Robert Groysman, MD, 6957 W Plano Pkwy, suite 2100, Plano, TX (2026)

03/06/2026

Speaking fluently was never an issue. Now you stop mid-sentence because the word vanishes. It was right there.

This is not dementia. Or aging. This is a specific pattern of vascular-cognitive dysfunction that is both measurable and treatable.

Endothelial damage from COVID reduces cerebral blood flow, particularly to the brain regions responsible for language retrieval. When perfusion drops, those neural networks receive less oxygen and glucose. The rapid coordination required for speech slows. Words that were automatic become effortful.

A second, overlapping process compounds the problem. Mitochondrial dysfunction in neurons reduces ATP production. The high-speed synaptic activity that underlies word selection and articulation requires energy. When that energy is insufficient, retrieval falters.

Both mechanisms are detectable. Cerebral perfusion imaging can reveal reduced flow in the language centers. Neurocognitive testing can identify a selective pattern of lexical retrieval deficits that distinguishes this from generalized cognitive decline.

Treatment addresses both layers, vascular-protective strategies and anti-inflammatory support for the endothelial injury, alongside mitochondrial cofactors to restore neuronal energy output. Many patients experience measurable improvement in language function once the underlying mechanisms are identified and treated.

The loss of fluency is frightening. Recognizing it has a physiological basis is the first step toward getting it back.

Volume 6 of The Complete Long COVID Handbook covers endothelial dysfunction, cerebral perfusion, and the vascular mechanisms behind cognitive symptoms including word-finding difficulty.

03/06/2026

Perfume gives you a migraine. Cleaning products make you dizzy. Walking through the detergent aisle triggers brain fog. Your doctor says it's anxiety.

It's not anxiety. It's immunological.

Volatile organic compounds enter the nasal passages and interact with mast cells lining the nasal mucosa. The nasal lining contains a high concentration of mast cells, which are easily irritated. After COVID, mast cells become chronically hypersensitive. Ordinary household chemicals, fragrances, and cleaning products that never bothered you before now provoke degranulation. Histamine and other inflammatory mediators release, causing skin flushing, rapid heart rate, dizziness, and cognitive impairment.

People who've never been allergic before suddenly react to scented lotions, cleaning sprays, and even their own medications. Standard allergy testing comes back negative because this is not an IgE-mediated allergy. This is mast cell activation, and it requires different testing. MCAS evaluation, including prostaglandin D2 and tryptase levels, can confirm the mechanism.

Management starts with reducing the trigger load, unscented personal care products, HEPA air filtration, ventilation, and removing fragranced items from the home. Once the mast cell activation is addressed with stabilizers and trigger avoidance, the sensitivity threshold can gradually improve.

This condition is real, measurable, and treatable. You are not imagining the symptoms.

Volume 5 of The Complete Long COVID Handbook covers mast cell sensitization, environmental triggers, and the testing and treatment pathway for chemical sensitivity.

03/06/2026

Physical therapy improves deconditioning. It can worsen mitochondrial dysfunction. Same symptom. Different mechanism. Different outcome.

Deconditioning responds to graded exercise because the muscles and cardiovascular system need retraining. The protocol starts low, increases gradually, and rebuilds aerobic capacity over time. For patients whose fatigue comes from inactivity, this approach works.

Mitochondrial dysfunction is a different problem entirely. The cells cannot generate sufficient ATP during activity. The electron transport chain is impaired, and overexertion produces excess reactive oxygen species that the body cannot clear fast enough. The result is not muscle soreness. It is a metabolic crash that can arrive 12 to 72 hours after the activity that caused it.

This is the push-crash cycle. A patient feels well enough to exercise, pushes through the session, and then cannot function for days afterward. The delay between activity and crash is what makes it so difficult to connect cause and effect. Patients are told to push harder. They do. They get worse. The cycle repeats.

