High Somatization Rates, Frequent Spontaneous Recovery, and a Lack of Organic Biomarkers in Post-Covid-19 Condition, 2024, Tröscher et al.

SNT Gatchaman

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High Somatization Rates, Frequent Spontaneous Recovery, and a Lack of Organic Biomarkers in Post-Covid-19 Condition
Anna Tröscher; Patrick Gebetsroither; Marc Rindler; Vincent Böhm; Rainer Dormann; Tim von Oertzen; Anna Heidbreder; Raimund Helbok; Judith Wagner

INTRODUCTION
Many patients report neuropsychiatric symptoms after SARS-CoV-2 infection. Data on prevalence of post-COVID-19 condition (PCC) vary due to the lack of specific diagnostic criteria, the report of unspecific symptoms, and reliable biomarkers.

METHODS
PCC patients seen in a neurological outpatient department were followed for up to 18 months. Neurological examination, SARS-CoV-2 antibodies, Epstein–Barr virus antibodies, and cortisol levels as possible biomarkers, questionnaires to evaluate neuropsychiatric symptoms and somatization (Patient Health Questionnaires D [PHQ-D]), cognition deficits (Montreal Cognitive Assessment [MoCA]), sleep disorders (ISS, Epworth Sleepiness Scale [ESS]), and fatigue (FSS) were included.

RESULTS
A total of 175 consecutive patients (78% females, median age 42 years) were seen between May 2021 and February 2023. Fatigue, subjective stress intolerance, and subjective cognitive deficits were the most common symptoms. Specific scores were positive for fatigue, insomnia, and sleepiness and were present in 95%, 62.1%, and 44.0%, respectively. Cognitive deficits were found in 2.3%. Signs of somatization were identified in 61%, who also had an average of two symptoms more than patients without somatization. Overall, 28% had a psychiatric disorder, including depression and anxiety. At the second visit (n = 92), fatigue (67.3%) and insomnia (45.5%) had decreased. At visit three (n = 43), symptom load had decreased in 76.8%; overall, 51.2% of patients were symptom-free. Biomarker testing did not confirm an anti-EBV response. SARS-CoV-2-specific immune reactions increased over time, and cortisol levels were within the physiological range.

CONCLUSIONS
Despite high initial symptom load, 76.8% improved over time. The prevalence of somatization and psychiatric disorders was high. Our data do not confirm the role of previously suggested biomarkers in PCC patients.

Link | PDF (Brain and Behavior) [Open Access]
 
Despite the main focus on psychosomatisation and FND, this paper has some useful data.

Although patients displayed a high symptom load at the first visit, more than half were symptom-free, and 76.7% had improved clinically at the last follow-up.

We investigated cortisol levels in the serum, which have been shown to be decreased in PCC patients (Klein et al. 2023; Su et al. 2022). However, we were not able to replicate those results, as in our cohort most patients were well within the physiological range.

On the other hand, we did find an increase of SARS-CoV-2 IgG. This is most likely due to repeated exposure to the virus and the kinetics of antibody development against SARS-CoV2 (Movsisyan et al. 2022). Other studies show low SARS-CoV-2 titer but higher response to other viruses, which was interpreted as undirected chronic immune activation (Spatola et al. 2023; Su et al. 2022; Gaebler et al. 2021). However, in this study, we could show that PCC patients do have a high immune response, specifically against SARS-CoV-2. This is also in line with a study, which showed good viral clearing in PCC patients over time, indicating a good immune response against SARS-CoV-2 (Hoeggerl et al. 2023). Hence, our results do not point toward undirected immune activation but rather to a potent defense against SARS-CoV-2, confirming other previously published data (Klein et al. 2023; Hoeggerl et al. 2023).

Viral persistence is one of the candidate mechanisms, with data pro and against. I don't think having high IgG necessarily means viral components are all being cleared.
 
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But then there's the usual claptrap —

[Our] data suggest that long COVID is related to functional neurological disorders. The connection between a Covid infection and functional neurological symptoms is controversially discussed. The main challenge in diagnosing symptoms as functional rests in the low yield of positive features. The diagnosis is therefore mainly made on the basis of missing pathological findings in clinical and paraclinical examinations. However, positive features do exist in functional neurological disorders, most of all temporal inconsistency of symptoms (Teodoro et al. 2023). This was present in the majority of our patients, who reported significant fluctuations in the severity of their complaints, inconsistent with any organic disorder.

Right. Fluctuating symptoms are not seen in any other organic neurological disease such as — oh I don't know, MS?? MS, a demyelinating disease which is famously characterised to have "symptoms varying spatially and temporally".

There are several ways in which a Covid infection might be related to a functional neurological disorder. Depression is associated with cognitive deficits. The prevalence of depressive disorders has risen during the pandemic (Casjens et al. 2024). Hence, some patients may have suffered from depression. This is of particular relevance due to the high frequency of cognitive symptoms (“brain fog”) in PCC (Ball et al. 2020). Furthermore, media coverage may have induced enhanced introspection. This may trigger other pathophysiological mechanisms associated with functional disorders, such as a disruption in predictive processing, where an imbalance in the integration of sensory data and top-down predictions leads to the symptoms experienced by the patient (Mavroudis et al. 2024).

