Postoperative hemiparesis due to conversion disorder after moderate sedation: a case report

Summary

Peri‐operative conversion disorder that manifests as postoperative muscle weakness is an uncommon diagnosis made through exclusion of neurological, metabolic or iatrogenic aetiologies. We present a case where a patient with a considerable history of physical and psychological trauma suffered from prolonged right‐sided hemiparesis following a breast biopsy under moderate‐to‐deep sedation. Conversion disorder following moderate‐to‐deep sedation has yet to be discussed in the literature, as all previous cases have described postoperative conversion disorder in the setting of general or central neuraxial anaesthesia. Our recommendation is for practitioners to keep conversion disorder on the list of differential diagnoses, despite the depth of sedation or type of anaesthetic utilised, and perform the same detailed neurological, metabolic and psychiatric assessment when considering postoperative weakness.

Introduction

Postoperative conversion disorder is a rare occurrence that has previously only been reported following general or neuraxial anaesthesia. Conversion disorder, as defined by the Diagnostic and Statistical Manual of Mental Disorders 5th Edition (DSM‐5), is a functional neurological deficit that is a diagnosis of exclusion without any attributable medical cause or malingering, typically affecting motor and/or sensory function or even causing transient loss of consciousness ¹. Recent studies looking to define a neurological aetiology through functional imaging of symptomatic patients have suggested a diathesis model of aberrant neural circuitry stemming from the prefrontal cortex or cingulate gyrus that may serve as the nexus for inhibitory motor or sensory pathways ². Thus, certain patients may have a higher susceptibility for conversion disorder, although currently there are minimal screening guidelines or tools to formally identify patients at increased risk. While there is no known prevalence of conversion disorders in peri‐operative settings, it has a lifetime prevalence of 0.023% in the general population ³.

Numerous stressors exist within the peri‐operative period including, but not limited to: anxiety; pain; postoperative nausea and vomiting; intra‐operative recall; and postoperative rehabilitation. However, the interplay between peri‐operative stress and conversion disorders is not fully understood. The current literature on peri‐operative conversion disorders consists primarily of case reports where symptoms typically present postoperatively, highlighting the delay between a potential precipitating surgical or anaesthetic aetiology and the symptoms ^{4, 5, 6, 7, 8, 9}. These cases, while rare, may be of interest to anaesthetists as patients with peri‐operative conversion disorders may endure prolonged hospitalisation, increased utilisation of hospital resources to rule out more common diagnoses and a higher risk of iatrogenic errors ⁵. Perhaps most importantly, conversion disorders tend to improve over time with supportive care and reassurance to the patient that these symptoms are neurological and functional rather than a manifestation of their psychological state ².

Report

A 39‐year‐old woman presented for a right breast mass excision and biopsy. Her past medical history was significant for migraine headaches and her past psychiatric history significant for childhood trauma, right upper extremity burns and domestic abuse as an adult. Her past surgical history included an appendicectomy, Spigelian hernia repair and septoplasty, all performed at other hospitals. At the time of her pre‐operative visit, she denied any complications with previous anaesthetics and did not appear anxious.

For this operation, her anaesthetic consisted of moderate‐to‐deep sedation, composed of midazolam 2 mg, propofol infusion between 60 – 90 μg.kg⁻¹.min⁻¹, fentanyl 75 μg and no neuromuscular blocking drug. Twenty millilitres of bupivacaine 0.25% was injected around the incision by the surgeon. The patient tolerated the 35‐min procedure well. Of note, she was alert and oriented to person, place and time, and conversant immediately postoperatively.

One hour postoperatively, she was noted to have right upper and lower extremity paresis without discernible temperature sensation and no withdrawal to noxious stimuli. She continued to be conversant, alert and oriented. Her vital signs were within normal limits. Her cranial nerve examination was unremarkable. No hypertonia, hyperreflexia or posturing was observed and proprioception remained normal. Routine bloodwork showed normal electrolyte levels, renal function and blood counts.

