I am transitioning off a waitlist and gearing up for big news! Stay tuned and please direct virtual and in office consultation requests to drmichaelscoma@gmail.com and they will be answered in the order in which they are received. #MECFS #LongCovid #MCAS #LymeDisease

Treatment is highly individualized, guided by symptom clusters and medication tolerability, and may involve pharmacologic interventions targeting autonomic dysfunction, neuroinflammation, sleep disruption, and HPA axis dysregulation.

Clinically, patients often articulate frustration with being "exhausted but unable to relax or sleep." This phenotype requires recognition as a distinct manifestation of neurophysiological dysfunction secondary to elevated sympathetic nervous system activity.

Patients with Long COVID and ME/CFS frequently present with "wired fatigue," a paradoxical state of profound exhaustion coupled with hyperarousal. This symptom reflects underlying autonomic dysfunction and impaired hypothalamic-pituitary-adrenal (HPA) axis dysregulation.

In practice, I utilize intravenous glutathione pushes adjunctively in patients with post-viral syndromes. When appropriately timed and dosed, they can accelerate recovery by enhancing antioxidant capacity and reducing neuroinflammatory burden.

Low glutathione means poor activation of cellular defense (e.g. the NRF2 pathway), leading to sustained inflammation and fatigue. Restoring levels - via NAC, glycine, or liposomal glutathione - can support mitochondrial repair and cognitive recovery.

Long Covid patients have depleted glutathione and heightened oxidative stress, especially in the brain and blood vessels. This impairs energy, slows immune recovery, and allows residual viral proteins to linger.

Glutathione and Long COVID. Glutathione, an antioxidant, regulates redox balance, immune function and detoxification. In Long COVID, oxidative stress and mitochondrial dysfunction are rampant - low glutathione is both a marker and a mechanism of persistent symptoms.

Neurocognitive impairment in ME/CFS and Long COVID is a clinically observable, functionally devastating deficit. Underrecognized by clinicians, yet central to disability, this is not “brain fog.” It’s neurological dysfunction and should be treated as such.

Patients frequently state: “I can tolerate being bedbound. I can adapt to POTS. What I can’t endure is losing cognitive capacity.” Loss of ability to perform remote work, synthesize information, or engage in abstract reasoning = loss of identity & autonomy.

In ME/CFS and Long COVID, the most disabling symptom is often not fatigue or orthostatic intolerance, but neurocognitive dysfunction. Impairments in processing speed, working memory, attention, and executive function are profound. This is acquired cognitive injury.

Treatment may include SNRIs for autonomic imbalance, low-dose aripiprazole for neuroinflammation and fatigue, lamotrigine for cortical excitability and mood, and gradual sensory desensitization to reduce CNS hyperreactivity with neuroimmune targets essential.

These symptoms are likely driven by autonomic dysfunction, chronic neuroinflammation, sensory overload, and sustained stress response (HPA axis dysregulation). Hypoperfusion and impaired interoception also contribute to altered self-environment integration.

Depersonalization and Derealization. Depersonalization and derealization are dissociative symptoms marked by altered self-perception or a sense of unreality. In ME/CFS and Long COVID, patients may describe feeling detached from their body, emotions, or surroundings.

⏰⏰⏰ How time flies. three months later and Pemivibart receipt = 40 and 30-60 day antiviral courses > 60 with ongoing significant and sustained clinical improvements - in particular the neurological phenotypes.

Accurate differentiation requires longitudinal assessment, pattern recognition, and high clinical suspicion. In the absence of pathognomonic findings, experienced clinical judgment remains the cornerstone of diagnosis and therapeutic planning.

Testing including specialty labs (e.g., IgeneX), may increase sensitivity but lack standardization and specificity. False positives and negatives occur. Diagnosis remains clinical - guided by history, exposure risk, and symptom progression.

ME/CFS, Long COVID, and chronic tick-borne illnesses (ie., Borrelia burgdorferi) present with overlapping symptoms: exertional intolerance, cognitive impairment, dysautonomia, and fatigue. Absence of definitive biomarkers complicates differential diagnosis.

Reduced vagal tone, low HRV, and dysfunctional insular processing lock the CNS in a pro-inflammatory threat mode. The poisoned sensation is not symbolic - it's a brain-body error signal reflecting disordered interoception and failed homeostasis. It's CDR.

Glial priming and neuroinflammation in the brainstem and limbic structures amplify autonomic output. Sympathetic excess and impaired baroreflex cause cerebral hypoperfusion, orthostatic intolerance, and a centrally mediated sense of systemic collapse.