Differentiating Functional Cognitive Disorder from Early Neurodegeneration: A Clinic-Based Study, 2021, Ball, Pennington et al

Abstract

Functional cognitive disorder (FCD) is a relatively common cause of cognitive symptoms, characterised by inconsistency between symptoms and observed or self-reported cognitive functioning. We aimed to improve the clinical characterisation of FCD, in particular its differentiation from early neurodegeneration.

Two patient cohorts were recruited from a UK-based tertiary cognitive clinic, diagnosed following clinical assessment, investigation and expert multidisciplinary team review: FCD, (n = 21), and neurodegenerative Mild Cognitive Impairment (nMCI, n = 17). We separately recruited a healthy control group (n = 25). All participants completed an assessment battery including: Hopkins Verbal Learning Test-Revised (HVLT-R), Trail Making Test Part B (TMT-B); Depression Anxiety and Stress Scale (DASS) and Minnesota Multiphasic Personality Inventory (MMPI-2RF).

In comparison to healthy controls, the FCD and nMCI groups were equally impaired on trail making, immediate recall, and recognition tasks; had equally elevated mood symptoms; showed similar aberration on a range of personality measures; and had similar difficulties on inbuilt performance validity tests. However, participants with FCD performed significantly better than nMCI on HVLT-R delayed free recall and retention (regression coefficient −10.34, p = 0.01). Mood, personality and certain cognitive abilities were similarly altered across nMCI and FCD groups. However, those with FCD displayed spared delayed recall and retention, in comparison to impaired immediate recall and recognition. This pattern, which is distinct from that seen in prodromal neurodegeneration, is a marker of internal inconsistency. Differentiating FCD from nMCI is challenging, and the identification of positive neuropsychometric features of FCD is an important contribution to this emerging area of cognitive neurology.

Open access, https://www.mdpi.com/2076-3425/11/6/800/htm

 

I remember reading about an elderly man who had been a fanatical chess player throughout life, and he was extremely good at it. He seemed to be mentally alert, and still an excellent chess player well into old age. I don't know how it arose, but he had an MRI scan showing massive degeneration in his brain as a result of Alzheimer's, despite still playing chess at a high level regularly. Somehow his apparent high intelligence and his constant use of his mental faculties disguised his cognitive problems until his Alzheimer's was very severe.

The idea that cognitive disorders could be functional is abhorrent to me. It's like a doctor saying to a patient with cognitive problems that "you tell me you have issues but we've tested you and you are fine so you must be lying".

At what stage do doctors ever test people for vitamin B12 deficiency, nutrient deficiencies generally, minor strokes, tumours, anaemia etc. The number of causes for cognitive difficulty must be immense and some of them could be reversible. And yet a doctor believing that a patient is lying about their cognitive abilities effectively shuts the door on any other investigation. As an example, CBT won't work for B12 deficiency but B12 tablets or injections will - and not only that, they would be cheaper than CBT and the patient may have decades of good quality of life ahead of them.

https://www.youtube.com/watch?v=QqjyAeOLyKM

 

Surely if you lack pre morbid scores for the individuals in the various groups the only way to reliably avoid risk of selection bias is to use sufficiently large cohorts to ensure you are looking at representative population differences not individual differences? Could groups sizes of 21, 17 and 25 ever guarantee scores reliably representative of their entire populations?

Also correct me if I am wrong, I am not familiar with the current literature, but isn’t internal inconsistency a feature of early stage dementias?

Further internal variability or inconsistency is not of itself prima facie evidence of functional or psychogenic symptoms, it is equally theoretically possible to have symptom variation linked to a biological mechanism, as is seem in PEM in people with ME. Also the impact of fatigue can fluctuate significantly in many other conditions from cancer to MS.

I often think of a subject I studied with amongst other things very specific reading disorders in the context of dysphasia and hemiplegia following a CVA. There was no doubt of the robustness of his disorder directly linked to focal brain damage. He was a very well studied subject, his weekly routine being one day going swimming, one day visiting the grandchildren and one day coming into the university to be studied by neuropsychologists.

In one instance he struggled to read aloud the word ‘gauge’, and after various attempts he turn aside to me and said ‘I can never read gauge’, then returned back to the screen still failing to read the word ‘gauge’. Most clinicians working with acquired neurological conditions expect variation and inconsistencies on the edge of people’s abilities, biological systems are rarely as tidy as we would like them. No reasonable clinician or researcher would doubt the organic basis of his condition. He did display variability but only in the context of very narrowly defined psycholinguistic categories.

Presumably however the committed FCD/FND believer would say that this patient displayed a significant functional component reinforced by the regular interaction with intelligent interested academics and post graduate students and the sense that he was helping push forward the boundaries of science.

(I must admit I am so sceptical of these claims on the basis of such small sample sizes and further don’t believe there are currently any meaningful criteria to diagnose functional cognitive disorder that I have not bothered to waste time on reading the article. However even if their FCD group was rather ‘people perceived by a narrow section of physicians as having FCD’ I still remain sceptical that this study could produce any meaningful results, even though I am actually interested in the question what prompts such functional diagnoses, be it patient related factors such as being female or doctor related factors such as personal beliefs.)

 

The New Scientist had a feature article on this. One of the mysteries was why intellectual people deteriorated so quickly when they developed Alzheimers. By considering patients like the above they discovered that is was because these people were not diagnosed until late in the day because their symptoms were masked.

The chess player had gone to see his doctor because he said he could only see five moves ahead now instead of 10. You can imagine the reception he got!

This is important for FND because they make such a big thing about symptoms being "incongruent" It has been said that one of the problems with modern medicine is that students are taught classic case definitions but in the real word no patient will match that exactly.

I also suspect that they magnify normal variation to get a group that is somehow different so they can restate that FND exists. Like an imaginary line where those below are "real" and those above are FND but with very little to distinguish them. All results are bundled to give averages.