Lennon and colleagues report on the associations between sport-related concussion (SRC), non-sports-related concussion (nSRC) and long-term cognitive and behavioural outcomes in a longitudinal cohort of community-dwelling adults. Findings suggest that those with SRC showed no long-term cognitive or behavioural deficits compared with those with no concussions. Moreover, it is suggested those with SRC showed better performance in working memory and verbal reasoning at the study baseline which is hypothesized to be due to the ‘benefits of sport’ in the form of physical, social and economic benefits. The authors suggest these findings will help inform physicians and public health authorities when communicating the risks and benefits of community sports to patients and the public.
As the authors note, their findings are “at odds with much of the SRC literature”. This is likely a contributing factor to the media coverage of this research. At the time of writing, The Times, The Telegraph and the Guardian have all reported on the studies finding with variations on the benefits of ‘amateur sport’ outweighing the risk of concussion. The NIHR Applied Health Research and Care South West Peninsula, that supported the research, has also hosted a press release titled ‘Sports concussions in non-athletes not linked to long-term brain problems’. There is a common feature to all the press coverage so far: all have used images of adults or children playing what appears to be contact ru...
Lennon and colleagues report on the associations between sport-related concussion (SRC), non-sports-related concussion (nSRC) and long-term cognitive and behavioural outcomes in a longitudinal cohort of community-dwelling adults. Findings suggest that those with SRC showed no long-term cognitive or behavioural deficits compared with those with no concussions. Moreover, it is suggested those with SRC showed better performance in working memory and verbal reasoning at the study baseline which is hypothesized to be due to the ‘benefits of sport’ in the form of physical, social and economic benefits. The authors suggest these findings will help inform physicians and public health authorities when communicating the risks and benefits of community sports to patients and the public.
As the authors note, their findings are “at odds with much of the SRC literature”. This is likely a contributing factor to the media coverage of this research. At the time of writing, The Times, The Telegraph and the Guardian have all reported on the studies finding with variations on the benefits of ‘amateur sport’ outweighing the risk of concussion. The NIHR Applied Health Research and Care South West Peninsula, that supported the research, has also hosted a press release titled ‘Sports concussions in non-athletes not linked to long-term brain problems’. There is a common feature to all the press coverage so far: all have used images of adults or children playing what appears to be contact rugby.
Any reader would reasonably assume then that this research had a clear focus on ‘contact sports’. Especially so given the senior author is quoted in the NIHR press release explicitly saying, “This study suggests that there could be long-term benefits from sport which could outweigh any negative effects of concussions, which could have important implications for policy decisions around contact sport participation”. But what seems to be missing from the research article is information about exactly what ‘sport’ the participants did across the groups created for analysis.
In the supplementary material, Table S3 shows the ‘Head injury scenario questions’ used to categorise these groups. Yet little clarity is offered here. The sport-related concussion group appears to have been categorised based on responses to two questions: 1) Have you ever had a blow to the head while biking? (cycling), 2) Have you ever had a blow to the head while playing sports? (football, baseball, basketball etc). This is a very wide category to group as ‘SRC’. Without further clarification, this could plausibly include any of the following head injury events: falling off a bicycle whilst riding to work, falling over playing table tennis, being punched in the head whilst boxing or receiving a high-impact tackle playing rugby. Clearly, the context of each of these varies significantly. Interestingly, this instrument also seems to categorise head injuries sustained from rollerblading/skateboarding, horse riding and skiing as ‘Non-sport related’. Furthermore, given the focus on the benefits of ‘sport’ for long-term cognitive health, it is surprising that the sporting backgrounds of those that were in the ‘nSRC’ and ‘Mixed concussion group’ were not reported.
The definition and conceptualisation of what constitutes ‘sport’ is not clear in the article which makes interpretation of the findings difficult. ‘Community sport’ is used but what this is referring to is not explained. Given the ongoing public health concerns with brain health in contact sports specifically, accuracy is paramount. We urge the authors to clarify the sporting backgrounds of their participants so the scientific community, policy makers, the public and the media can be better placed to evaluate these findings.
Dear Editor,
I read with interest the recent systematic review by Trinidade et al. on predictors of persistent postural-perceptual dizziness (PPPD) following peripheral vestibular disorders (1). The authors provided a thoughtful synthesis of the literature and identified key psychological factors associated with PPPD development. However, I believe the review overlooked some relevant evidence regarding additional predictors and pathophysiological mechanisms of chronic dizziness.
Specifically, the authors did not discuss the potential role of cervical spine dysfunction and somatosensory abnormalities as PPPD risk factors. Several studies have identified exaggerated cervical spine proprioceptive signals and impaired cervical graviceptive processing in patients with PPPD (2). Additionally, there is evidence that migraine and migraine-related vestibulopathy may predispose individuals to developing chronic subjective dizziness after acute peripheral vestibular events (3,4). Investigation of these factors may provide further insight into PPPD pathophysiology.
Moreover, the authors focused their review on peripheral vestibular disorders as PPPD triggers. However, central vestibular disorders like vestibular migraine can also lead to PPPD, especially among those with pre-existing migraine. (5) A review incorporating evidence from central vestibular precipitants could offer a more comprehensive view of PPPD development.
In summary, while Trinidade et al. pre...
Dear Editor,
I read with interest the recent systematic review by Trinidade et al. on predictors of persistent postural-perceptual dizziness (PPPD) following peripheral vestibular disorders (1). The authors provided a thoughtful synthesis of the literature and identified key psychological factors associated with PPPD development. However, I believe the review overlooked some relevant evidence regarding additional predictors and pathophysiological mechanisms of chronic dizziness.
Specifically, the authors did not discuss the potential role of cervical spine dysfunction and somatosensory abnormalities as PPPD risk factors. Several studies have identified exaggerated cervical spine proprioceptive signals and impaired cervical graviceptive processing in patients with PPPD (2). Additionally, there is evidence that migraine and migraine-related vestibulopathy may predispose individuals to developing chronic subjective dizziness after acute peripheral vestibular events (3,4). Investigation of these factors may provide further insight into PPPD pathophysiology.
Moreover, the authors focused their review on peripheral vestibular disorders as PPPD triggers. However, central vestibular disorders like vestibular migraine can also lead to PPPD, especially among those with pre-existing migraine. (5) A review incorporating evidence from central vestibular precipitants could offer a more comprehensive view of PPPD development.
In summary, while Trinidade et al. presented a helpful systematic review, consideration of these additional predictors and vestibular disorders may provide a more complete understanding of PPPD pathophysiology. This could inform future research directions and lead to improved early identification of at-risk patients.
References:
1. Trinidade A, Cabreira V, Goebel JA, Staab JP, Kaski D, Stone J. Predictors of persistent postural-perceptual dizziness (PPPD) and similar forms of chronic dizziness precipitated by peripheral vestibular disorders: a systematic review. J Neurol Neurosurg Psychiatry. 2023 Nov;94(11):904-915. doi: 10.1136/jnnp-2022-330196. Epub 2023 Mar 20. PMID: 36941047.
