A Case of Functional Neurological Disorder With Cognitive Symptoms: Emotion-Focused Psychotherapeutic Insights 2023 Millstein, Perez and Langfitt

[Andy]

Section snippets

Case Report
A 59-year-old woman, Mrs. A, was referred for an outpatient telemedicine psychotherapy consultation in the department of neurology at a large academic medical center. Five years earlier, she had begun experiencing neurological symptoms including gait and balance difficulties, confusion, difficulty concentrating, and cognitive fatigue. She had received a diagnosis of FND 1 year earlier through her neurologist based on “rule in” signs for a functional gait disorder. Her gait and balance...

Discussion
This case highlights the potential for emotion-focused psychotherapy in the treatment of FND with cognitive symptoms. Here, both the initial interview and subsequent therapy targeted in-session emotional experience guided by both Mrs. A's reporting and observable physical signs of anxiety discharge. Through tracking patterns of anxiety (and affect) manifesting in outwardly presenting bodily symptoms (e.g., muscle tension), the therapist and Mrs. A were able to identify potential nonconscious...

Paywall, https://www.sciencedirect.com/science/article/abs/pii/S2667296023000010

 

[rvallee]

Without fail, those FND papers merely recount what they do. They describe the steps they took and what they think of it. And that's it, it's assumed that it must be good and that all it takes is simply to describe it in order to make it valid.

Very guru-like. They even ascribe themselves absurd powers close to mind-reading. And they describe things they do in clinical practice, then talk about how it has potential, or is promising. Which essentially admits that they're just winging it and aren't actually interested in any evidence, they consider merely describing what they do as evidence for doing what they do. The only truly circular discipline: it exists because it has existed before, and continues to exist simply by describing its existence and promoting its aspirations as accomplished facts. One of the biggest and most harmful cons in history.

 

[bobbler]

is the cliffhanger approach normal for the abstract to what tantalise the reader into what happened next. It only seems to be something I see with FND papers so I guess that defines them as 'the next level in storytelling-focused 'researchers' vs the CFS stuff. Pay to read more and find out if the patient lived type stuff?

 

[Charles B.]

Step 1: Decide that somebody’s persistent physical symptoms are the product of some psychological process.

Step 2: Manufacture evidence for Step 1 by observing anodyne bodily sensations and deeming them an expression of the psychological processes you’ve already asserted exist; I.e. exactly what a medium, clairvoyant, or other charlatan would do.

Step 3: Reassert the conclusion, ignoring the fact that you randomly assigned normal actions as proof of psychological distress, and you still failed to connect your fictitious distress to the troublesome symptoms.

All this garbage does is get allegedly “heartsink” patients away from the medical establishment. Nobody reasonable is reading what these quacks have to say.

 

[SNT Gatchaman]

Five years earlier, she had begun experiencing neurological symptoms including gait and balance difficulties, confusion, difficulty concentrating, and cognitive fatigue.

Her gait and balance difficulties improved with education and physical therapy.

Brain magnetic resonance imaging revealed a stable basal ganglia cavernoma that was felt to be incidental to her presentation. Imaging was otherwise unremarkable. Neuropsychological testing did not identify any objective cognitive impairments and suggested average/high-average intelligence levels. She denied depression and had no prior psychiatric history, including no history of childhood maltreatment. She was not on any psychoactive medications.

Presumably imaged 5 years prior with her initial symptoms and therefore able to be judged as stable. "Cavernoma" is an outdated term, more correctly a slow-flow venous malformation. See Radiopaedia and Wikipedia.

From Functional Neuroanatomy of the Basal Ganglia (2012) —

The “basal ganglia” refers to a group of subcortical nuclei responsible primarily for motor control, as well as other roles such as motor learning, executive functions and behaviors, and emotions.

