The review is relevant to an estimated 44% to 60% of perimenopausal women who report cognitive changes such as forgetfulness and trouble concentrating, commonly described as brain fog. These symptoms can affect productivity, work, daily routines and quality of life, and no FDA-approved pharmacological intervention is currently available specifically for them. Researchers who conducted the review cautioned that the evidence is too limited to recommend either ADHD medication for menopausal brain fog.

Larger studies would be needed first to establish whether the drugs are safe and effective for this use, and the review does not establish that the benefits reported by participants were caused by changes in their underlying cognitive ability. To assess the potential role of existing ADHD treatments, the researchers conducted a scoping review of original research involving lisdexamfetamine, a stimulant, and atomoxetine, a non-stimulant. The eligible population consisted of biological women aged 45 to 60 whose last menstrual period had occurred less than 10 years earlier.

Studies were excluded if they involved transgender women, disordered sleep, surgical menopause, primary ovarian insufficiency, premature or early menopause, or a previous or current cancer diagnosis. These criteria were intended to focus the evidence on women experiencing the natural menopause transition, but they also restricted the size and composition of the evidence base and limit how widely its findings can be generalized. The biological rationale proposed by the researchers centers on the substantial decline and fluctuation in estrogen during menopause.

The menopause transition is associated with quantifiable deficits in working memory, attentional control and processing speed, and these domains overlap with core symptoms of ADHD. The authors suggested that ADHD medications may influence signaling pathways disrupted during the transition in a way that improves subjective executive function. Neuroimaging findings from a subset of women taking lisdexamfetamine were described as further supporting this interpretation, although the research release did not provide the sample size or detailed methods of that imaging analysis.

Evidence linking ADHD symptoms with menopausal experiences remains incomplete. Cross-sectional data showed a positive correlation between ADHD symptom severity and the intensity of menopause symptoms, indicating an association in the populations studied rather than proof of a causal relationship. Findings were inconsistent about whether a formal ADHD diagnosis was associated with somatic or psychological complaints.

Those limitations, together with the minimal or nonsignificant effects of both medications on objective cognitive measures, mean the review cannot demonstrate that lisdexamfetamine or atomoxetine improves cognition during menopause.

Subject of Research: Scoping review of ADHD medications for self-reported executive dysfunction during the menopause transition

Article Title: ADHD medications offer promise in managing menopausal brain fog

Article References: ADHD medications offer promise in managing menopausal brain fog. Original publication (Bibliographic details unavailable.)

Image Credits: AI Generated

DOI: Not provided

Keywords: menopause, brain fog, ADHD, lisdexamfetamine, atomoxetine, executive function, cognition, perimenopause, scoping review, medications, offer, promise

The study, led by Sharron Hinchliff of the University of Sheffield and Kristina Potočnik of the University of Edinburgh, forms part of the MARIE-UK project, a large-scale international research initiative investigating unmet needs across perimenopause, menopause, and post-menopause. The researchers conducted in-depth, semi-structured interviews with 50 women aged between 43 and 67 years, with a mean age of 52.3 years, drawn from a larger cohort of 1,043 UK women who had completed a quantitative survey. Participants were recruited through digital platforms, NHS Trust websites, clinics, and community venues including places of worship, and the sample deliberately captured variation in age, menopausal stage, ethnicity, and employment circumstances.

To analyse the interviews, the team used collaborative reflexive thematic analysis, a rigorous qualitative method in which multiple researchers independently code the same transcripts and then compare interpretations to reach consensus. The analysis produced 13 themes and 46 subthemes, and the researchers interpreted the findings through the lens of Conservation of Resources (COR) theory, a well-established psychological framework which holds that individuals strive to obtain, retain, and protect resources they value, such as time, energy, health, and social support. When demands deplete these resources faster than they can be replenished, a loss spiral begins: each loss makes people more vulnerable to further losses, compounding strain and diminishing wellbeing.