Once the type of fatigue is identified, the approach changes. Mitochondrial support (coenzyme Q10, riboflavin, targeted cofactors) addresses the energy production deficit. Pacing protocols and heart rate zone monitoring prevent the oxidative overload that triggers crashes. Over weeks, energy reserves improve and patients can tolerate modest increases in activity without relapse.

The distinction between deconditioning and mitochondrial dysfunction is the difference between an intervention that helps and one that harms.

Volume 3 of The Complete Long COVID Handbook covers mitochondrial energy production, the push-crash cycle, and the pacing and supplementation protocols that support gradual rebuilding.

03/05/2026

Mast cell activation syndrome is not one disease. It is a spectrum with distinct clinical patterns. Here is how we differentiate them.

Histamine-dominant subtype. Flushing, gastrointestinal upset, headaches, and itching. These patients respond to H1 and H2 receptor blockers and cromolyn sodium. Testing focuses on serum histamine and 24-hour urine methylhistamine. This is the subtype most clinicians recognize, and antihistamines often provide visible relief.

Prostaglandin-dominant subtype. Abdominal cramping, diarrhea, musculoskeletal pain, and bronchospasm. These patients do not respond well to antihistamines alone because the dominant mediators are prostaglandin D2 and leukotriene E4. Testing requires 24-hour urine prostaglandin D2 and leukotriene E4 levels. Treatment emphasizes COX inhibitors, leukotriene receptor antagonists, and mast cell stabilizers like ketotifen.

Tryptase-elevating subtype. Systemic degranulation with anaphylactoid reactions, hypotension, and diffuse urticaria. Serum tryptase measured during an acute episode and at baseline distinguishes this pattern. These patients require epinephrine autoinjectors and careful trigger avoidance.

Mixed subtype. Two or more mediators elevated simultaneously. The clinical picture combines flushing, pain, and systemic reactions. The full panel (histamine, prostaglandin, leukotriene, tryptase) is necessary. Treatment is individualized based on which mediator dominates.

In Long COVID, mast cells become chronically hypersensitive after infection. Non-histamine mediators, particularly prostaglandins and leukotrienes, are often the dominant drivers. This explains why many patients try antihistamines, see partial improvement, and assume nothing more can be done. The mediator profile determines the treatment path. Without subtyping, treatment remains incomplete.

Triggers span food additives, environmental chemicals, physical stressors like temperature extremes, and hormonal fluctuations. Identifying both the subtype and the trigger pattern allows precise, targeted therapy.

Volume 5 of The Complete Long COVID Handbook covers MCAS mediator profiles, subtype-specific testing protocols, and the treatment strategies that differ based on which pathway is driving symptoms.

03/05/2026

Insomnia is one of the most common symptoms people with Long COVID report. But it is important to understand something first.

Before anyone asks how to fix insomnia in Long COVID, the first step is figuring out which mechanisms are causing your Long COVID.

Insomnia in this condition is usually not a primary sleep disorder. It is often a downstream symptom of underlying biological problems that COVID triggered.

Treating sleep alone rarely works if the real issue is coming from the nervous system, mitochondria, hormones, or inflammation.

At the same time, we should also be careful not to miss basic sleep issues that can exist in anyone, including Long COVID patients. Things like sleep hygiene and obstructive sleep apnea (OSA) still need to be evaluated. Long COVID does not eliminate the possibility of common sleep disorders.

So both things matter:
1. Evaluate standard sleep issues
2. Identify the Long COVID mechanisms driving insomnia

Here are some of the most common mechanisms that can cause insomnia in Long COVID.

1. Dysautonomia (Fight or Flight Overactivation)
Many Long COVID patients develop autonomic nervous system dysfunction. The sympathetic nervous system becomes dominant while the parasympathetic “rest and digest” system is suppressed.

This can cause:
• Racing heart at night
• Adrenaline surges
• Waking up around 2–4 AM
• Feeling wired but exhausted

Your body literally cannot shift into sleep mode.

2. Neuroinflammation
COVID can trigger inflammation in the brain that affects sleep-regulating centers like the hypothalamus and brainstem.

Inflammatory cytokines disrupt normal sleep signaling and fragment sleep cycles.