2. Jooyeon, Jamie, Im., Seunghee, Na., Hyeonseok, S., Jeong., Yong-An, Chung. A Review of Neuroimaging Studies in Persistent Postural-Perceptual Dizziness (PPPD).. Nuclear Medicine and Molecular Imaging, (2021). doi: 10.1007/S13139-020-00675-2
3. Brian, A., Neff., Jeffrey, P., Staab., Scott, D.Z., Eggers., Matthew, L., Carlson., William, R., Schmitt., Kathryn, M., Van, Abel., Douglas, K., Worthington., Charles, W., Beatty., Colin, L., W., Driscoll., Neil, T., Shepard. Auditory and vestibular symptoms and chronic subjective dizziness in patients with Ménière's disease, vestibular migraine, and Ménière's disease with concomitant vestibular migraine.. Otology & Neurotology, (2012). doi: 10.1097/MAO.0B013E31825D644A
4. Yoon, Hee, Cha., Robert, W., Baloh. Migraine associated vertigo.. Journal of Clinical Neurology, (2007). doi: 10.3988/JCN.2007.3.3.121
5. Stephen, P., Cass., Jennifer, K., P., Ankerstjerne., Sertac, Yetiser., Joseph, M., Furman., Carey, D., Balaban., Barlas, Aydogan. Migraine-Related Vestibulopathy:. Annals of Otology, Rhinology, and Laryngology, (1997). doi: 10.1177/000348949710600302
To the Editor,
I am writing to commend and engage with the recently published study, "Cognition in patients with myelin oligodendrocyte glycoprotein antibody-associated disease: a prospective, longitudinal, multicentre study of 113 patients (CogniMOG-Study)." (1). This pioneering work addresses a crucial yet underexplored aspect of MOGAD, namely its impact on cognitive function. The study represents a significant advancement in understanding cognitive impairments associated with this rare but impactful condition.
Significance of Findings: The CogniMOG-Study provides a comprehensive assessment of cognitive function in MOGAD patients, revealing that while cognitive deficits are present, they are relatively limited compared to other neuroinflammatory conditions. The observed impairments in semantic fluency and processing speed are particularly noteworthy. These findings suggest that cognitive deficits in MOGAD primarily affect verbal and information processing domains, which are critical for daily functioning and quality of life.
The study’s longitudinal design is a particular strength, allowing for the observation of cognitive changes over time. The absence of significant cognitive decline over the follow-up periods is an encouraging finding, suggesting stability in cognitive function among MOGAD patients. However, it also raises questions about the factors contributing to cognitive stability and the potential for practice effects, which merit fur...
To the Editor,
I am writing to commend and engage with the recently published study, "Cognition in patients with myelin oligodendrocyte glycoprotein antibody-associated disease: a prospective, longitudinal, multicentre study of 113 patients (CogniMOG-Study)." (1). This pioneering work addresses a crucial yet underexplored aspect of MOGAD, namely its impact on cognitive function. The study represents a significant advancement in understanding cognitive impairments associated with this rare but impactful condition.
Significance of Findings: The CogniMOG-Study provides a comprehensive assessment of cognitive function in MOGAD patients, revealing that while cognitive deficits are present, they are relatively limited compared to other neuroinflammatory conditions. The observed impairments in semantic fluency and processing speed are particularly noteworthy. These findings suggest that cognitive deficits in MOGAD primarily affect verbal and information processing domains, which are critical for daily functioning and quality of life.
The study’s longitudinal design is a particular strength, allowing for the observation of cognitive changes over time. The absence of significant cognitive decline over the follow-up periods is an encouraging finding, suggesting stability in cognitive function among MOGAD patients. However, it also raises questions about the factors contributing to cognitive stability and the potential for practice effects, which merit further investigation.
Clinical and Research Implications: The identification of cerebral lesions as a predictor of cognitive deficits is a critical insight. This association underscores the importance of considering cerebral involvement when evaluating cognitive function in MOGAD patients. It also highlights the need for further research into the specific neurobiological mechanisms that link cerebral lesions with cognitive impairment.
The study’s findings have important implications for clinical practice. Understanding that MOGAD patients may experience specific cognitive challenges can inform the development of targeted cognitive rehabilitation strategies. Moreover, recognizing the relatively mild nature of cognitive impairments compared to conditions like NMOSD can guide more nuanced patient assessments and management plans.
Limitations and Future Directions: While the study is a valuable contribution, several limitations should be acknowledged. The use of normative data that may not reflect current population characteristics could impact the interpretation of cognitive test results. Additionally, the exclusion of severely affected patients from neuropsychological testing may limit the generalizability of the findings. Future research should address these limitations by incorporating updated normative data and including a broader range of patients.
Furthermore, the study highlights the need for ongoing longitudinal research to explore cognitive changes beyond the 2-year follow-up. Longer-term studies could provide deeper insights into the trajectory of cognitive function in MOGAD and help distinguish between genuine cognitive changes and methodological artifacts such as practice effects.
Conclusion: In conclusion, the CogniMOG-Study is a significant step forward in understanding the cognitive profile of MOGAD patients. It provides valuable insights into the nature and extent of cognitive impairments associated with this condition and sets the stage for future research and clinical advancements. I applaud the authors for their meticulous work and look forward to continued exploration in this vital area of research.
References
1. Passoke S, Stern C, Häußler V, et alCognition in patients with myelin oligodendrocyte glycoprotein antibody-associated disease: a prospective, longitudinal, multicentre study of 113 patients (CogniMOG-Study)Journal of Neurology, Neurosurgery & Psychiatry Published Online First: 30 July 2024. doi: 10.1136/jnnp-2024-333994
Dear Editor,
I am writing to offer a comprehensive analysis and reflection on the manuscript titled "Oral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapse" (1). This study, which delves into the intricate nuances of managing MOGAD, presents crucial findings that could significantly impact clinical practice and patient outcomes.
The complexity of MOGAD lies not only in its diverse clinical presentations but also in its variable response to treatment modalities. As highlighted in the manuscript's introduction, MOGAD encompasses a spectrum of neurological manifestations, ranging from optic neuritis and transverse myelitis to acute disseminated encephalomyelitis. The recent establishment of consensus diagnostic criteria marks a pivotal advancement in early recognition and intervention, underscoring the urgency for evidence-based therapeutic strategies.
One of the most compelling aspects of the study is its exploration of the optimal corticosteroid regimen at MOGAD onset, aiming to delay the time to first relapse (TTFR) while minimizing cumulative corticosteroid exposure. By retrospectively analyzing data from a multicenter cohort comprising 109 patients, the authors meticulously assessed the relationship between corticosteroid dosage and taper duration and the subsequent risk of relapse. The utilization of Cox proportional hazards models, along...
