Functional neurological disorder and its complex comorbidities

Functional neurological disorder (FND), classified under the somatic symptoms and related disorders in the Diagnostic and Statistical Manual of Mental Disorders (DSM5) , is characterised by involuntary neurological symptoms which are not explained by a known neurological or other medical condition, or by another mental health disorder. Previously in DSM4, FND was a diagnosis of exclusion, but the description changed in DSM5, which specifies FND as a ‘rule-in’ diagnosis. The criteria now include clinical evidence of incompatibility between symptoms and recognised neurological or medical conditions, hence positive differentiation. Furthermore, the requirement for a preceding stressor is removed, although still included as a clinical note. International Classification of Diseases (ICD11) similarly uses the positive differentiation of FND, but with the addition of a cognitive symptom sub-type.

FND is characterised by the presence of involuntary neurological symptoms, such as weakness, paralysis, blindness, or non-epileptic seizures, that are not explained by a known neurological condition.¹ As a result, FND is associated with significant disability, causing a negative impact on the day-to-day lives of those affected. FND is the second most common cause of neurology clinic visits after headaches, with an incidence rate of four-to-12 per 100,000. It is more common among women aged 35-to-50 years and those of lower socioeconomic status.² FND is a costly condition at the interface of psychiatry and neurology. Importantly, however, the overall misdiagnosis rate is thought to be between 1-to-4 per cent, and 10 per cent of those may be multiple sclerosis-related.¹²

Although the list of predisposing risk factors for FND is extensive, the most common include a history of sexual abuse or trauma, stress, anxiety, chronic pain, and family or personal history of any neurological or other medical condition.⁴ A prior stressor is only present in up to 30 per cent of FND cases.⁵ Many patients who are diagnosed with FND have comorbid psychiatric illnesses. The rates of those with depression are between 20-to-40 per cent,^6,7,8 while those with anxiety are close to 40 per cent.⁹ Additionally, dissociative disorder has been linked with FND for the past 200 years.⁶ However, previous research has shown that the diagnosis of FND is less common in those with psychosis.³ Furthermore, another study has shown that while 75 per cent of patients with FND had a psychiatric disorder, only 7 per cent had psychotic symptoms, while the majority had depressive disorder (41 per cent) and phobic disorder (15 per cent).⁶

Dissociative disorders are characterised by disruption of the normal integration of consciousness, memory, identity, emotion, perception, body representation, motor control, and behaviour. Dissociative symptoms can include ‘positive’ symptoms, such as fragmentation of identity, depersonalisation, and derealisation, or ‘negative’ symptoms such as dissociative amnesia. In this paper, the clinical presentation, management, and the complex interplay between psychosis, FND, and dissociation are described.

Discussion

Based on this woman’s presenting symptoms, a co-morbid diagnosis of dissociative disorder was made, with associated identity change and loss of autobiographical memory. She was also diagnosed with FND, which led her to experience motor symptoms as well as deterioration of speech. Her transient psychotic symptoms were attributed to a dissociative cause. Symptoms, such as believing that she was evil, along with the somatic and sensory symptoms, are explicable in the context of dissociation.

Dissociation is a defence mechanism associated with the development of FND along with other defence mechanisms such as denial. Changes in psychiatric classification have contributed to a changed understanding of the term dissociation. Dissociative processes can be divided into detachment related – causing a separation from the self or world – or compartmentalisation-related – causing a reversible loss of voluntary control over intact processes.¹³

This case was unusual in that it displayed the complex interplay between psychosis, FND, and dissociation. Increased interest in the study of FND has shed new light on its pathophysiology, however, its mechanism is rather complex, requiring the interaction of both neurobiological and psychological mechanisms.³ A recent systematic review discussing the link between conversion and dissociative disorder stated that a pathophysiological process is a plausible hypothesis in explaining conversion symptoms in dissociative disorder,³ although more studies are needed in order to establish a deeper understanding and support for the proposed interplay between the two disorders.¹⁰ A meta-analysis regarding the relationship between dissociative disorder and symptoms of psychosis indicated a strong association between the two conditions.¹¹ A possible explanation for this finding was suggested to be the presence of trauma-related memory (which was present in this case), that could trigger symptoms of depersonalisation/derealisation, and in turn trigger the development of psychosis.

Conclusions

While these findings indicate a strong interplay between FND and dissociative disorders, as well as between dissociative disorder and psychosis, no clear association has been established between psychosis and FND. It is postulated that the presence of a dissociative disorder comorbid with FND also triggered the development of transient psychosis. However, in this patient’s case, the initial presentation of psychosis could indicate a reciprocal influence on the development of FND.

Treatment approaches for FND focus on regaining normal function and retraining the brain (Figure 2). In this specific case, the ongoing management of dissociative/psychotic symptoms required low dose maintenance anti-psychotic medication alongside FND specific psychological therapy, resulting in a positive outcome. Flexibility and person-centred approaches are key to improving patient outcomes. 

Case Report

Ms A is a 35-year-old single artist, with no formal past psychiatric history who initially presented with a brief psychotic episode requiring psychiatric admission and anti-psychotic treatment. She subsequently presented with functional neurological disorder (FND) and co-morbid psychotic-like symptoms, necessitating admission for investigation under the neurology team. Within weeks she presented with symptoms of FND with motor symptoms, prominent dissociative phenomena, such as altered sense of reality, depersonalisation, and hallucinatory experiences. The case highlights the co-occurrence of FND, dissociative symptoms, and psychotic symptoms within the same episode.

The patient had no past medical history of note. She attended counsellors twice in the previous five years for symptoms of low mood, with no formal diagnosis of major depressive disorder. At the time of presentation, the patient was unemployed due to pandemic restrictions. She was the eldest of three children. She consumed alcohol occasionally and had used cannabis occasionally in the past. In childhood, she reported parental discord and disharmony, but no abuse. She notably learned to dissociate while observing arguments.

