Neurobiology, 76(2), 77–98.

Calcia, M. A., et al. (2016). Stress and neuroinflammation: A systematic review. Psychopharmacology, 233(9), 1637–1650.

Tang, S. C., et al. (2022). The neuroendocrine-immune axis and the pathophysiology of neuroinflammation. Frontiers in Neuroendocrinology, 65, 101002.

Morimoto, K., & Nakajima, K. (2019). Role of microglia in neuroinflammation in metabolic and neurodegenerative diseases. Frontiers in Endocrinology, 10, 232.

Fujino, T., et al. (2022). Plasmalogens as the missing link in age-related neurodegeneration. Frontiers in Cellular Neuroscience, 16, 878345.

Huang, E. J., & Reichardt, L. F. (2001). Neurotrophins: Roles in neuronal development and function. Annual Review of Neuroscience, 24(1), 677–736.

Perera, T. D., et al. (2016). The clinical research evidence base for rTMS in depression and beyond. Psychiatric Clinics of North America, 39(1), 97–113.

George, M. S., & Post, R. M. (2011). Daily left prefrontal repetitive transcranial magnetic stimulation for acute treatment of medication-resistant depression. American Journal of Psychiatry, 168(4), 356–364.