Dear Editor,
I am writing to offer a comprehensive analysis and reflection on the manuscript titled "Oral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapse" (1). This study, which delves into the intricate nuances of managing MOGAD, presents crucial findings that could significantly impact clinical practice and patient outcomes.
The complexity of MOGAD lies not only in its diverse clinical presentations but also in its variable response to treatment modalities. As highlighted in the manuscript's introduction, MOGAD encompasses a spectrum of neurological manifestations, ranging from optic neuritis and transverse myelitis to acute disseminated encephalomyelitis. The recent establishment of consensus diagnostic criteria marks a pivotal advancement in early recognition and intervention, underscoring the urgency for evidence-based therapeutic strategies.
One of the most compelling aspects of the study is its exploration of the optimal corticosteroid regimen at MOGAD onset, aiming to delay the time to first relapse (TTFR) while minimizing cumulative corticosteroid exposure. By retrospectively analyzing data from a multicenter cohort comprising 109 patients, the authors meticulously assessed the relationship between corticosteroid dosage and taper duration and the subsequent risk of relapse. The utilization of Cox proportional hazards models, along with Simon-Makuch and Kaplan-Meier plots, provided a robust framework for elucidating these intricate dynamics.
The key findings of the study underscore the critical role of corticosteroids in modulating disease activity at MOGAD onset. Notably, the recommendation of initiating a prednisone dose of 12.5 mg/day (0.16 mg/kg/day for children) for a minimum duration of 3 months yielded a remarkable 88% reduction in the risk of relapse compared to alternative regimens. Moreover, the absence of severe adverse events among patients receiving this dosage further accentuates its safety profile, reassuring clinicians of its therapeutic viability.
However, amidst the optimism surrounding these findings, it is imperative to acknowledge the inherent limitations of retrospective studies, including potential selection biases and variability in clinical practices across centers. The authors' candid acknowledgment of these limitations underscores the need for further prospective studies to validate and refine the proposed therapeutic approach.
Beyond its immediate clinical implications, the study prompts broader contemplation on the intricacies of balancing therapeutic efficacy with long-term safety considerations. The delicate interplay between relapse prevention and corticosteroid-related adverse effects necessitates a nuanced and patient-centered approach to treatment decision-making. The proposed regimen represents a commendable stride towards achieving this equilibrium, offering a pragmatic framework for optimizing patient outcomes while mitigating potential risks.
In conclusion, the manuscript makes a significant contribution to the evolving landscape of MOGAD management, offering evidence-based insights that have the potential to revolutionize clinical practice. By delineating a clear roadmap for corticosteroid optimization at disease onset, the study empowers clinicians with valuable tools to navigate the complexities of MOGAD management effectively.
References
1. Trewin BP, Dale RC, Qiu J, et alOral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapseJournal of Neurology, Neurosurgery & Psychiatry Published Online First: 14 May 2024. doi: 10.1136/jnnp-2024-333463
I am writing to provide a more in-depth discussion on the recently published article, "Cognitive trajectory in the first year after first-ever ischaemic stroke in young adults: the ODYSSEY study." [1]. This study offers valuable insights into the intricate dynamics of cognitive recovery following ischaemic strokes in young adults, shedding light on the challenges and potential predictors of cognitive outcomes.
The central finding, highlighting the persistent prevalence of cognitive impairment in young stroke patients even one year post-event, underscores the gravity of the issue. The study's longitudinal design, incorporating cognitive assessments at distinct time points within the first year, provides a nuanced understanding of the trajectory of cognitive changes. Notably, the observation of specific improvements in processing speed, visuoconstruction, and executive functioning among initially cognitively impaired patients adds granularity to our comprehension of post-stroke recovery.
The study's discussion on the complex factors influencing cognitive recovery, such as age and lesion volume, enriches the narrative. However, the candid acknowledgment of the challenges in predicting cognitive recovery at an individual level reflects the intricate nature of post-stroke outcomes. Exploring the potential role of post-stroke fatigue and the absence of uniform predictors for recovery contribute to the depth of the article. The...
I am writing to provide a more in-depth discussion on the recently published article, "Cognitive trajectory in the first year after first-ever ischaemic stroke in young adults: the ODYSSEY study." [1]. This study offers valuable insights into the intricate dynamics of cognitive recovery following ischaemic strokes in young adults, shedding light on the challenges and potential predictors of cognitive outcomes.
The central finding, highlighting the persistent prevalence of cognitive impairment in young stroke patients even one year post-event, underscores the gravity of the issue. The study's longitudinal design, incorporating cognitive assessments at distinct time points within the first year, provides a nuanced understanding of the trajectory of cognitive changes. Notably, the observation of specific improvements in processing speed, visuoconstruction, and executive functioning among initially cognitively impaired patients adds granularity to our comprehension of post-stroke recovery.
The study's discussion on the complex factors influencing cognitive recovery, such as age and lesion volume, enriches the narrative. However, the candid acknowledgment of the challenges in predicting cognitive recovery at an individual level reflects the intricate nature of post-stroke outcomes. Exploring the potential role of post-stroke fatigue and the absence of uniform predictors for recovery contribute to the depth of the article. The use of the Reliable Change Index (RCI) as a method for assessing cognitive recovery, though rigorous, prompts thoughtful consideration of its implications and potential impact on the observed outcomes.
Nevertheless, it is crucial to address the inherent limitations in the study to ensure a balanced interpretation of the results. The exclusion of cognitive data for patients with more severe strokes introduces a potential bias that warrants cautious generalization of the findings. The absence of information on interventions such as cognitive rehabilitation and the wide temporal range of baseline assessments pose challenges to the study's precision. These limitations, conscientiously noted in the article, emphasize the importance of interpreting the results within a nuanced context.
In conclusion, the "ODYSSEY study" significantly advances our understanding of cognitive recovery after ischaemic strokes in young adults. The enduring challenges faced by this population are well-captured, but a meticulous consideration of the study's limitations is paramount. Future research endeavors should strive to address these limitations, providing a more comprehensive understanding of post-stroke cognitive trajectories and guiding effective interventions for young stroke patients.
References
1. Schellekens MMI, Springer RCS, Boot EM, et alCognitive trajectory in the first year after first-ever ischaemic stroke in young adults: the ODYSSEY studyJournal of Neurology, Neurosurgery & Psychiatry Published Online First: 30 December 2023. doi: 10.1136/jnnp-2023-332104
I recently had the opportunity to read your article titled "Prognostic Value of Spinal Cord Lesion Measures in Early Relapsing-Remitting Multiple Sclerosis" [1] and I want to extend my appreciation for the significant contribution your research has made to the field of multiple sclerosis (MS). Your study investigated the relation of whole spinal cord lesion number (SCLN) and volume (SCLV) to the future occurrence and type of confirmed disability accumulation (CDA) in patients with relapsing-remitting MS. The manual delineation of SC lesions and the subsequent analyses provided valuable insights into the prospective value of these measures in predicting clinical outcomes. The significant association between the absence of SC lesions and reduced CDA risk suggests the importance of SC lesions as a prognostic indicator in MS. Additionally, the close correlation between SCLN and SCLV, and their independent association with CDA, provide further support for the relevance of these measures in predicting disability accumulation.
