Acute psychogenic mutism following total hip arthroplasty under general anesthesia in an elderly patient: a case report

Abstract

Postoperative neuropsychiatric complications most commonly manifest as delirium or cognitive impairment; however, acute isolated mutism in the absence of frank delirium or structural brain injury—referred to in some literature as acute psychogenic mutism (APM)—represents an exceedingly rare and poorly understood postoperative phenomenon. This report presents a case of APM in a 69-year-old woman following elective total hip arthroplasty under general anesthesia. The patient developed acute selective aphonia upon emergence from anesthesia, despite preserved comprehension and nonverbal communication abilities, with symptoms resolving spontaneously 44 h postoperatively. Emergent neuroimaging revealed no evidence of acute ischemic or hemorrhagic stroke, making a macro-scale cerebrovascular event unlikely.This case is notable for three distinctive features: (1) context-dependent preoperative anxiety, reflected by an Observational Anxiety Scale (OAS) score of 0 in the presence of family preoperatively, which escalated to elevated situational anxiety (HADS-A score 12, suggesting clinically relevant anxiety but not necessarily pathological) upon entry into the operating room; (2) the potential contribution of severe cerebral white matter lesions (Fazekas grade III), which may have disrupted prefrontal-limbic regulation under anesthetic stress; and (3) its occurrence in an older patient undergoing orthopedic surgery, challenging the prior association of APM predominantly with younger plastic surgery patients. We propose a tripartite etiological model integrating environmental triggers, neural vulnerability, and psychogenic dissociation, offering preliminary insights into perioperative mental health risk stratification that warrant further investigation. Non-convulsive status epilepticus was considered unlikely given the patient’s alertness and interactive behavior, though EEG was not performed acutely.

Introduction

Acute postoperative mutism, even after excluding obvious organic etiologies like stroke or structural damage, remains an exceedingly rare phenomenon [1]. While the majority of reported postoperative mutism cases are attributed to organic causes—particularly damage to the dentato-thalamo-cortical pathway—a small subset with features suggestive of a psychogenic or functional origin has been described [2–4].However, existing reports of postoperative psychogenic mutism are almost exclusively limited to younger plastic surgery patients, with body image anxiety proposed as a trigger [5]. Whether this entity occurs in elderly orthopedic populations—and what risk factors may predispose such patients—remains unknown.

Postoperative neuropsychiatric complications in the elderly, particularly delirium and cognitive dysfunction, are common and well-studied, affecting up to 40% of high-risk surgical patients [6, 7]. In contrast, isolated, reversible mutism in an otherwise alert patient represents a far rarer and diagnostically challenging presentation.

Here, we report a 69-year-old woman who developed acute, transient psychogenic mutism following total hip arthroplasty under general anesthesia, with spontaneous resolution 44 h postoperatively. This case extends the literature in three ways: (1) context-dependent preoperative anxiety unmasked by operating room entry, (2) severe cerebral white matter disease (Fazekas grade III) as a potential neural vulnerability, and (3) occurrence in an elderly orthopedic patient, challenging the prior association with younger plastic surgery cohorts. We propose a tripartite model integrating environmental triggers, neural fragility, and psychogenic dissociation to inform perioperative risk stratification.

Case presentation

A 69-year-old woman (body mass index 27.1 kg/m²) was admitted for elective right total hip arthroplasty due to femoral head necrosis accompanied by progressive pain and mobility limitation. Her medical history included hypertension, managed with nifedipine and irbesartan, and a prior cerebral infarction without residual neurological deficits. Preoperative magnetic resonance imaging revealed Fazekas grade III leukoaraiosis, old lacunar infarcts, and cerebral atrophy. Cardiac evaluation demonstrated frequent ventricular premature beats and 70% stenosis of the left anterior descending artery, for which she received bisoprolol, antiplatelet therapy, and potassium supplementation. The patient had no prior diagnosis of depression, anxiety disorder, post-traumatic stress disorder, or conversion disorder. She denied any history of psychological trauma or previous episodes of functional neurological symptoms. Her preoperative Hospital Anxiety and Depression Scale-Depression subscale (HADS-D) score was 3, indicating no clinically significant depressive symptoms. A structured psychiatric assessment was not performed by a psychiatrist at the bedside due to the acute setting and spontaneous resolution. However, a detailed clinical interview was conducted by the attending anesthesiologist and neurologist using a standardized template, covering past psychiatric history, trauma history, conversion symptoms, and family history. The absence of prior or current major depressive disorder, generalized anxiety disorder, post-traumatic stress disorder, or conversion disorder was confirmed by patient and family report. No formal structured diagnostic interview (e.g., SCID) was administered, which is a limitation.