Applied to menopause, COR theory reframes the transition not simply as a biological event but as a demand that drains the very resources women need to function and thrive at work. The majority of participants in the study reported cognitive changes, particularly difficulties with working, short-term, and episodic memory, alongside the phenomenon popularly known as brain fog, characterized by trouble focusing on tasks, following instructions, or retrieving words. These difficulties struck many women with startling speed and severity. One participant, given the pseudonym Bree, described how after more than two decades in her job she had been the colleague everyone consulted for policy knowledge, yet suddenly found herself unable to work out how to resize her computer screen. The abruptness of the change, she said, made her feel as though she had almost shrunk as a person.

The consequences rippled far beyond day-to-day task performance. Women described their brains filling up too quickly, forcing them to write everything down, and several reported forgetting what they were saying mid-sentence or retracing their steps to check whether tasks had been completed. This perceived decline in efficiency fed directly into career decisions: some participants declined promotions because they no longer felt competent enough to take them on, despite years of accumulated expertise. Others described a vicious cycle in which forgetting triggered worry about forgetting, which in turn dominated their thoughts and deepened their anxiety. Several women articulated a striking sense of imposter syndrome, feeling like frauds in roles they were demonstrably qualified to hold, a perception that chipped away at confidence and professional self-concept.

Perhaps the most emotionally resonant finding concerned identity. Many participants said they no longer recognized themselves, and one described the experience as being like a bereavement, a loss of the self accompanied by a thousand and one emotions. The researchers note that this profound alteration in professional identity, closely tied to cognitive changes, represents a gap in the existing literature, which has documented the impact of menopausal symptoms on quality of life but rarely explored how cognitive disruption intersects with identity reconstruction in occupational settings. Thirty-six of the participants reported feeling overwhelmed at work, and the mental health toll was measurable: at the time of interview, 39 women reported depression and/or anxiety as menopause symptoms, compared with only 12 who reported such conditions before their menopausal transition.

The study also revealed how the personal and professional domains of women’s lives became intertwined in a reciprocal relationship. Sleep disruption associated with menopausal symptoms contributed to fatigue, which participants believed impaired their memory and concentration, with knock-on effects on work performance. Workplace stress, in turn, intensified symptoms that did not simply switch off when women moved between the office and home. Many participants first noticed their cognitive symptoms during the COVID-19 pandemic, and they reflected that lockdowns, staffing shortages, and pervasive uncertainty had likely exacerbated the effects, a compounding factor the researchers argue has been overlooked in existing pandemic preparedness frameworks.

Faced with declining performance, many women adopted masking strategies, deliberately concealing their difficulties from line managers to avoid being seen as less competent. One participant, Rachel, noted that no one had brought her declining performance to her attention because she had managed to fool them into thinking she was still functioning properly, even though she knew she was not. Masking sometimes worked, but the effort of maintaining the facade was itself deeply stressful, and the persistent fear of being found out carried tangible risks, including demotion or enforced reductions in working hours, threats that loom especially large for women approaching the later stages of their careers and concerned about financial security before retirement.

Workplace support emerged as the critical variable determining whether women remained trapped in the resource loss spiral or escaped it. Those with flexible hours, empathetic line managers, colleagues experiencing similar symptoms, or the option to work from home reported better coping and a regained sense of control. One participant described a manager who granted her a paid wellbeing day to attend a menopause retreat. Yet support was far from universal, and shared demographics offered no guarantee of understanding. One woman, Isabelle, whose line manager was of a similar age, requested an Occupational Health referral to explore available support, only to have the referral submitted with poor performance listed as the reason, despite no performance conversation ever having taken place. The manager also suggested a demotion, an outcome Isabelle found deeply distressing. The researchers conclude that limited awareness of the diversity of menopausal experiences, rather than a lack of shared characteristics, drives unsupportive responses.