The classification of CDA events into progression independent of relapse activity (PIRA) and relapse-associated worsening (RAW) facilitated a nuanced analysis of their association with SC lesion measures. The significant association with PIRA, but not RAW, hints at distinct underlying mechanisms for different types of disability progression, which could have implications for treatment strategies.
While your study provides valuable insi...
I recently had the opportunity to read your article titled "Prognostic Value of Spinal Cord Lesion Measures in Early Relapsing-Remitting Multiple Sclerosis" [1] and I want to extend my appreciation for the significant contribution your research has made to the field of multiple sclerosis (MS). Your study investigated the relation of whole spinal cord lesion number (SCLN) and volume (SCLV) to the future occurrence and type of confirmed disability accumulation (CDA) in patients with relapsing-remitting MS. The manual delineation of SC lesions and the subsequent analyses provided valuable insights into the prospective value of these measures in predicting clinical outcomes. The significant association between the absence of SC lesions and reduced CDA risk suggests the importance of SC lesions as a prognostic indicator in MS. Additionally, the close correlation between SCLN and SCLV, and their independent association with CDA, provide further support for the relevance of these measures in predicting disability accumulation.
The classification of CDA events into progression independent of relapse activity (PIRA) and relapse-associated worsening (RAW) facilitated a nuanced analysis of their association with SC lesion measures. The significant association with PIRA, but not RAW, hints at distinct underlying mechanisms for different types of disability progression, which could have implications for treatment strategies.
While your study provides valuable insights, I also acknowledge the limitations you outlined. A prospective design, although challenging, would have strengthened the study's findings. Furthermore, the relatively low number of patients with disability worsening necessitated classifying only the first CDA event, limiting the exploration of potential later events and subsequent subgroup analyses. The use of three different MRI scanners might have increased data heterogeneity, but it also enhanced the generalizability of the results.
Differentiating between symptomatic and asymptomatic SC lesions and considering the potential benefits of using 3D gradient-recalled echo sequences for lesion detection could have further enriched the study's findings.
Notwithstanding these limitations, your research is a valuable addition to the existing literature on MS prognostication. Your findings hold promise for improving patient care by providing clinicians with valuable prognostic information to guide treatment decisions.
Once again, I commend you and your team for your excellent work. Your dedication to advancing our understanding of multiple sclerosis is commendable, and I look forward to seeing how your research progresses in the future.
References
1. Markus L, Julian M, Matthias B, et al. Prognostic value of spinal cord lesion measures in early relapsing-remitting multiple sclerosis. Journal of Neurology, Neurosurgery & Psychiatry. 2023:jnnp-2023-331799. doi: 10.1136/jnnp-2023-331799.
Dear Editor,
I am writing to express my appreciation for the enlightening article titled "Childbirth Delivery Mode and the Risk of Multiple Sclerosis: A Prospective Population-Based Study" [1] recently published in your esteemed journal. The study, which examines the potential relationship between childbirth mode and the subsequent risk of multiple sclerosis (MS) development, presents a comprehensive analysis and incites intriguing discussions. The authors embarked on a commendable endeavor by conducting a meticulous prospective cohort study encompassing individuals born in Norway between 1967 and 2003. Their investigation aimed to unravel the potential influence of caesarean section (CS) births on the risk of adult-onset MS. The findings unveil an association suggesting an 18% elevated risk of MS among individuals born via CS, as compared to those born vaginally, after considering an array of confounding factors. However, the authors astutely highlight that this association does not persist when a sibling-matched analysis is undertaken. Furthermore, this intriguing connection appears to be primarily confined to individuals born preterm or via emergency CS. Such nuanced insights underline the complexities underlying the childbirth mode and MS risk paradigm, necessitating a thoughtful interpretation of the findings.
The authors acknowledge the divergent findings from previous studies, emphasizing the discrepancies between their results and those report...
Dear Editor,
I am writing to express my appreciation for the enlightening article titled "Childbirth Delivery Mode and the Risk of Multiple Sclerosis: A Prospective Population-Based Study" [1] recently published in your esteemed journal. The study, which examines the potential relationship between childbirth mode and the subsequent risk of multiple sclerosis (MS) development, presents a comprehensive analysis and incites intriguing discussions. The authors embarked on a commendable endeavor by conducting a meticulous prospective cohort study encompassing individuals born in Norway between 1967 and 2003. Their investigation aimed to unravel the potential influence of caesarean section (CS) births on the risk of adult-onset MS. The findings unveil an association suggesting an 18% elevated risk of MS among individuals born via CS, as compared to those born vaginally, after considering an array of confounding factors. However, the authors astutely highlight that this association does not persist when a sibling-matched analysis is undertaken. Furthermore, this intriguing connection appears to be primarily confined to individuals born preterm or via emergency CS. Such nuanced insights underline the complexities underlying the childbirth mode and MS risk paradigm, necessitating a thoughtful interpretation of the findings.
The authors acknowledge the divergent findings from previous studies, emphasizing the discrepancies between their results and those reported in an Iranian case–control study. This retrospective analysis, while reporting a substantial increase in MS risk among individuals born by CS, utilized self-reported data and was susceptible to potential biases [2]. The contrast between this study and a Danish nationwide cohort study also warrants consideration [3]. In both studies, similar estimates were observed when adjusting for pertinent factors, indicating a convergence of findings.
The study delves into intriguing potential mechanisms underlying the observed associations. The authors propose that alterations in gut microbiota, delayed immune system development, and differential cytokine responses may underpin the relationship between CS births and MS risk. The exploration of these pathways adds a layer of depth to the investigation, urging further research into the intricate interplay between childbirth experiences and immune-mediated diseases.
While the study boasts numerous strengths, such as its large population-based cohort, prospective design, and verification of MS cases by neurologists, the authors candidly delineate its limitations. The lack of generalizability to other populations due to the exclusive focus on Norwegian individuals is acknowledged, as is the absence of maternal smoking information for certain cohorts. Despite these limitations, the sibling-matched analyses and comprehensive data integration fortify the study's robustness.
In conclusion, the study "Childbirth Delivery Mode and the Risk of Multiple Sclerosis: A Prospective Population-Based Study" significantly advances our understanding of the intricate relationship between childbirth mode and MS risk. The authors' astute exploration of potential mechanisms, combined with the meticulous consideration of confounding factors, highlights the need for cautious interpretation. The association identified between CS births and MS risk, particularly in subgroups with complicated pregnancies, beckons further investigation into the underlying confounders shaping this relationship. This study underscores the importance of ongoing research into the nexus between early life experiences and long-term health outcomes, contributing valuable insights into our understanding of immune-mediated diseases.