At first presentation, Ms A reported an 18-month history of work-related stress and mid-insomnia. She reported hearing second person auditory hallucinations criticising her and predicting death. The voice accused her of bringing evil spirits into the house and had been intermittent for several weeks. She also alluded to a feeling that she may cause harm to her parents, yet denied having made any plans to do so. She was not expressing any delusional beliefs. There were no objective depressive features. She was child-like at presentation, holding her mother’s hand. There was no evidence of guardedness or suspicion, and no hostility. She was orientated to time and place and had partial insight. She was admitted on a voluntary basis and prescribed olanzapine 5mg once daily. Physical examination, routine bloods, and CT brain were unremarkable.

On day four review, the patient was casually dressed, with a relaxed posture, and her speech was normal in terms of rate and volume. She denied ongoing auditory hallucinations or other psychotic symptoms. She was compliant with medication, which had been increased to olanzapine 20mg once daily. Her symptoms gradually improved and she appeared engaged, relaxed, and denied any abnormal experiences. She had good insight. She was discharged after two weeks on olanzapine 20mg once daily.

At subsequent follow-up two weeks post-discharge, Ms A reported having “spasms” and “seizures”. Video footage taken by her mother showed the patient sitting on a chair with her head back, mouth open, and eyes rolled back with a rigid posture. There was no evidence of any tremors, tongue biting, or incontinence. She reported feeling “absent from her body” during these episodes. During mental state examination, she appeared distracted at times, but calm. Her mood was subjectively and objectively euthymic, and speech was normal in rate, rhythm, and volume. There was no evidence of overt auditory hallucinations or other psychotic symptoms. Additionally, no extrapyramidal features were evident at examination. She was keen to stop olanzapine altogether, having already discontinued treatment. The risk of relapse was emphasised.

Two months later, the patient was admitted medically due to deteriorating motor symptoms. Collateral history from her mother indicated she would start speaking in a childlike manner and with an altered accent and would have a lisp similar to when she was a child. Her speech would deteriorate over time to the point where she could not articulate certain consonants, such as S, V, and R, anymore.

At interview, Ms A’s speech was almost inaudible, but she answered appropriately. Unusual eye movements and truncal movements extending to her shoulders, along with scrunching of eyes and face were evident. She denied feeling depressed. Psychotic symptoms were not directly elicited during the interview. She was perplexed and restless. Investigations to rule out an underlying organic cause, such as anti-N-methyl-D-aspartate (NMDA) receptor encephalitis and voltage gated potassium channel complex antibody encephalitis, were sent off. The following day, Ms A tried to get out through the bathroom window in the medical ward. She appeared agitated and would hit her head against the bed frame while talking to herself. The nurse was unable to decipher what she was saying to herself at the time. At this point, 2mg of lorazepam was given orally, which settled her symptoms. A dose of 1.5mg of risperidone mane and 3mg nocte was prescribed to treat underlying psychotic symptoms, given the previous history. Over a week later, after symptoms had stabilised, the patient was discharged home on risperidone 4mg daily, which was well tolerated.

In order to rule out an organic cause of neurological symptoms, CT brain, thorax, abdomen, and pelvis was performed, and came back negative. This was followed by MRI brain and electroencephalogram, both of which were also negative. An extensive autoantibody screen was performed and sent to Oxford, Berlin, and Germany, to rule out limbic encephalitis and paraneoplastic encephalomyelitis (Table 1). While awaiting autoantibody results, Ms A was placed on 20mg of prednisolone once daily. Prednisolone was discontinued once negative results were returned. Cerebrospinal fluid analysis revealed no abnormalities in white cell count, protein, or glucose levels. HSV1/2, VZV and enterovirus screen came back negative. Rheumatoid factor levels and anti-nuclear and anti-phospholipid antibodies were not detected in serum. Copper levels were within normal range. It was reported that 48 hours after steroids were stopped, the patient started experiencing cognitive symptoms, such as poor concentration and loss of autobiographical memory.

A diagnosis of FND was made, based on the presenting complaints, clinical features, and investigation findings. A second opinion admission to Cork University Hospital, organised independently by family, ensued, where the diagnosis of FND was affirmed. Since the patient presented to hospital with no psychotic symptoms on admission, the psychiatry liaison team, in collaboration with the neurology team in the second opinion centre, opted to discontinue the antipsychotic medication.

Two weeks after discharge, Ms A experienced symptoms of psychosis again. She thought she was evil and seeing examples of evil faces, believing that she changed into Donald Trump or the Coronavirus. She then developed further functional neurological symptoms, including language dysfunction, such as anomia and dysphonia. She was recommenced on 2.5mg risperidone (0.5mg mane, 2mg nocte) to treat her psychotic symptoms, which settled quickly. She was managed on risperidone (0.5mg mane, 2mg nocte) as well as sertraline 50mg daily for her anxiety. She engaged with clinical psychology as an outpatient for psychological work for FND and dissociative symptoms. Ms A continued on a combination of risperidone 2.5mg daily and sertraline 50mg daily, with liaison psychiatry follow-up. Subsequent brief recurrences secondary to stressors were managed with brief psychological work for FND and low dose risperidone 0.5mg daily.

Authors: Dr Catherine Corby, Consultant Liaison Psychiatrist, Department of Liaison Psychiatry and Psychological Medicine, University Hospital Limerick/Adjunct Associate Clinical Professor at the School of Medicine, University of Limerick, and Dr Edris Adel, BMBS, SHO in General Internal and Geriatric Medicine, University Hospital Limerick.