The findings arrive at a pivotal moment for UK policy. Women’s employment rates have risen steadily, with 68.6 percent of women aged 50 to 64 now employed, an increase of more than 20 percent since 1992, and menopause symptoms typically begin in a woman’s forties. The UK Employment Rights Act 2025 introduced a mechanism through which large employers, those with at least 250 employees, may be required to publish equality action plans addressing the gender pay gap and support for employees experiencing menopause, with voluntary publication possible since April 2026 and mandatory publication intended from spring 2027, subject to secondary legislation. The researchers argue that legal frameworks should go further, mandating employer education, enforcing compliance with menopause policies, and incentivizing evidence-based interventions such as cognitive screening, mental health support, managerial training, and resources like the Menopause Information Pack for Organizations. They caution against framing hormone replacement therapy as a panacea for cognitive health, noting that some participants using HRT still reported substantial cognitive challenges. As the proportion of menopausal women in paid employment continues to grow, the study’s central message is unambiguous: menopausal cognitive changes are legitimate occupational health concerns, and workplaces that fail to recognize them risk perpetuating gender inequalities, losing skilled workers, and compounding the mental health burdens that women already carry through one of the most demanding transitions of their lives.

Subject of Research: Cognitive changes at menopause and their impact on women's workplace performance, identity, and mental health

Article Title: Understanding the interplay between cognitive changes at menopause, the workplace, and mental health: qualitative findings from the MARIE-UK (WP2a) project

Article References: Hinchliff, S., Potočnik, K., Delanerolle, G., Taylor, J., Elliot, K., Fontana, D., Saraswat, L., Panay, N., Talaulikar, V., Atkinson, C., Kemp, H. F., Kurmi, O., Rathnayake, N., Al-Kharusi, L., Pathiraja, V., Al-Riyami, N., Palanisamy, R., Eleje, G. U., & Phiri, P. (2026). Understanding the interplay between cognitive changes at menopause, the workplace, and mental health: qualitative findings from the MARIE-UK (WP2a) project. Frontiers in Global Women's Health, 7, Article 1878423. https://doi.org/10.3389/fgwh.2026.1878423

Image Credits: AI Generated

DOI: 10.3389/fgwh.2026.1878423

Keywords: menopause, brain fog, cognitive changes, workplace, mental health, Conservation of Resources theory, qualitative research, women's health, occupational health, MARIE-UK, gender inequality, UK policy

The clinical picture itself helps explain why progress has been so slow. Long COVID is strikingly heterogeneous, with manifestations that include debilitating fatigue, cognitive dysfunction often described as brain fog, and persistent respiratory compromise, all affecting multiple organ systems. Despite intensive research efforts, the underlying pathophysiological mechanisms remain elusive, and that gap in understanding has directly impeded the development of effective therapies. It is precisely this fragmentation that the special issue set out to address, assembling studies that approach the syndrome from complementary angles rather than competing hypotheses.

The first strand of evidence concerns the lungs, where structural damage from acute infection can linger long after the virus itself has cleared. A team led by Garg and colleagues examined survivors of severe COVID-19 acute respiratory distress syndrome and demonstrated that specific imaging patterns on computed tomography correlate with ongoing symptoms. In particular, reticulations and septal thickening, the fine net-like changes that appear when lung architecture is disrupted, were positively associated with symptomatic dyspnoea, the distressing breathlessness that many survivors report. The researchers also found that parenchymal and atelectatic bands, linear scars within the lung tissue, were associated with reduced forced vital capacity, a standard measure of how much air the lungs can hold.

What makes that study significant, the editors note, is that it moves beyond simply documenting that abnormalities persist. By linking individual CT imaging patterns to both symptomatic and functional measures, the work establishes concrete associations between what radiologists see on a scan and what patients actually feel and how well their lungs perform. That kind of correlation is a prerequisite for using imaging as a meaningful clinical tool in follow-up care, rather than as a descriptive curiosity. It also provides a framework for stratifying patients, since different patterns of lung injury may reflect different underlying processes and may therefore respond differently to future treatments.

A companion study in the same issue addresses a practical barrier to long-term lung surveillance: radiation dose. Devkota and colleagues evaluated ultra-low-dose CT, a technique that dramatically reduces radiation exposure compared with standard protocols, in patients recovering from moderate to severe acute COVID-19 pneumonia. Their results showed that ultra-low-dose CT is comparable to standard-dose CT in accurately detecting persistent lung abnormalities. The authors reported a diagnostic accuracy of 95.0 percent overall, rising to 98 percent among non-obese subjects. Those figures matter because repeated surveillance imaging is only feasible, and ethically justifiable, if the cumulative radiation burden can be kept low. A technique that preserves diagnostic performance while cutting exposure makes serial monitoring of recovering patients a far more realistic proposition for clinics and hospitals.