Thank you for providing a platform for this thought-provoking study, and I look forward to witnessing future advancements in this evolving field.
References
1. Akash, K., et al., Childbirth delivery mode and the risk of multiple sclerosis: a prospective population-based study. Journal of Neurology, Neurosurgery & Psychiatry, 2023: p. jnnp-2023-331241.
2. Maghzi, A.H., et al., Cesarean delivery may increase the risk of multiple sclerosis. Mult Scler, 2012. 18(4): p. 468-71.
3. Nielsen, N.M., et al., Cesarean section and offspring's risk of multiple sclerosis: a Danish nationwide cohort study. Mult Scler, 2013. 19(11): p. 1473-7.
There are several shortcomings in the commentary by White et al. For brevity, this response focuses on four main points.
1. New case definition
In the past 20 years, multiple case definitions have been published that require post-exertional malaise (PEM) as a core feature of ME/CFS, such as the Canadian Consensus Criteria (CCC), International Consensus Criteria (ICC), and the Institute of Medicine (IOM) criteria. NICE’s definition is based on the latter.
These case definitions are the ones used in research and clinical practice today. White et al. refer to the 1994 criteria developed by the Centers for Disease Control and Prevention (CDC) but the CDC no longer seems to use this case definition. Instead, they advise healthcare providers to diagnose ME/CFS using the IOM criteria where PEM is a required symptom.
NICE evaluated scientific evidence for ME/CFS as it is currently defined and not for a case definition that was published nearly 30 years ago. Other reviews on ME/CFS, such as the recent one by IQWIG in Germany, have used a similar approach. (1)
It is incorrect to state that NICE “downgraded nearly thirty years of research.” The previous NICE guidance from 2007 on ME/CFS already highlighted PEM as a core feature of ME/CFS, and studies that used this description were not downgraded in the evidence review. Neither were studies that used the CCC, ICC, or IOM criteria mentioned above.
There are several shortcomings in the commentary by White et al. For brevity, this response focuses on four main points.
1. New case definition
In the past 20 years, multiple case definitions have been published that require post-exertional malaise (PEM) as a core feature of ME/CFS, such as the Canadian Consensus Criteria (CCC), International Consensus Criteria (ICC), and the Institute of Medicine (IOM) criteria. NICE’s definition is based on the latter.
These case definitions are the ones used in research and clinical practice today. White et al. refer to the 1994 criteria developed by the Centers for Disease Control and Prevention (CDC) but the CDC no longer seems to use this case definition. Instead, they advise healthcare providers to diagnose ME/CFS using the IOM criteria where PEM is a required symptom.
NICE evaluated scientific evidence for ME/CFS as it is currently defined and not for a case definition that was published nearly 30 years ago. Other reviews on ME/CFS, such as the recent one by IQWIG in Germany, have used a similar approach. (1)
It is incorrect to state that NICE “downgraded nearly thirty years of research.” The previous NICE guidance from 2007 on ME/CFS already highlighted PEM as a core feature of ME/CFS, and studies that used this description were not downgraded in the evidence review. Neither were studies that used the CCC, ICC, or IOM criteria mentioned above.
2. Blinding and subjective outcomes
White et al. write: “The NICE committee decided to downgrade all fatigue outcomes based on the premise that it is a subjective measure.” This is incorrect. Fatigue outcomes in studies with a low risk of bias such as the double-blind Rituximab trial were not downgraded.
NICE did downgrade quality of evidence when subjective outcomes (not just fatigue, but also pain, sleep, quality of life, etc.) were used in trials where participants and therapists were not blinded as this combination creates a high risk of bias. This grading is in accordance with the Cochrane Handbook which states that “the potential for bias cannot be ignored even if the outcome assessor cannot be blinded." (2) In the case of patient-reported outcome measures such as fatigue, the Cochrane Handbook considers patients to be the outcome assessor.
Moreover, trials of GET and CBT also included objective measurements such as fitness tests, actigraphy, and employment data and these indicated no clinically relevant improvements. (3)
3. Long-term follow-up
The largest studies on GET and CBT — the PACE (4) and GETSET (5) trials — failed to find significant benefits of these interventions at their longest follow-up. This suggests that initial improvements might be due to response bias or a placebo effect. It is questionable to recommend treatments if the long-term follow-up shows no benefit.
In both GETSET and PACE, a sensitivity analysis indicated that additional treatment received after randomization was unlikely to explain the null results. The authors of GETSET reported that “there is no evidence that the improvements observed in the SMC group were due to them having received more exposure to therapy than the GES group after trial completion.” (5) Similarly, in the PACE trial the control group caught up on the intervention group and “there was some evidence from an exploratory analysis that improvement after the 1-year trial final outcome was not associated with receipt of additional treatment with CBT or GET.” (4)
4. Harms
The Cochrane review on GET included only randomized trials but concluded: “We are uncertain about the risk of serious adverse reactions because the certainty of the evidence is very low.” (6) There was too little data on adverse effects to form a conclusion.
Surveys and qualitative studies, on the other hand, have consistently found a negative impact of GET on some ME/CFS patients. This has been reported for several decades, in multiple countries, and with little indication that harms are due to improper implementation of GET. (7) Considering the adage ‘primum non nocere’, it is sensible to use a lower threshold for evaluating evidence on the potential harms of a medical intervention compared with its potential benefits.
At the NICE Roundtable Discussion prior to Guideline release (8), health profession stakeholders had ample opportunity to raise concerns. Following clear, succinct responses from a representative of the committee, consistent with our comments above, no further objections were raised.
2. Higgins JPT, Thomas J, Chandler J, Cumpston M, Li T, Page MJ, et al. Cochrane Handbook for Systematic Reviews of Interventions. 2nd Edition. Chichester (UK): John Wiley & Sons; 2019.
3. Vink M, Vink-Niese A. Graded exercise therapy for myalgic encephalomyelitis/chronic fatigue syndrome is not effective and unsafe. Re-analysis of a Cochrane review. Health Psychol Open. 2018 Dec;5(2):2055102918805187.
4. Sharpe M, Goldsmith KA, Johnson AL, Chalder T, Walker J, White PD. Rehabilitative treatments for chronic fatigue syndrome: long-term follow-up from the PACE trial. Lancet Psychiatry. 2015 Dec 1;2(12):1067–74.
5. Clark LV, McCrone P, Pesola F, Vergara-Williamson M, White PD. Guided graded exercise self-help for chronic fatigue syndrome: Long term follow up and cost-effectiveness following the GETSET trial. J Psychosom Res. 2021 Jul 1;146:110484.
7. Geraghty K, Hann M, Kurtev S. Myalgic encephalomyelitis/chronic fatigue syndrome patients’ reports of symptom changes following cognitive behavioural therapy, graded exercise therapy and pacing treatments: Analysis of a primary survey compared with secondary surveys. J Health Psychol. 2019 Sep;24(10):1318–33.