Time for the :banghead: emoji.

Concluding —

The high rate of somatization supports a role for neurologists in the diagnosis of exclusion of organic disease but points out the need for a multidisciplinary team, including psychosomatic support, to properly manage this disease.

Last time I looked no-one was properly managing this disease, least of all the psychosomagicians. As evidenced by the official statistics of 17m in the US and 2m in the UK.
 
Number of patients
First visit 175
Second visit 92
Third visit 43

How can they conclude anything about recovery rates when only a quarter of the sample are included?

Especially if you consider the iller some one is the less likely they are to continue in the study. Without clear evidence (sorry haven’t checked the actual paper) on why people dropped out, the loss of 75% of the sample renders the final assessments meaningless.
 
An impressive display of the extreme biases needed to promote psychosomatic ideology. The drop-out rate for follow-up (75%) alone that they use to conclude a 78% spontaneous recovery would be impressive in itself, but the fact that they define 'somatization' as having symptoms and seeking medical care is just all icing and no cake. They even feature the "it was covered in the press therefore nocebo" by circular reasoning, in that they are saying that because other people have said that before. No evidence needed.

And, yeah, they did define 'somatization' explicitly as absence of evidence from standard tests:
According to the ICD-10 catalog, somatization disorders are defined as the repeated presentation of physical symptoms together with persistent requests for medical investigations, in spite of repeated negative findings and reassurances by doctors that the symptoms have no physical basis. If any physical disorders are present, they do not explain the nature and extent of the symptoms or the distress and preoccupation of the patient. This discrepancy as well as the accompanying affective and cognitive components were explicitly elicited during the clinical consultation (ICD 2019). To evaluate the impact of somatization on the symptom load, we calculated the frequency distribution of all recorded symptoms according to somatization status. Furthermore, we evaluated the overall complaint load depending on the somatization status.
What is 'somatization status' you might ask? No idea, it's just something they're winging I guess. But this indicates that they simply use PHQ-D, which mostly overlaps with the very kind of illness they are pretending to study:
To evaluate the effect of somatization on the prevalence of PCC symptoms, we split the patient cohort according to the result on the PHQ-D somatization questionnaire
So in a study where they assess a medical condition known for a wide range of symptoms with no obvious pathophysiology, they assume that those much be 'somatization' since they... can't find obvious pathophysiology. Holy circular reasoning, Batman. And they use a depression questionnaire, but conclude that it's somatization. Which I guess means they believe that depression is somatization. Who knows?

They can mention 'standardized' and 'well-validated' questionnaires all they want, it means nothing. They all feature overlapping questions and explicitly ask questions that psychologize the very kind of illness they are researching. Those questionnaires are just as 'validated' and 'standardized' as Meyers-Briggs was when it was considered valid and widely used. They can even talk about depression and anxiety being psychiatric disorders, obviously they aren't that on their own, and again there's the overlapping questions anyway that makes this all ridiculous. The entire concept makes no sense here, it's just ridiculous.

They even feature the assertion that this must be the conversion disorder / functional whatever, but that even though it lacks the fake 'rule-in' signs for FND, it still must be that because, possibly, nocebo. Again no evidence needed, this is basically someone said because someone said because someone said.

Impressive twist in shifting PEM to stress intolerance, showing how stress is perfectly equivalent to exertion in almost all cases where it's used. An extremely biased choice that makes no sense outside of working with pre-achieved conclusions and given how much PEM has featured in LC data.

Just straight up bizarre:
In summary, we found a high subjective symptom load in patients presenting at the PCC outcome clinic but could not objectify cognitive deficits or laboratory anomalies. Most patients showed significant improvement over time. Notably, 61% of patients were positive for somatization according to the PHQ-D, indicating a substantial overlap with other PCC symptoms. These findings support pandemic-related stress and anxiety as important factors contributing to PCC.
Conversion disorder explicitly defined on absence of evidence for known diagnoses and using a depression questionnaire with overlapping questions leads to conclusions of pandemic-related stress and anxiety. Pulled straight out of a donkey.

Actually things are even worse than that on drop-outs, they only have any follow-up data for 92, but of those only 55 filled in the questionnaires, so most of the data is literally missing:
The questionnaires were filled out in 55/92 (60.0%) of the patients at the second visit
And it continues further still, they actually only have full data sets for 21/175:
Due to the high drop-out rate (only 21/175 [12%] patients filled out the questionnaires three times), no score analyses were performed for the third visit
So they only have full data for 12% of participants.

So an absolute joke of a 'study'. Which is typical in psychosomatic ideology, a concept that obviously exists in extreme bias. They aren't hiding it much either:
The high rate of somatization supports a role for neurologists in the diagnosis of exclusion of organic disease but points out the need for a multidisciplinary team, including psychosomatic support, to properly manage this disease.
This is major crisis level of bias and regression. None of this is normal for any group of professionals, but it has become 'standardized' and 'well-validated' in health care. Completely absurd.
 
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