The special issue then widens the anatomical scope, because the abnormalities associated with Long COVID are not confined to the lungs. In a retrospective CT angiography study, Goksu and colleagues identified significantly enlarged carotid bodies in patients previously hospitalized with COVID-19 pneumonia. The carotid bodies are small paired organs at the bifurcation of the carotid arteries that sense hypoxaemia, low oxygen levels in the blood, and modulate sympathetic nervous system activity in response. Enlargement of these structures in post-COVID patients could reflect prolonged chemoreceptor stimulation resulting from the pathophysiological changes of Long COVID, suggesting that the syndrome’s reach extends well past the respiratory system into the machinery that regulates breathing and cardiovascular tone.

The carotid body finding also raises pointed mechanistic questions. These organs are rich in ACE2 receptors, the same molecular doorway that SARS-CoV-2 uses to enter cells, and they are central to chemoreception. That combination leaves open two possibilities that are not mutually exclusive: the enlargement may be the result of direct viral injury to the tissue, or of chronic hypoxic stimulation as the body adapts to persistently disturbed oxygen dynamics, or of both acting in concert. Disentangling those mechanisms will be important, because a viral injury model and a maladaptive stimulation model would point toward very different therapeutic strategies.

Moving from structure to immunology, Kawaguchi and colleagues investigated serological profiles in an effort to identify clinically useful biomarkers for Long COVID’s heterogeneous manifestations. Their study covered 275 patients with Omicron-related Long COVID, a cohort of particular interest because most of the world’s current infections involve Omicron-lineage viruses. The team found that nucleocapsid N-antibody titers were positively associated with acute disease severity and with antiviral immune responses. Conversely, lower titers of antibodies against the spike protein’s S-antigen correlated significantly with memory impairment, the brain fog that is among the most disabling of Long COVID’s neurocognitive symptoms, and with reduced quality of life.

Those results expand understanding of the immunological underpinnings of neurocognitive symptoms and suggest that a blood test capable of flagging patients at risk of cognitive sequelae may one day be feasible. The authors are careful, however, to flag the interpretive pitfalls. Vaccination status and the time elapsed since infection both shape antibody profiles, and any biomarker built on serology must account for those variables before it can be trusted in the clinic. The caution is a reminder that in a post-vaccine, repeatedly exposed population, the immune signature of Long COVID is layered over a complex history of immunological events.

Finally, the issue turns from diagnosis to treatment, and to an organ system that has become a focal point of Long COVID research: the gut. Amoroso and colleagues conducted a randomized, double-blind, placebo-controlled trial in which patients with Long COVID received four weeks of probiotic supplementation or placebo. The probiotic arm achieved a significantly greater reduction in clinically relevant fatigue scores than placebo, with 24.24 percent of treated patients reaching that threshold compared with 6.06 percent on placebo. Crucially, the clinical improvement was accompanied by concurrent changes in gut microbial taxa, in microbiota-associated metabolites and in immune-related pathways, offering a plausible biological mechanism rather than an unexplained statistical signal. The editors caution that the modest sample size warrants restraint, but they describe the result as an exciting indication that gut-directed therapies deserve serious consideration in the Long COVID treatment landscape.

Read as a whole, the five studies converge on a single conclusion that the editors of the issue emphasize: Long COVID is a syndrome of genuine complexity, and no single measurement, organ or discipline will capture it alone. Continued research using diverse and integrated methodologies, spanning imaging, immunological, physiological and microbiome-related measures, will be essential for improving the characterization, monitoring and treatment of the condition. Much remains unresolved in elucidating the underlying causes of Long COVID, let alone alleviating the burden it places on patients and health systems. But the trajectory on display in this collection, from structural imaging that predicts symptoms, to immune markers that track cognitive decline, to microbial interventions that measurably reduce fatigue, illustrates how multidisciplinary work can turn a bewildering syndrome into a set of tractable, testable questions. The British Journal of Biomedical Science has signalled its commitment to serving as a forum for exactly that kind of rigorous, cross-cutting research, and the field will need more of it if the legacy of the pandemic is to be met with answers rather than open questions.