The authors revised this Rapid Response at BMJ's request in line with BMJ's Terms and Conditions for Rapid Responses.
Dear Editor,
In the article ‘Anomalies in the review process and interpretation of the evidence in the NICE guideline for chronic fatigue syndrome and myalgic encephalomyelitis’ published in the Journal of Neurology, Neurosurgery & Psychiatry on 10th July 2023, the authors claim NICE invented a new definition of ME. These claims are unfounded as NICE used the Institute of Medicine (IOM) criteria which is now 8 years old and was created using a more robust process than many other definitions as it drew on samples from different countries and compared the most widely used definitions of ME.
One area where NICE felt there was a gap in the IOM criteria was the lack of an empirical process alongside other methods. Leonard Jason's four-item empiric criteria were the only criteria that used adequate empiric methods, and this aligned very closely with the IOM criteria. As a result, NICE operationalised the IOM criteria for use in the NHS, with the four-item criteria helping to substantiate their approach.
NICE does not measure a trial’s success based on the researchers’ own terms but by analysing the raw data and applying the committee's agreed protocol. This allows NICE to measure whether a treatment had an effect or not. This is striking when looking at the assertion that research showed that the favoured treatment...
The authors revised this Rapid Response at BMJ's request in line with BMJ's Terms and Conditions for Rapid Responses.
Dear Editor,
In the article ‘Anomalies in the review process and interpretation of the evidence in the NICE guideline for chronic fatigue syndrome and myalgic encephalomyelitis’ published in the Journal of Neurology, Neurosurgery & Psychiatry on 10th July 2023, the authors claim NICE invented a new definition of ME. These claims are unfounded as NICE used the Institute of Medicine (IOM) criteria which is now 8 years old and was created using a more robust process than many other definitions as it drew on samples from different countries and compared the most widely used definitions of ME.
One area where NICE felt there was a gap in the IOM criteria was the lack of an empirical process alongside other methods. Leonard Jason's four-item empiric criteria were the only criteria that used adequate empiric methods, and this aligned very closely with the IOM criteria. As a result, NICE operationalised the IOM criteria for use in the NHS, with the four-item criteria helping to substantiate their approach.
NICE does not measure a trial’s success based on the researchers’ own terms but by analysing the raw data and applying the committee's agreed protocol. This allows NICE to measure whether a treatment had an effect or not. This is striking when looking at the assertion that research showed that the favoured treatments of CBT and GET were safe, when, in reality, safety data either was not collected or was incomplete or uninterpretable. These treatments have led to many complaints from people with ME that they were harmful and led to deterioration. This was illustrated in the MEAction UK 2019 report, ME services in the UK Not Fit For Purpose.
The authors of this critique also claim that NICE didn't aggregate data properly, but there are hundreds of pages of meta-analysis proving they were meticulous and gave detailed consideration to every trial they looked at. The real complaint here seems to be that NICE didn't aggregate data in the way the authors of this paper wish they had. For example, the Cochrane review of exercise in ME, which many of these authors favour, pools results from multiple different interventions with very different protocols, and this has been argued to provide an evidence base for GET by extension. But that would be like pooling the evidence for CBT, DBT, ABA, psychoanalysis and counselling, and then claiming this proves ABA alone is effective. NICE sensibly grouped "like with like", so that trials with similar protocols were grouped together, improving the accuracy and specificity of their analysis.
The criticism that NICE gave too much weight to survey evidence, and the lived experience of people with ME, was factored into the committee's decisions alongside other evidence. ‘NICE considers all types of evidence in its evaluations. This includes evidence from published and unpublished data, data from non-UK sources, databases of ongoing clinical trials, end-to-end studies, conference proceedings, and data from registries, real-world evidence and other observational sources.’
The complaint that energy management isn't evidenced is bizarre. Energy management isn't offered as a therapy and it isn't curative. It is essentially the same as the activity management of the last guideline - which many of the same authors were happy to accept when they contributed to that guideline. Energy management is essentially a continuation of those same principles of care but it is not offered or presented as a treatment. The Forward ME group of charities has also endorsed this approach.
With regard to GET and whether fixed increments in activity were required, NICE had to look at the evidence from the trials. Numerous trials refer to increments that are fixed and shouldn't be changed except with the approval of the clinician. The PACE manual for therapists explains that GET is based on the deconditioning model and discourages reductions in exercise when in a crash, ‘A central concept of GET is to MAINTAIN exercise as much as possible during a CFS/ME setback. This is to reduce the many negative consequences of rest, and to allow the body to habituate to the increase in activity. If activity and exercise is reduced at this time, the boom/bust cycle continues, and the body is not able to desensitise to the increase in activity: which is, of course, an essential component of a graded increase in exercise and activity.’ If the treatment was delivered in a different way in practice it would indicate that the GET as researched wasn’t effective in clinical settings.
Similarly, it cannot be merely assumed that because one approach is helpful elsewhere, that it is helpful here. There is no treatment that is suitable for all diseases. Chronic primary pain isn't ME and asthma isn't diabetes and it should be self-evident that different illnesses need different treatments.
We are also concerned that news coverage about this paper (and previous news coverage quoting the same authors) continues to paint people with ME as unreliable witnesses to their own illness and lives. This is a long-standing form of bias against disabled people.
In conclusion, this article reads as an attack on the 2021 NICE guideline for ME/CFS by a group of researchers who have focussed on treating ME with Graded Exercise Therapy and CBT. By contrast, the patient community welcomes the NICE guideline and the robust review of the evidence that NICE carried out. The guideline is a real improvement on the previous version and the removal of Graded Exercise Therapy as a recommended treatment was greeted with relief. It is now time for researchers and medical staff to work with people living with ME to implement the NICE guideline throughout the NHS. Further delay and obstruction will cause more harm and increase the suffering of a very vulnerable group of people.
Whilst long overdue this paper represents a good start, to me. However it leaves me with several questions. Here are a few of them.
Will we see an immediate reduction in the number of ‘dustbin’ FND diagnoses, including amongst people deemed to be in the FND Subtypes? Will patients be empowered to define what a ‘dustbin’ diagnosis is?
Do the authors believe that the FND Society will promptly appoint an equalities expert as their new Patient Engagement Executive? I am not alone in receiving a suboptimal response from them, especially when compared to their approach to FND Portal. I was happy that he got ‘rockstar’ treatment; I got ‘appalling contempt’ and what amounts to ‘we control the narrative, you’re not welcome here’ which was interpreted as their attempt to silence women.
Was the decision not to include patient representation in the FND Subtypes paper made by a feminist?
Same question regarding the lumping of Conversion Disorder under FND in DSM, which has made it harder than ever for people with rare conditions such as Stiff Person Syndrome and Moyamoya Disease to record an initial misdiagnosis of Conversion Disorder.
