Functional neurological disorder: an evolutionary perspective

Abstract

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Functional neurological disorder (FND) is among the commonest disorders in neurological practice with an estimated prevalence of 80–140 per 100 000 individuals and a female predominance of ~70% [1]. It is characterized by symptoms involving an excess or decrease in voluntary movement or sensory pathways such as seizures, paralysis, tremor, and visual loss leading to disability and distress [1]. FND has been documented worldwide since antiquity [1, 2]. Formerly known as hysteria and conversion disorder, FND lies at the neurology-psychiatry interface and has long been stigmatized and neglected. In recent years, the field has undergone a renaissance, with a growing consensus that FND has characteristic clinical features that allow a rule-in diagnosis [2].

Magnetic resonance imaging (MRI) and other investigations are typically normal, but functional MRI and neurophysiological studies shed light on new underlying mechanisms of FND [1, 3]. At the brain network level, data suggest a breakdown in communication between the recently evolved prefrontal cortex and more conserved brain regions like amygdala, periaqueductal gray (PAG), and insula, governing threat detection. FND symptoms are hypothesized to arise from mismatches between predicted and ‘bottom-up’ sensory experience, with associated disruption in sense of agency (the feeling that one has initiated and is in control of one’s own movements and their outcomes) [1, 3]. This pattern is distinct from feigning [2]. Psychosocial mechanisms—sometimes related to stress and past adversity—also play an important role in many people with FND.

Some studies have explored genes potentially involved in FND (e.g. TPH2 in the serotonin pathway) [4]. In addition, many common FND comorbidities such as anxiety and nociplastic pain (pain from chronic alteration of central nervous system processing, not from inflammation or injury [5]) have a strong genetic basis. However, genome-wide association studies specific to FND are lacking, and there is no evidence that any gene involved in FND has undergone a selective sweep (a sign of past natural selection).