Subject of Research: Multidisciplinary biomedical research on the pathophysiology, biomarkers and treatment of Long COVID

Article Title: Editorial: Long COVID in the biomedical sciences

Article References: Kunnath, A. P., Kavanagh, O., & Tan, S. C. (2026). Editorial: Long COVID in the biomedical sciences. British Journal of Biomedical Science, 83, Article 17822. https://doi.org/10.3389/bjbs.2026.17822

Image Credits: AI Generated

DOI: 10.3389/bjbs.2026.17822

Keywords: Long COVID, PASC, SARS-CoV-2, computed tomography, carotid body, serological biomarkers, brain fog, probiotics, gut microbiome, fatigue, ARDS, British Journal of Biomedical Science

The scale of the problem justifies the effort. The most recent estimates cited by the authors suggest that roughly six percent of United States adults and half a percent of children and adolescents are still living with new or persistently worsened symptoms that began shortly after an acute SARS-CoV-2 infection. For clinical purposes, the authors define Long COVID as new or worsened symptoms developing after confirmed or suspected infection and persisting for more than three months, a deliberately broad formulation that sidesteps the stricter laboratory-confirmation requirements of research definitions. The dominant symptoms cluster around fatigue, post-exertional malaise, cognitive impairment often called brain fog, and orthostatic intolerance, the lightheadedness and palpitations that appear or worsen when a patient stands upright.

What makes the review distinctive is its use of clinical vignettes that mirror how patients actually describe their lives. In one case, a 32-year-old woman with a history of anxiety reports four months of fatigue that is qualitatively different from anything she has felt before. After minimal activity, she describes crashing, as though wearing a lead coat, with profound exhaustion and difficulty thinking that can persist for hours to days. Even preparing meals or answering emails has become a hurdle, and she has cut back her work hours. Her symptoms began about a month after a mild COVID-19 infection, a temporal link that might easily be missed if a clinician never asks about preceding illness.

A second vignette captures the dysautonomia pattern: a previously athletic 19-year-old develops palpitations, lightheadedness, and near-fainting on standing, symptoms that improve when she lies down. She recalls an upper respiratory illness two weeks before onset, and although she never tested herself, multiple family members had confirmed COVID-19 at the time. A third describes a 45-year-old aerospace engineer whose forgetfulness, word-finding difficulty, and slowed processing speed have cost him deadlines at work, all despite a normal basic laboratory evaluation. Together, the cases illustrate the review’s central message: Long COVID frequently announces itself through recognizable symptom clusters, and related conditions such as myalgic encephalomyelitis/chronic fatigue syndrome and postural orthostatic tachycardia syndrome often ride alongside it.

Beneath the clinical patterns, the authors propose a three-part conceptual framework for what SARS-CoV-2 actually leaves behind. The first category is a hit-and-run phenomenon, in which acute infection causes direct end-organ tissue injury with lasting consequences, such as pulmonary fibrosis or vascular events. The second is a stressor effect, in which the infection reduces physiological reserve and unmasks or accelerates chronic diseases like diabetes, hypertension, or rheumatoid arthritis in the following weeks and months. The third and most scientifically contested category is ongoing biological dysregulation, encompassing persistent viral reservoirs, immune dysregulation, gut dysbiosis, mitochondrial dysfunction, and microvascular clotting, processes repeatedly identified in basic science studies but largely invisible to current clinical diagnostic tools. Management of the first two categories follows standard practice, the authors note, while the third currently rests on rehabilitation and supportive care.

Diagnostically, the review resists exotic testing. Because no clinically available biomarker can confirm or exclude Long COVID, and severe symptoms can coexist with entirely normal conventional results, the workup serves mainly to rule out competing diagnoses and addressable sequelae. The authors recommend a focused physical examination guided by the patient’s symptoms, with particular attention to orthostatic vital signs, which are often skipped and frequently abnormal in this population. Targeted laboratory and imaging studies, including complete blood count, metabolic panel, thyroid function, and inflammatory markers, follow the same logic a primary care clinician would apply to any undifferentiated complaint. A validated ten-item questionnaire for post-exertional malaise, the DSQ-PEM, can help document a symptom that patients often struggle to articulate.