Is it ethical (from a feminist perspective or any other) to use the word ‘functional’ to aid acceptance of a FND diagnosis on the basis that it doesn’t overtly point to a mental disorder diagnosis?
Can the authors assure your readers that ‘functional’ no longer means ‘hysteric...
Whilst long overdue this paper represents a good start, to me. However it leaves me with several questions. Here are a few of them.
Will we see an immediate reduction in the number of ‘dustbin’ FND diagnoses, including amongst people deemed to be in the FND Subtypes? Will patients be empowered to define what a ‘dustbin’ diagnosis is?
Do the authors believe that the FND Society will promptly appoint an equalities expert as their new Patient Engagement Executive? I am not alone in receiving a suboptimal response from them, especially when compared to their approach to FND Portal. I was happy that he got ‘rockstar’ treatment; I got ‘appalling contempt’ and what amounts to ‘we control the narrative, you’re not welcome here’ which was interpreted as their attempt to silence women.
Was the decision not to include patient representation in the FND Subtypes paper made by a feminist?
Same question regarding the lumping of Conversion Disorder under FND in DSM, which has made it harder than ever for people with rare conditions such as Stiff Person Syndrome and Moyamoya Disease to record an initial misdiagnosis of Conversion Disorder.
Is it ethical (from a feminist perspective or any other) to use the word ‘functional’ to aid acceptance of a FND diagnosis on the basis that it doesn’t overtly point to a mental disorder diagnosis?
Can the authors assure your readers that ‘functional’ no longer means ‘hysterical’ and is no longer used to convey one meaning to patients and another to their doctors (as per http://dx.doi.org/10.1136/jnnp-2011-300992)?
Given the patient demographic, the next feminist perspective paper I’d like to read could be titled ‘what is ‘functional’ doing in the overarching vestibular disorders diagnostic Venn diagram?’ Will I/we be reading that any time soon?
Lennon and colleagues report on the associations between sport-related concussion (SRC), non-sports-related concussion (nSRC) and long-term cognitive and behavioural outcomes in a longitudinal cohort of community-dwelling adults. Findings suggest that those with SRC showed no long-term cognitive or behavioural deficits compared with those with no concussions. Moreover, it is suggested those with SRC showed better performance in working memory and verbal reasoning at the study baseline which is hypothesized to be due to the ‘benefits of sport’ in the form of physical, social and economic benefits. The authors suggest these findings will help inform physicians and public health authorities when communicating the risks and benefits of community sports to patients and the public.
As the authors note, their findings are “at odds with much of the SRC literature”. This is likely a contributing factor to the media coverage of this research. At the time of writing, The Times, The Telegraph and the Guardian have all reported on the studies finding with variations on the benefits of ‘amateur sport’ outweighing the risk of concussion. The NIHR Applied Health Research and Care South West Peninsula, that supported the research, has also hosted a press release titled ‘Sports concussions in non-athletes not linked to long-term brain problems’. There is a common feature to all the press coverage so far: all have used images of adults or children playing what appears to be contact ru...
Show MoreDear Editor,
Show MoreI read with interest the recent systematic review by Trinidade et al. on predictors of persistent postural-perceptual dizziness (PPPD) following peripheral vestibular disorders (1). The authors provided a thoughtful synthesis of the literature and identified key psychological factors associated with PPPD development. However, I believe the review overlooked some relevant evidence regarding additional predictors and pathophysiological mechanisms of chronic dizziness.
Specifically, the authors did not discuss the potential role of cervical spine dysfunction and somatosensory abnormalities as PPPD risk factors. Several studies have identified exaggerated cervical spine proprioceptive signals and impaired cervical graviceptive processing in patients with PPPD (2). Additionally, there is evidence that migraine and migraine-related vestibulopathy may predispose individuals to developing chronic subjective dizziness after acute peripheral vestibular events (3,4). Investigation of these factors may provide further insight into PPPD pathophysiology.
Moreover, the authors focused their review on peripheral vestibular disorders as PPPD triggers. However, central vestibular disorders like vestibular migraine can also lead to PPPD, especially among those with pre-existing migraine. (5) A review incorporating evidence from central vestibular precipitants could offer a more comprehensive view of PPPD development.
In summary, while Trinidade et al. pre...
To the Editor,
Show MoreI am writing to commend and engage with the recently published study, "Cognition in patients with myelin oligodendrocyte glycoprotein antibody-associated disease: a prospective, longitudinal, multicentre study of 113 patients (CogniMOG-Study)." (1). This pioneering work addresses a crucial yet underexplored aspect of MOGAD, namely its impact on cognitive function. The study represents a significant advancement in understanding cognitive impairments associated with this rare but impactful condition.
Significance of Findings: The CogniMOG-Study provides a comprehensive assessment of cognitive function in MOGAD patients, revealing that while cognitive deficits are present, they are relatively limited compared to other neuroinflammatory conditions. The observed impairments in semantic fluency and processing speed are particularly noteworthy. These findings suggest that cognitive deficits in MOGAD primarily affect verbal and information processing domains, which are critical for daily functioning and quality of life.
The study’s longitudinal design is a particular strength, allowing for the observation of cognitive changes over time. The absence of significant cognitive decline over the follow-up periods is an encouraging finding, suggesting stability in cognitive function among MOGAD patients. However, it also raises questions about the factors contributing to cognitive stability and the potential for practice effects, which merit fur...
Dear Editor,
Show MoreI am writing to offer a comprehensive analysis and reflection on the manuscript titled "Oral corticosteroid dosage and taper duration at onset in myelin oligodendrocyte glycoprotein antibody-associated disease influences time to first relapse" (1). This study, which delves into the intricate nuances of managing MOGAD, presents crucial findings that could significantly impact clinical practice and patient outcomes.
The complexity of MOGAD lies not only in its diverse clinical presentations but also in its variable response to treatment modalities. As highlighted in the manuscript's introduction, MOGAD encompasses a spectrum of neurological manifestations, ranging from optic neuritis and transverse myelitis to acute disseminated encephalomyelitis. The recent establishment of consensus diagnostic criteria marks a pivotal advancement in early recognition and intervention, underscoring the urgency for evidence-based therapeutic strategies.
One of the most compelling aspects of the study is its exploration of the optimal corticosteroid regimen at MOGAD onset, aiming to delay the time to first relapse (TTFR) while minimizing cumulative corticosteroid exposure. By retrospectively analyzing data from a multicenter cohort comprising 109 patients, the authors meticulously assessed the relationship between corticosteroid dosage and taper duration and the subsequent risk of relapse. The utilization of Cox proportional hazards models, along...
Dear Editor,
I am writing to provide a more in-depth discussion on the recently published article, "Cognitive trajectory in the first year after first-ever ischaemic stroke in young adults: the ODYSSEY study." [1]. This study offers valuable insights into the intricate dynamics of cognitive recovery following ischaemic strokes in young adults, shedding light on the challenges and potential predictors of cognitive outcomes.