Back to the case report —

The biopsychosocial formulation for Mrs. A identified several predisposing, precipitating, and/or perpetuating factors. These included an action-oriented coping style, onset in the context of familial stressors, ongoing caretaking responsibilities, and anxiety around familial stressors. During this [initial] session, Mrs. A was able to observe the role of bodily-held anxiety as well as underlying emotional avoidance (e.g., anger, grief) in disrupting cognitive processes.

Over the course of 2 subsequent emotion-focused psychotherapy sessions, she noted further symptom relief because of learning to “actually feel feelings” and “digest them.” At the 18-month follow-up, she shared that her cognitive symptoms remained in remission despite ongoing life and familial stressors.

Through tracking patterns of anxiety (and affect) manifesting in outwardly presenting bodily symptoms (e.g., muscle tension), the therapist and Mrs. A were able to identify potential nonconscious emotions and relational conflicts that may be contributing to symptoms.

The supplementary data contains a post-treatment video interview between therapist and patient.

 

[SNT Gatchaman]

An "action-oriented coping style" does not seem pathological. From Resilience Factors Contributing to Mental Health Among People Affected by the Fukushima Disaster: Development of Fukushima Resilience Scale (2020) —

The factor “action-oriented approach” was regarded as an important measure for resilient people, and represents several individual abilities related to making something to do on one’s own, playing some social roles, and having leisure time. These results suggest the possibility that an “action- oriented approach” could contribute to the promotion of mental health among people affected by a major disaster. A previous study examining the influence of individual coping skills on psychological resilience also reported the significance of an action-oriented approach.

 

[NelliePledge]

Yes @SNT Gatchaman my gut reaction to that reference to action centred coping was that yet again they are having cake and eating it.

 

[Peter T]

Yes @SNT Gatchaman my gut reaction to that reference to action centred coping was that yet again they are having cake and eating it.

It does seem that this post hoc psychologising is used to explain radically diverse outcomes. An explanation that can be used to explain contradictory outcomes is not a meaningful explanation. I am reminded of a homeopath I saw (when I was at the trying anything and everything stage) who said if my symptoms seemed to have improved that the tincture was doing its job, but my symptoms seemed to worsen then the tincture had successfully done its job and now was the time to move on to a different dilution of brandy that may or may not have any molecules of the supposed active ingredient.

Also the fact that an intervention appears to have an effect does not mean that it is doing what the practioner believes it to be doing. For example, under the old NICE guidelines, people going through the UK specialist services may report in the short term that GET has helped them, but what outcome measures for the UK services we have from then suggest following intervention patients worked on average fewer hours and claimed more benefits. Further I have come across a number of people making comments on social media along the lines of, ‘my ME/CFS seemed to be getting worse, so I did a couple of weeks of GET to get myself back on track’. Given GET starts with establishing a stable activity base line, a reasonable explanation of these findings could be that rather than being curative, any subjective improvement comes from people doing less and being given a structure that unconsciously encourages pacing.

Similarly physiotherapy for a motor problem might provide a context for a patient to better manage their presenting symptoms without it actually having any impact on the underlying condition, for example someone with one leg shorter than the other may learn to walk better with physiotherapy but it would be unreasonable to state that the intervention has resulted in the shorter leg growing without objective measurements of changes in length.

In such situations post hoc explanations might give hints for future research, but they do not enable firm conclusions without a theoretical model that allows predictions that can be then confirmed by changes in objective measurements. What we are seeing here is a lot of conjecture and possibilities that are never subjected to meaningful validation.

 

[SNT Gatchaman]

For anyone interested, here are a couple of references looking at the neurological effects and BBB disruption associated with these lesions. The literature retains the terms "cavernoma" and "cerebral cavernous malformations". Possibly the lesions visible on imaging are only the tip of the iceberg, with a more generalised cellular problem in handling inflammation and redox that I could imagine might lead to symptoms variable in time and (neurological) space — i.e. could underlie a subset of what is called FND. At the very least I don't think it's reasonable to dismiss a positive imaging finding in this patient as "something we feel is incidental."