On treatment, the message is sobering but constructive: there is no cure, and no FDA-approved medication, yet validation and education alone can meaningfully improve quality of life. The authors emphasize that mental health conditions are not the cause of Long COVID, but the illness frequently produces new or worsened depression and anxiety, partly because patients do not feel believed by clinicians or loved ones. Nonpharmacologic strategies form the backbone of care. Activity pacing, energy conservation, and task modification, such as spreading grocery shopping and meal preparation across separate days or using a scooter and a seated chopping station, help patients live within their energy envelope. Referral to therapists experienced with chronic fatiguing illnesses, typically in neurorehabilitation rather than orthopedic settings, can be transformative: physical therapy for fatigue and activity intolerance, occupational therapy for self-care and job demands, and speech therapy for attention, memory, and breathing discomfort despite normal pulmonary tests.

One warning stands out with unusual force. While some patients tolerate gradual, supervised exercise progression, graded exertion must be approached with extreme caution in patients with post-exertional malaise. The authors cite evidence that even seemingly minor overexertion can trigger delayed symptom flares and has been associated with amyloid deposition, reduced mitochondrial enzyme activity, and signs of severe skeletal muscle damage in affected patients. For those with orthostatic intolerance, simpler measures carry real benefit: increasing daily fluid intake to 2.5 to 3.5 liters and sodium to 2.8 to 4 grams, equivalent to 7 to 10 grams of salt, alongside compression garments such as waist-high stockings or an abdominal binder, provided no contraindications exist.

Pharmacologic management remains symptom-based, borrowing indications from other contexts: beta blockers or ivabradine for POTS, stimulants for attention-dominant brain fog, gabapentinoids for neuropathic pain, and SSRIs for new or worsened mood symptoms. Two off-label options receive special mention. Low-dose naltrexone, an opioid receptor blocker, has been associated in some patients with improved pain, fatigue, and cognition, and a 2026 systematic review and meta-analysis examined the evidence base. Patients with suspected mast cell activation syndrome triggered by Long COVID sometimes report relief from combined H1 and H2 antihistamines. The authors also address the longer arc of illness: symptoms persist beyond one year in roughly a quarter of patients and beyond two years in about ten percent, making documentation of functional impact, workplace accommodation letters, and disability paperwork an essential, billable-worthy part of primary care.

Perhaps the most practical contribution is a set of principles for delivering all of this within a standard visit. The authors advise screening for preceding illness and symptom duration in the history, asking which symptom is most bothersome right now, and tackling only one or two symptoms per visit while leveraging longitudinal follow-up. Medication trials should be stepwise, one intervention at a time, starting low and titrating slowly, with de-prescribing of drugs that may worsen fatigue or cognition. Written after-visit summaries matter disproportionately for patients with cognitive symptoms, and telehealth or first-appointment scheduling can spare fatigued patients the exertion of a waiting room. On prevention, the review is equally concrete: vaccination shows a dose-dependent reduction in Long COVID risk, early outpatient antivirals offer modest protection, with nirmatrelvir/ritonavir associated with a 26 percent relative risk reduction, molnupiravir 14 percent, and ensitrelvir 45 percent, while metformin was linked to a 41 percent reduction in incidence in a randomized trial. Indoor air filtration, N95 or KN95 masking, and isolation during infectivity round out the defensive toolkit. Until reliable biomarkers and curative therapies arrive, the authors argue, the frontline of Long COVID medicine will remain the primary care office, and clinicians equipped with a structured approach can already change what the illness means for the patients living with it.