Based on neurology recommendations, a magnetic resonance image of the brain, head and cervical neck was performed and ruled‐out stroke, haemorrhage, mass or any structural cause for paresis. It was significant only for mild congenital stenosis and a slight disc bulge seen at C5‐C6 with no myelopathy. Overnight video electroencephalography did not show any activity concerning for seizure. Normal muscle‐specific kinase autoantibody and acetylcholine receptor binding antibody tests ruled out myasthenia gravis and peripheral electromyelography studies showed no peripheral nerve or muscular aetiology for weakness. Given her normal white blood cell count, lack of fever and isolated neurological findings, cerebrospinal fluid testing was deferred due to minimal concern for a neuro‐infectious aetiology.

On day three of her admission, with continued right‐side hemiparesis, our multidisciplinary team believed that there was enough evidence to investigate psychosomatic diagnoses and psychiatrists were consulted. The psychiatry team diagnosed the patient with a postoperative conversion disorder based on continued functional neurological symptoms with a low suspicion of malingering or secondary gain. As per their recommendations, no psychopharmacology was started as the patient lacked any mood symptoms or acute psychosis. Instead, she was evaluated by physical medicine for rehabilitation and eventually transferred to their care. The care team was instructed to avoid any unnecessary diagnostic testing and rather focus on affirming the patient's symptoms as being ‘organic’ and ‘functional’ as opposed to ‘psychogenic.’ After 28 days of inpatient rehabilitation focusing on upper and lower extremity strength‐building exercises, cognitive behavioural therapy and continued affirmation of her symptoms in a low acuity setting, the patient eventually regained her baseline motor function and was discharged home.

Discussion

We present a case of hemiparesis secondary to conversion disorder in the peri‐operative period following a detailed and extensive neurologic, psychiatric and metabolic workup. While postoperative conversion disorders are rare occurrences in practice, previous published case studies have detailed similar clinical scenarios, each arriving at the diagnosis through exclusion of more common aetiologies of peri‐operative neurological deficits such as stroke or residual paralysis ^{4, 5, 6, 7, 8, 9}. There is currently uncertainty whether anaesthesia has a protective or causative role to play in the development of conversion disorder. It stands to reason that if the stress or trauma of surgery is a triggering factor for functional neurological symptoms, then general anaesthesia or appropriate surgical coverage with regional or neuraxial anaesthesia would be protective in preventing their onset.

To our knowledge, this is the first report of conversion disorder following moderate‐to‐deep sedation. Based on our experience, we propose that conversion disorder is possible even in lighter planes of anaesthesia, without neuraxial instrumentation and should be considered a differential regardless of the anaesthetic utilised. The inclusion of conversion disorders in the setting of monitored sedation suggests that the type of anaesthetic may not be as triggering of a factor as previously thought, given that profound symptoms are possible across a wide spectrum of anaesthetics and surgical procedures. Notably, it has been suggested that the use of sedation with propofol may even be therapeutic for severe symptoms stemming from conversion disorder. Stone et al. reported a case series where five out of eleven patients treated had complete resolution of neurological symptoms following monitored sedation ¹⁰. These authors propose that the use of Gamma aminobutyric acid‐ (GABA‐) modulating sedatives in sub‐general anaesthetic dosages may block the inhibitory pathways driving functional symptoms. Yet it is unclear why transient states of sedation could uncouple these aberrant pathways. If future research elucidates and substantiates this treatment modality, it may better define the role anaesthetists can play in the prevention or potentially the treatment of peri‐operative conversion disorders.

Finally, this case highlights the importance of assessing a patient's social and trauma history during the peri‐operative period and the need to carefully manage conversion disorders with the appropriate team of specialists in order to facilitate the supportive care necessary for recovery from a functional standpoint. This patient's hemiparesis likely represented an unconscious manifestation of stress resulting in the somatisation of her psychological state. This may explain the lateralisation of her symptoms to her right, given her right‐sided upper extremity burns as a child and the concern for a right‐side breast lesion. Much of the nuance and emotionality around the patient's past psychiatric history was only elucidated by the psychiatry team days after the onset of her symptoms. While knowledge of the patient's complex social history would not have deterred a thorough work‐up of more common diagnoses, it might have changed the manner in which the medical team interacted with her. The patient did not begin to see return of function to the right side of her body until her care was de‐escalated to a unit focused on supportive care rather than diagnostic testing and monitoring. Indeed, the management of peri‐operative conversion disorders represents the metaphorical tightrope walk between a vigilant and methodical diagnostic rule‐out of more nefarious aetiologies and defusing the patient's very tension and stress that may be fuelling the onset of these symptoms.