Metacognition in functional cognitive disorder- a potential mechanism and treatment target

ABSTRACT

Introduction: Functional Cognitive Disorder (FCD) is common. Despite this, there is no evidence-based consensus on how to treat FCD. Poor metacognitive ability has been suggested as a key mechanism underlying the disorder. This paper evaluates the proposal that strategies which improve metacognition could provide a mechanistically plausible translational therapy.

Methods: We reviewed the existing literature relating to metacognition in FCD, previous strategies to improve metacognitive ability in FCD and whether metacognitive performance can be modulated.

Results: Though limited, there is evidence to suggest that metacognition is impaired in FCD. Converging evidence from neuroimaging studies suggests that metacognitive performance can be modulated. The effectiveness of existing strategies to improve metacognition including cognitive training, psychoeducation and lifestyle interventions have been equivocal. Recently, a potential treatment option has emerged in the form of a computer-based metacognitive training paradigm.

Conclusions: There is an urgent need for effective treatments in FCD. Impaired metacognition may be a plausible therapeutic target but, in the first instance, further research is required to demonstrate deficits in “local” metacognitive ability in FCD patients when measured objectively. If so, clinical trials of interventions, such as computerised metacognitive training, are required to evaluate their effectiveness in improving FCD symptoms.

KEYWORDS:

• Functional cognitive disorder
• metacognition
• treatment
• mechanism

Acknowledgements

RH, RB and JH conceived this paper. RB drafted the paper with all authors (RH, AM, SF, JH) critically reviewing it and suggesting amendments to the content and structure prior to submission. All authors take responsibility for the integrity of the paper.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

This research received no specific grant from any funding body. RB is supported by an NIHR Academic Clinical Fellowship. JH and RH are supported by the NIHR Biomedical Research Centre at University College London Hospitals NHS Foundation Trust and University College London. AM is supported by the Mental Health and Justice Project funded by the Wellcome Trust [grant number 203376/2/16/Z]. The Wellcome Centre for Human Neuroimaging is supported by core funding from the Wellcome Trust [grant number 203147/Z/ 16/Z]. SF is supported by a Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society [grant number 206648/Z/17/Z].