Subject of Research: Clinical evaluation and management of Long COVID in primary care

Article Title: Long COVID in Primary Care: A Practical Approach to Evaluation and Management

Article References: Chopra, A., Bonilla, H. F., & Cheng, A. L. (2026). Long COVID in Primary Care: A Practical Approach to Evaluation and Management. Journal of General Internal Medicine. https://doi.org/10.1007/s11606-026-10901-w

Image Credits: AI Generated

DOI: 10.1007/s11606-026-10901-w

Keywords: Long COVID, primary care, SARS-CoV-2, post-exertional malaise, dysautonomia, POTS, brain fog, ME/CFS, diagnosis, rehabilitation, antivirals, prevention

ETS is an established surgical treatment for focal hyperhidrosis, the condition in which the palms, armpits, or face sweat excessively, and it is also offered for refractory facial blushing. During the procedure, a surgeon inserts a thoracoscope through small incisions and interrupts the thoracic sympathetic chain, typically at spinal levels T2 to T4, using cauterization, resection, or titanium clips. The interruption abolishes the overactive sweating signals traveling to the target region, and most patients enjoy immediate and durable dryness where it matters most to them. But the sympathetic trunk is not a set of isolated wires serving single destinations. It is a longitudinally interconnected conduit carrying afferent and efferent signals between the brain, spinal cord, and virtually every organ below the neck, and the new study argues that cutting it inevitably perturbs far more than sweat glands in the hands.

The research team, led by surgeons at Linkou Chang Gung Memorial Hospital in Taiwan, developed a dedicated instrument called the Chang Gung Sympathetic Function Questionnaire to capture this broader picture. The 60-item survey rates each symptom on a 0 to 10 numeric scale, allowing respondents to classify complaints as none, mild, moderate, or severe, with scores of 8 or above counted as severe. Before deploying it, the team validated the questionnaire psychometrically: internal consistency was excellent across all domains, with Cronbach’s alpha values between 0.89 and 0.96, sampling adequacy was high, and exploratory factor analysis confirmed that the items clustered into the four theoretical domains the researchers had predicted, explaining 65 to 81 percent of total variance. The survey was distributed anonymously in English and Mandarin through closed online communities dedicated to hyperhidrosis support between April and August 2025.

The most striking finding concerned compensatory sweating, the phenomenon in which the body, deprived of its ability to sweat in the denervated upper regions, redirects sweat output to areas below the neck. More than 80 percent of ETS patients reported compensatory sweating in the chest, back, abdomen, buttocks, thighs, calves, or feet, and in multiple regions the severity reached the severe threshold in more than 40 percent of patients. The data also revealed that this burden grows with time: chest sweating severity correlated moderately with postoperative duration, and receiver operating characteristic analysis identified a cutoff of roughly 16.75 years after surgery as the point at which severe chest sweating became most predictable. In other words, the longer patients live with the operation, the more likely their compensatory sweating is to become disabling.

Beyond sweating, the survey documented a constellation of vascular and sensory disturbances that few patients are warned about. Facial, hand, and foot blushing were reported by 43 to 53 percent of ETS patients, compared with 15 to 29 percent of controls, suggesting persistent vasomotor dysregulation. Erythromelalgia, a condition marked by burning redness in the extremities, was present in 40 percent of patients versus 11.3 percent of controls. Hand and foot paresthesia, abnormal tingling sensations, were both more frequent and more severe after surgery, and skin complaints including itchiness, dermatitis, and discoloration were consistently worse. The researchers attribute these changes to the loss of sympathetic vasoconstrictor tone in cutaneous arterioles, which destabilizes blood flow regulation and microcirculation rather than merely drying the skin.

Perhaps the most provocative results concern the brain. After compensatory sweating, the central nervous system was the most frequently affected system in the survey. ETS patients reported markedly higher severity of cognitive complaints, including inattention, memory loss, brain fog, and a disturbing sense of loss of reality, along with affective symptoms such as anxiety, depression, loss of motivation, loss of interest, tiredness, and insomnia. For several of these items, severe ratings of 8 or above occurred in more than 30 percent of patients. Notably, some symptoms, such as sound sensitivity and tiredness, showed similar prevalence in both groups but significantly greater severity among ETS patients, suggesting that the surgery intensifies underlying central dysregulation rather than creating new symptoms from nothing.