While the patient was alert and fully communicative on the ward (Observational Anxiety Scale score = 0) in the presence of her family, she developed acute situational anxiety immediately upon entering the operating room (Hospital Anxiety and Depression Scale-Anxiety subscale score = 12, which falls within the borderline-to-clinical range for anxiety symptoms). This was accompanied by selective mutism-she stopped speaking entirely—and overt avoidance behaviors, including turning away from operating room personnel and attempting to sit up from the supine position. Of note, she did not utter a single word from operating room entry until induction of anesthesia, and there was no interval period of normal speech. Her family confirmed postoperatively that such mutism and avoidant behavior had never been observed previously under any circumstance.

Immediately following extubation, the patient presented with acute mutism that was phenomenologically similar to her preoperative mutism in the operating room: she was awake and alert, made eye contact, followed commands (e.g., “squeeze my hand,” “show me two fingers” ), and communicated non-verbally by nodding but remained completely unable to produce any vocalization. Unlike her preoperative mutism, which occurred in the setting of overt anxiety and avoidance, her postoperative mutism occurred without observable distress or agitation. EEG was not performed during the acute episode, as the patient’s alertness, ability to follow commands, and lack of any motor phenomena made non-convulsive status epilepticus unlikely.

This case underscores acute psychogenic mutism as a rare perioperative psychological complication, which was associated in this patient with significant preoperative anxiety and underlying cerebral white matter disease.

Discussion

Postoperative neuropsychiatric complications, especially in elderly patients undergoing non-cardiac surgery, represent a growing clinical and public health challenge, garnering increasing research attention worldwide [8–10]. Although preoperative anxiety is a well-established risk factor for postoperative neuropsychiatric impairment [11–13], its manifestation as isolated mutism following general anesthesia is exceedingly rare. Here, we discuss the diagnostic workup, differential diagnoses, and proposed mechanisms of this case.

Acute psychogenic mutism, classified as a conversion disorder (or functional neurological symptom disorder), is characterized by a sudden inability to speak in the absence of structural pathology, typically precipitated by acute psychological trauma. While more common in children, it is rare in adults and seldom reported in the perioperative setting [14, 15]. A comparable case from 2024 described a 75-year-old woman who developed transient aphasia following surgery for a humeral fracture. She retained the ability to follow commands and communicate in writing but lost vocalization; MRI showed no new lesions, hemorrhage, or residual drug effects [16]. Her symptoms resolved abruptly after interaction with family. Similarly, our patient presented with acute, reversible mutism without an organic cause. However, our case was distinctively accompanied by a history of cerebral infarction, significant situational anxiety upon operating room entry, and postoperative ICU isolation—factors that likely compounded psychological distress and functional vocal loss. To confirm the diagnosis, common differentials including transient ischemic attack, laryngeal injury, residual anesthetic effects, or primary emotional disturbances must be ruled out [17–20].

To strengthen the diagnostic validity, we applied the DSM-5 criteria for conversion disorder (functional neurological symptom disorder) to this case. The patient met all required criteria: (A) she demonstrated one symptom of altered voluntary motor function (complete loss of vocalization with preserved comprehension and nonverbal communication); (B) clinical and neuroimaging findings ruled out an organic cause (negative emergent CT/MRI for stroke, no laryngeal injury, no residual anesthetic effects); (C) there was evidence of incompatibility between the symptom and recognized neurological disease (isolated aphonia without aphasia, intact writing and gesturing, and spontaneous resolution); and (D) the symptom caused clinically significant distress but not a better explained by another medical or psychiatric disorder. The duration criterion for persistent conversion disorder (>6 months) does not apply given the acute and transient nature (44 h). This retrospective application of DSM-5 criteria supports the diagnosis of acute psychogenic mutism as a functional neurological disorder.