People may sleep but never reach deep restorative sleep.

3. Circadian Rhythm Disruption
Some patients develop circadian rhythm problems after COVID.

Common patterns include:
• Delayed sleep phase (falling asleep at 3–5 AM)
• Reversed cortisol rhythm
• Difficulty waking in the morning

When the body clock is disrupted, sleep timing becomes unstable.

4. Mitochondrial Dysfunction
The brain requires large amounts of cellular energy to regulate sleep cycles.

If mitochondria are impaired, sleep becomes non-restorative.

This is why many patients say:
“I slept 9 hours but still feel exhausted.”

5. Hormone Imbalances
Long COVID frequently disrupts several hormones involved in sleep regulation:

• Cortisol rhythm
• Thyroid hormones
• Testosterone in men
• Progesterone in women
• Melatonin signaling

Hormonal shifts alone can completely disrupt sleep quality.

6. Histamine and Mast Cell Activation
Histamine is actually a wake-promoting neurotransmitter.

When mast cells are activated, histamine levels can increase and make it difficult to fall asleep or stay asleep.

Some patients notice sleep improves with antihistamines.

7. Gut Dysbiosis
The gut microbiome plays a role in serotonin and melatonin production.

COVID-related microbiome disruption can alter sleep signaling through the gut-brain axis.

I treat all if these mechanisms.

Long COVID insomnia is usually a symptom, not the root problem.

Trying to treat sleep directly without addressing the mechanisms often leads to frustration.

But at the same time, we should not ignore basic sleep medicine principles:

• Evaluate sleep hygiene
• Screen for obstructive sleep apnea
• Review medications that disrupt sleep
• Consider circadian rhythm disorders

Once those are addressed, the next step is identifying which Long COVID mechanisms are present.

For many patients the main drivers are:

• Dysautonomia
• Mitochondrial dysfunction
• Gut dysbiosis
• Histamine / mast cell activation
• Endothelial dysfunction and microclots
• Hormone imbalance

When the underlying mechanisms begin improving, sleep often improves as well.

That is why a mechanism-based approach to Long COVID matters so much.

03/05/2026

The current evidence suggests Long COVID is a multi-mechanism syndrome, often post-infectious, rather than driven by ongoing viral replication. Consistent, replicated data is key to understanding its complexities.

03/05/2026

Long COVID isn't one problem. It's six interconnected mechanisms disrupting multiple body systems. The Complete 7-Volume Series gives you the full framework: dysautonomia, mitochondrial dysfunction, endothelial damage, gut dysbiosis, mast cell activation, and hormone imbalance. Each volume breaks down one mechanism in depth: what's broken, why it's broken, and how to start fixing it. You'll understand the biology behind your symptoms, what tests to request, and which treatments target which mechanisms. This is the comprehensive system for understanding Long COVID and building your recovery strategy. All seven volumes, one complete roadmap.

Get the complete series: https://www.longcovidfamily.com/product/full-handbook-series/

03/05/2026

Small fiber neuropathy can often sound like permanent nerve damage.

The condition divides into two forms. Structural small fiber neuropathy which involves axon loss. Or inflammatory small fiber neuropathy which is a functional disturbance. (The nerve fibers remain intact but signal abnormally while inflammation persists.)

In Long COVID, the functional inflammatory form can predominate. Symptoms can fluctuate with activity, stress, and autonomic demand.

A skin punch biopsy can distinguish the two forms of nerve damage. Quantitative sudomotor axon reflex testing (QSART) measures sudomotor nerve function and frequently demonstrates reduced sweat output despite normal structural findings.

This distinction matters because the treatment pathway is not the same.

Inflammatory SFN my include reducing the immune activation that is disrupting nerve signaling.

Most patients with small fiber neuropathy after COVID experience meaningful do have options. The diagnosis is not a sentence. It is a starting point for targeted treatment.

Volume 2 of The Complete Long COVID Handbook covers autonomic neuropathy, small fiber testing, and the treatment protocols that address the inflammatory component.