The study offers a physiologically coherent explanation for these neuropsychological effects. The sympathetic nervous system governs arousal, vigilance, and emotional modulation, and surgical interruption of the thoracic chain alters the afferent feedback reaching the central autonomic network, a distributed set of cortical and subcortical structures including the insula, anterior cingulate cortex, amygdala, hypothalamus, and brainstem nuclei that integrates visceral signals and balances sympathetic and parasympathetic output. Physiological studies have documented parasympathetic predominance and reduced sympathetic drive after ETS, visible in heart rate variability and baroreflex sensitivity, supporting the idea of a systemic autonomic shift rather than an isolated peripheral denervation. In this framework, brain fog and mood disturbance after ETS are not imagined side effects but plausible consequences of rewiring the body’s stress and arousal circuitry.

The systemic reach of the surgery extended to the viscera as well. Cardiorespiratory complaints, including palpitations, shortness of breath, chest tightness, and chest tingling, were significantly more frequent and severe among ETS patients, each affecting more than half of respondents. Gastrointestinal symptoms such as heartburn, diarrhea, nausea, and indigestion were also elevated, consistent with the disruption of splanchnic sympathetic pathways that connect thoracic ganglia to the abdominal organs. Urogenital disturbances, particularly difficulty urinating and incomplete bladder emptying, increased markedly. Interestingly, a few symptoms moved in the opposite direction: dysmenorrhea and irregular menstrual cycles were less common in the ETS group, and shoulder and neck pain was less prevalent, though the authors caution that the ETS cohort was 70.4 percent male versus 10.1 percent of controls, so some of these apparent reductions likely reflect demographic imbalance rather than genuine protection.

The clinical implications are significant. The authors argue that the breadth of these findings supports more selective surgical techniques, such as limited ganglion resection or rami-only procedures, even though these carry a higher risk of hyperhidrosis recurrence. For patients already suffering severe complications, sympathetic trunk reconstruction, in which sural nerve or intercostal nerve grafts are used to restore continuity across the surgical gap, has emerged as the most definitive reversal option, and the Chang Gung team has pioneered robot-assisted microsurgical versions of this procedure with preliminary improvements in compensatory sweating and systemic symptoms. But reconstruction is complex surgery in its own right, and no pharmacologic or minimally invasive treatment currently exists that reliably reverses the systemic complications of ETS.

The study has limitations that temper but do not erase its message. Its cross-sectional design cannot prove causation, surgical details such as the exact level and extent of sympathectomy were self-reported and often incomplete, and recruitment through online hyperhidrosis communities may have overrepresented dissatisfied patients, potentially inflating symptom prevalence. The questionnaire has not yet been externally validated in independent cohorts, and no objective autonomic testing was performed. Even so, the sheer consistency of the signal across four symptom domains, measured against a validated instrument and a control group, makes a compelling case that ETS is not the localized procedure it is often portrayed to be. As the authors conclude, the operation produces global dysregulation of sympathetic control, and patients deserve preoperative counseling that reflects the true, multisystemic scope of what they are signing up for.

Subject of Research: Systemic adverse effects of endoscopic thoracic sympathectomy for hyperhidrosis

Article Title: The systemic adverse effects of endoscopic thoracic sympathectomy are underrecognized: a questionnaire-based study

Article References: Sung, C. W.-H., Chen, L. W.-Y., Lee, C.-H., Lu, J. C.-Y., Huang, J.-J., Chao, Y.-K., Chuang, D. C.-C., & Chang, T. N.-J. (2025). The systemic adverse effects of endoscopic thoracic sympathectomy are underrecognized: a questionnaire-based study. BMC Plastic and Reconstructive Surgery, 1(1), Article 7. https://doi.org/10.1186/s44452-025-00007-3

Image Credits: AI Generated

DOI: 10.1186/s44452-025-00007-3

Keywords: endoscopic thoracic sympathectomy, hyperhidrosis, compensatory sweating, autonomic nervous system, sympathetic chain, brain fog, vasomotor dysregulation, questionnaire study, sympathetic trunk reconstruction, patient counseling, central autonomic network, surgical complications