Transient ischemic attack (TIA) was considered a key differential diagnosis. While a TIA cannot be entirely ruled out by negative imaging alone, it is deemed improbable in this case for several clinical reasons. First, the patient’s symptoms (isolated, persistent aphonia for 44 h without any motor or sensory deficits) are highly atypical for a TIA in the territory of the middle or posterior cerebral arteries [21]. Second, the abrupt onset at emergence and the spontaneous, complete recovery without any antiplatelet or thrombolytic therapy are more consistent with a functional or metabolic etiology. Third, while intraoperative hypoxia or hypotension is not a prerequisite for TIA, its absence, combined with stable perioperative hemodynamics, further reduces its likelihood.Furthermore, the uncomplicated intubation procedure allowed for the exclusion of other potential causes, including migraine-related aura and intubation-induced laryngeal injury [18, 19, 22]. Residual neuromuscular blockade was considered unlikely given the patient’s intact comprehension and non-verbal communication abilities [23]. We acknowledge that the absence of radiographic evidence does not definitively exclude a TIA, as TIAs are clinical diagnoses [24]. However, the prolonged, non-fluctuating course over 44 h—exceeding the traditional 24-hour TIA time window—further argues against a cerebrovascular etiology. No conventional benzodiazepines (e.g., midazolam, diazepam) were administered during the perioperative period. Remimazolam, although also a benzodiazepine derivative, was used solely as part of the standard anesthesia protocol due to its ultra-short-acting properties; it was not administered as a treatment for mutism or anxiety symptoms. A “watchful waiting” approach with supportive care was adopted to avoid diagnostic confusion.

A critical differential diagnosis in this elderly patient with severe cerebral small vessel disease (Fazekas grade III) is hypoactive (or withdrawn) delirium. Delirium, particularly its hypoactive subtype, can present with psychomotor retardation, social withdrawal, and significantly reduced speech, closely mimicking a psychogenic or catatonic state. The patient’s pre-existing white matter disease is a well-established risk factor for postoperative delirium, potentially lowering the threshold for acute brain dysfunction under anesthetic stress [25, 26]. However, we ultimately favored the diagnosis of acute psychogenic mutism over hypoactive delirium for the following reasons. First, the mutism was isolated and context-dependent: upon emergence, the patient was awake, alert, and able to follow complex commands and communicate non-verbally (nodding, writing) without evidence of global cognitive clouding. This preservation of attention and receptive language is atypical for delirium. Second, the symptoms did not fluctuate—a hallmark feature of delirium—but instead resolved completely and abruptly after 44 h [27]. Third, we retrospectively applied the Confusion Assessment Method (CAM) criteria. Our patient fulfilled criterion (acute onset) but did not meet criteria for inattention or disorganized thinking. Therefore, while her leukoaraiosis likely conferred vulnerability, the clinical phenotype is more consistent with psychogenic mutism than with delirium. We acknowledge the absence of prospective CAM-ICU assessment as a limitation [28]. We do not claim that white matter disease is specific to psychogenic mutism. Rather, we propose that it serves as a neural vulnerability factor that lowers the threshold for both delirium and functional neurological disorders. In this patient, the clinical phenotype—isolated, non-fluctuating mutism with intact attention—favored the latter.

Although remimazolam was administered, the patient’s alert mental state and the isolated nature of the mutism argued against drug-induced delirium or psychosis, supporting a psychogenic etiology. Her MMSE score of 28, while not a delirium assessment tool, was consistent with intact cognitive function [29–31]. Classic aphasic syndromes (e.g., Broca’s or Wernicke’s aphasia) were also excluded, as the patient demonstrated preserved comprehension and non-verbal communication [32], alongside stable neuroimaging. Nevertheless, pre-existing white matter changes and a history of prior infarcts may have increased the patient’s vulnerability to functional speech inhibition under conditions of acute stress.