Oxidative stress and inflammation in cerebral cavernous malformation disease pathogenesis: Two sides of the same coin (2016)

Cerebral Cavernous Malformation (CCM) is a vascular disease of proven genetic origin, which may arise sporadically or is inherited as an autosomal dominant condition with incomplete penetrance and highly variable expressivity. CCM lesions exhibit a range of different phenotypes, including wide inter-individual differences in lesion number, size, and susceptibility to intracerebral hemorrhage (ICH). Lesions may remain asymptomatic or result in pathological conditions of various type and severity at any age, with symptoms ranging from recurrent headaches to severe neurological deficits, seizures, and stroke. To date there are no direct therapeutic approaches for CCM disease besides the surgical removal of accessible lesions. Novel pharmacological strategies are particularly needed to limit disease progression and severity and prevent de novo formation of CCM lesions in susceptible individuals.

Useful insights into innovative approaches for CCM disease prevention and treatment are emerging from a growing understanding of the biological functions of the three known CCM proteins, CCM1/KRIT1, CCM2 and CCM3/PDCD10. In particular, accumulating evidence indicates that these proteins play major roles in distinct signaling pathways, including those involved in cellular responses to oxidative stress, inflammation and angiogenesis, pointing to pathophysiological mechanisms whereby the function of CCM proteins may be relevant in preventing vascular dysfunctions triggered by these events. Indeed, emerging findings demonstrate that the pleiotropic roles of CCM proteins reflect their critical capacity to modulate the fine-tuned crosstalk between redox signaling and autophagy that govern cell homeostasis and stress responses, providing a novel mechanistic scenario that reconciles both the multiple signaling pathways linked to CCM proteins and the distinct therapeutic approaches proposed so far. In addition, recent studies in CCM patient cohorts suggest that genetic susceptibility factors related to differences in vascular sensitivity to oxidative stress and inflammation contribute to inter-individual differences in CCM disease susceptibility and severity.

This review discusses recent progress into the understanding of the molecular basis and mechanisms of CCM disease pathogenesis, with specific emphasis on the potential contribution of altered cell responses to oxidative stress and inflammatory events occurring locally in the microvascular environment, and consequent implications for the development of novel, safe, and effective preventive and therapeutic strategies.

mPR-Specific Actions Influence Maintenance of the Blood–Brain Barrier (BBB) (2022, International Journal of Molecular Sciences)

Cerebral cavernous malformations (CCMs) are characterized by abnormally dilated intracranial microvascular sinusoids that result in increased susceptibility to hemorrhagic stroke. It has been demonstrated that three CCM proteins (CCM1, CCM2, and CCM3) form the CCM signaling complex (CSC) to mediate angiogenic signaling.

Disruption of the CSC will result in hemorrhagic CCMs, a consequence of compromised blood–brain barrier (BBB) integrity. Due to their characteristically incomplete penetrance, the majority of CCM mutation carriers (presumed CCM patients) are largely asymptomatic, but when symptoms occur, the disease has typically reached a clinical stage of focal hemorrhage with irreversible brain damage.

We recently reported that the CSC couples both classic (nuclear; nPRs) and nonclassic (membrane; mPRs) progesterone (PRG)-receptors-mediated signaling within the CSC-mPRs-PRG (CmP) signaling network in nPR(−) breast cancer cells. In this report, we demonstrate that depletion of any of the three CCM genes or treatment with mPR-specific PRG actions (PRG/mifepristone) results in the disruption of the CmP signaling network, leading to increased permeability in the nPR(−) endothelial cells (ECs) monolayer in vitro.

Finally, utilizing our in vivo hemizygous Ccm mutant mice models, we demonstrate that depletion of any of the three CCM genes, in combination with mPR-specific PRG actions, is also capable of leading to defective homeostasis of PRG in vivo and subsequent BBB disruption, allowing us to identify a specific panel of etiological blood biomarkers associated with BBB disruption. To our knowledge, this is the first report detailing the etiology to predict the occurrence of a disrupted BBB, an indication of early hemorrhagic events.