03/05/2026

You feel your body vibrating from the inside. Your hands are steady. No one can see it. Nothing shows on a scan. But you feel it constantly.

Internal tremors are one of the most unsettling symptoms patients describe because there is no visible evidence. You feel shaking, buzzing, or vibration deep inside your body, sometimes in your chest, sometimes in your legs, sometimes everywhere at once. Every test comes back normal. You start to question whether it is real.

It is real. Internal tremors are a recognized pattern in autonomic dysfunction. The autonomic nervous system generates sensory signals that the brain interprets as vibration, even when there is no visible movement. Nerve conduction studies are often normal because the dysfunction is autonomic, not structural. Standard neurology workups check the wrong system.

Autonomic testing (QSART, sudomotor function, tilt table) evaluates the system that is actually involved. Heart rate variability monitoring can reveal the sympathetic overdrive that generates these signals.

This is one of the symptoms that responds to autonomic stabilization. Patients who felt they were vibrating for months or years describe gradual resolution as the nervous system rebalances. The tremors do not have to be permanent. They are a signal, not a sentence.

Volume 2 of The Complete Long COVID Handbook covers internal tremors, autonomic sensory signaling, and the testing and treatment pathway.

03/05/2026

People say I do not explain how to actually manage PEM. So here is exactly how to identify your triggers.

Post-exertional malaise is a delayed and exaggerated worsening of symptoms after physical, mental, or emotional effort. The crash does not show up during the activity. It arrives 12 to 72 hours later, which is exactly what makes it so difficult to connect cause and effect.

Here is a step-by-step tracking system that works.

Step 1: Log the activity - Write down what you did, how long, how intense, and what time of day. Include cognitive exertion (phone calls, decision-making, emotional conversations) alongside physical tasks.

Step 2: Log symptoms 24 to 72 hours later - Note what appeared, how severe, and when. Most people only track the day of. The delay is where the pattern hides.

Step 3: Look for patterns after two to three weeks - Which activities consistently trigger crashes? Is cognitive exertion worse than physical? Does time of day matter? Does combining two moderate activities in one day push you over the threshold when either alone would not?

Step 4: Identify your energy envelope - Or the total amount of physical, cognitive, emotional, and social activity you can sustain in a day without triggering PEM.

Once you see your pattern, you can pace within it. Pacing is not doing less forever. It is doing the right amount so your body can gradually rebuild without crashing.

Volume 3 of The Complete Long COVID Handbook covers PEM mechanisms, the energy envelope concept, and how to build a pacing protocol that fits your life.

03/04/2026

Long COVID patients who wake at 3 AM with a racing heart, drenched in sweat, wide awake with no explanation.

This is one of the patterns I see often. The patient falls asleep fine. Three or four hours later, the body jolts them awake. Heart pounding. Sheets soaked. Mind racing as if something dangerous just happened. Nothing did.

The sympathetic nervous system fires when it should be at its quietest. During deep sleep, the parasympathetic system is supposed to dominate, lowering heart rate, reducing cortisol, and allowing the body to repair. In autonomic dysfunction, that handoff fails. The sympathetic nervous system surges, releasing norepinephrine and cortisol at the exact hours when they should be at their lowest.

This is not a panic attack. It is not night terrors. It is not menopause (though hormonal shifts can layer on top of it). It is an autonomic misfire during the sleep cycle.

Cortisol timing tests (four-point saliva or dried urine), catecholamine levels, and overnight heart rate variability patterns can confirm the mechanism. Once confirmed, autonomic stabilization, cortisol rhythm repair, and vagus nerve support address the root cause rather than masking the symptom with sedation.

You are not anxious. Your nervous system is misfiring at 3 AM, and that is measurable.

Volume 2 of The Complete Long COVID Handbook covers autonomic regulation during sleep, sympathetic surges, and the specific testing that reveals this pattern.

03/04/2026

When cold hits, your body enters survival mode, activating fight or flight....

Robert Groysman, MD

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