Show MoreThe central finding, highlighting the persistent prevalence of cognitive impairment in young stroke patients even one year post-event, underscores the gravity of the issue. The study's longitudinal design, incorporating cognitive assessments at distinct time points within the first year, provides a nuanced understanding of the trajectory of cognitive changes. Notably, the observation of specific improvements in processing speed, visuoconstruction, and executive functioning among initially cognitively impaired patients adds granularity to our comprehension of post-stroke recovery.
The study's discussion on the complex factors influencing cognitive recovery, such as age and lesion volume, enriches the narrative. However, the candid acknowledgment of the challenges in predicting cognitive recovery at an individual level reflects the intricate nature of post-stroke outcomes. Exploring the potential role of post-stroke fatigue and the absence of uniform predictors for recovery contribute to the depth of the article. The...
I recently had the opportunity to read your article titled "Prognostic Value of Spinal Cord Lesion Measures in Early Relapsing-Remitting Multiple Sclerosis" [1] and I want to extend my appreciation for the significant contribution your research has made to the field of multiple sclerosis (MS). Your study investigated the relation of whole spinal cord lesion number (SCLN) and volume (SCLV) to the future occurrence and type of confirmed disability accumulation (CDA) in patients with relapsing-remitting MS. The manual delineation of SC lesions and the subsequent analyses provided valuable insights into the prospective value of these measures in predicting clinical outcomes. The significant association between the absence of SC lesions and reduced CDA risk suggests the importance of SC lesions as a prognostic indicator in MS. Additionally, the close correlation between SCLN and SCLV, and their independent association with CDA, provide further support for the relevance of these measures in predicting disability accumulation.
Show MoreThe classification of CDA events into progression independent of relapse activity (PIRA) and relapse-associated worsening (RAW) facilitated a nuanced analysis of their association with SC lesion measures. The significant association with PIRA, but not RAW, hints at distinct underlying mechanisms for different types of disability progression, which could have implications for treatment strategies.
While your study provides valuable insi...
Dear Editor,
Show MoreI am writing to express my appreciation for the enlightening article titled "Childbirth Delivery Mode and the Risk of Multiple Sclerosis: A Prospective Population-Based Study" [1] recently published in your esteemed journal. The study, which examines the potential relationship between childbirth mode and the subsequent risk of multiple sclerosis (MS) development, presents a comprehensive analysis and incites intriguing discussions. The authors embarked on a commendable endeavor by conducting a meticulous prospective cohort study encompassing individuals born in Norway between 1967 and 2003. Their investigation aimed to unravel the potential influence of caesarean section (CS) births on the risk of adult-onset MS. The findings unveil an association suggesting an 18% elevated risk of MS among individuals born via CS, as compared to those born vaginally, after considering an array of confounding factors. However, the authors astutely highlight that this association does not persist when a sibling-matched analysis is undertaken. Furthermore, this intriguing connection appears to be primarily confined to individuals born preterm or via emergency CS. Such nuanced insights underline the complexities underlying the childbirth mode and MS risk paradigm, necessitating a thoughtful interpretation of the findings.
The authors acknowledge the divergent findings from previous studies, emphasizing the discrepancies between their results and those report...
There are several shortcomings in the commentary by White et al. For brevity, this response focuses on four main points.
1. New case definition
In the past 20 years, multiple case definitions have been published that require post-exertional malaise (PEM) as a core feature of ME/CFS, such as the Canadian Consensus Criteria (CCC), International Consensus Criteria (ICC), and the Institute of Medicine (IOM) criteria. NICE’s definition is based on the latter.
These case definitions are the ones used in research and clinical practice today. White et al. refer to the 1994 criteria developed by the Centers for Disease Control and Prevention (CDC) but the CDC no longer seems to use this case definition. Instead, they advise healthcare providers to diagnose ME/CFS using the IOM criteria where PEM is a required symptom.
NICE evaluated scientific evidence for ME/CFS as it is currently defined and not for a case definition that was published nearly 30 years ago. Other reviews on ME/CFS, such as the recent one by IQWIG in Germany, have used a similar approach. (1)
It is incorrect to state that NICE “downgraded nearly thirty years of research.” The previous NICE guidance from 2007 on ME/CFS already highlighted PEM as a core feature of ME/CFS, and studies that used this description were not downgraded in the evidence review. Neither were studies that used the CCC, ICC, or IOM criteria mentioned above.
2. Blinding and subjective outcomes
Show MoreWhite...
The authors revised this Rapid Response at BMJ's request in line with BMJ's Terms and Conditions for Rapid Responses.
Dear Editor,
Show MoreIn the article ‘Anomalies in the review process and interpretation of the evidence in the NICE guideline for chronic fatigue syndrome and myalgic encephalomyelitis’ published in the Journal of Neurology, Neurosurgery & Psychiatry on 10th July 2023, the authors claim NICE invented a new definition of ME. These claims are unfounded as NICE used the Institute of Medicine (IOM) criteria which is now 8 years old and was created using a more robust process than many other definitions as it drew on samples from different countries and compared the most widely used definitions of ME.
One area where NICE felt there was a gap in the IOM criteria was the lack of an empirical process alongside other methods. Leonard Jason's four-item empiric criteria were the only criteria that used adequate empiric methods, and this aligned very closely with the IOM criteria. As a result, NICE operationalised the IOM criteria for use in the NHS, with the four-item criteria helping to substantiate their approach.
NICE does not measure a trial’s success based on the researchers’ own terms but by analysing the raw data and applying the committee's agreed protocol. This allows NICE to measure whether a treatment had an effect or not. This is striking when looking at the assertion that research showed that the favoured treatment...
Dear Editor,
Whilst long overdue this paper represents a good start, to me. However it leaves me with several questions. Here are a few of them.
Will we see an immediate reduction in the number of ‘dustbin’ FND diagnoses, including amongst people deemed to be in the FND Subtypes? Will patients be empowered to define what a ‘dustbin’ diagnosis is?
Do the authors believe that the FND Society will promptly appoint an equalities expert as their new Patient Engagement Executive? I am not alone in receiving a suboptimal response from them, especially when compared to their approach to FND Portal. I was happy that he got ‘rockstar’ treatment; I got ‘appalling contempt’ and what amounts to ‘we control the narrative, you’re not welcome here’ which was interpreted as their attempt to silence women.
Was the decision not to include patient representation in the FND Subtypes paper made by a feminist?
Same question regarding the lumping of Conversion Disorder under FND in DSM, which has made it harder than ever for people with rare conditions such as Stiff Person Syndrome and Moyamoya Disease to record an initial misdiagnosis of Conversion Disorder.
Is it ethical (from a feminist perspective or any other) to use the word ‘functional’ to aid acceptance of a FND diagnosis on the basis that it doesn’t overtly point to a mental disorder diagnosis?
Can the authors assure your readers that ‘functional’ no longer means ‘hysteric...
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