We propose a tripartite “environmental stress–neural fragility–psychogenic dissociation” model to elucidate the neural circuitry underlying acute psychogenic mutism (APM). The patient’s severe Fazekas grade III white matter disease likely disrupted prefrontal–limbic pathways—including the cingulum and fronto-occipital fasciculi—impairing top-down cognitive control [33]. Under anesthetic stress, compromised white matter integrity may have facilitated limbic hyperactivation due to failure of prefrontal inhibition, thereby triggering dissociative mutism as a defensive response [34]. Furthermore, age-related declines in neural plasticity and cholinergic function may have further reduced the patient’s resilience to acute stress [35].

The notable discrepancy between the patient’s preoperative Observational Anxiety Scale score (0 in the presence of family) and the elevated Hospital Anxiety and Depression Scale-Anxiety subscale score (12) upon entering the operating room highlights a critical limitation in current anxiety assessment methods: the concealing effect of social support on potentially clinically relevant underlying anxiety, which becomes unmasked upon exposure to the acute stress of the operative environment. Although concealed preoperative anxiety is a recognized risk factor for delirium and cognitive dysfunction [11, 13], its link to acute psychogenic mutism represents a novel finding. These observations underscore the necessity of developing more sensitive and context-specific tools for preoperative anxiety evaluation.

While acute psychogenic mutism (APM) has been predominantly reported in younger plastic surgery patients—potentially related to body image anxiety—this case underscores its relevance in elderly orthopedic populations, particularly among those with covert cerebral small vessel disease that impairs neural network stability [33]. Contributing factors such as the ICU environment, sleep disruption, and social isolation—for instance, restricted family visitation—may further aggravate perioperative psychological distress. The spontaneous resolution of symptoms without pharmacological intervention highlights the value of non-medical management strategies focused on psychological support. For high-risk patients—including those with a history of psychological trauma, silent cerebrovascular disease, or significant preoperative anxiety—we suggest considering multimodal preventive measures based on our clinical experience. These may include preoperative adaptation training (e.g., virtual reality-based operating room exposure), empathetic intraoperative care to reduce emergent stress, early postoperative psychological intervention accompanied by facilitated family presence, and multidisciplinary collaboration among anesthesiology, psychiatry, and neurology to design individualized awakening and recovery protocols.

Conclusion

To the best of our knowledge, this is among the few reported cases of acute psychogenic mutism following general anesthesia in an elderly patient undergoing orthopedic surgery. A multidisciplinary evaluation ruled out organic causes, leading us to propose a tripartite model that integrates environmental stress, white matter vulnerability, and psychogenic dissociation. APM should be included in the differential diagnosis of postoperative neurological complications, particularly for elderly patients with cerebral small vessel disease or significant preoperative anxiety. Clinicians should first exclude hypoactive delirium using validated screening tools such as CAM or 4AT before attributing postoperative mutism to a psychogenic cause. Future prospective studies with standardized psychiatric assessments and delirium screening tools are needed to validate our observations. Despite these limitations, this case highlights the importance of considering APM in the differential diagnosis of postoperative mutism, particularly in vulnerable elderly patients.

Abbreviations

APM

Acute Psychogenic Mutism

OAS

Observational Anxiety Scale

HADS-A

Hospital Anxiety and Depression Scale-Anxiety subscale

MMSE

Mini-Mental State Examination

TIA

Transient Ischemic Attack

MRI

Magnetic Resonance Imaging

CT

Computed Tomography

ICU

Intensive Care Unit

Authors’ contributions

W.Y. contributed to thesis ideation, revision, critical review, and manuscript submission. Y.G. and Y.D. contributed equally to thesis conception, data collection and analysis, and original draft writing. X.F., R.L., C.W., and Y.G. participated in thesis conception and manuscript revision. All authors read and approved the final manuscript.

Funding

This study was supported by the Gansu Provincial Key Research and Development Program (23YFFA00460), Lanzhou Municipal Healthcare Special Project (2023-1-47), Key Project of Gansu Joint Research Fund (25JRRA1199), Hospital Research Progect of Gansu Provincial Hospital 21GSSYA-7, and Gansu Provincial Science and Technology Program Project (21JR7RA675). The funders had no direct involvement in the study design, data collection, analysis, interpretation, or manuscript preparation.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

Ethical approval was waived by the institutional review board due to the retrospective nature of the case report.

Consent for publication

Full verbal and written consent has been obtained from the patient for submission of this manuscript for publication.

Competing interests

The authors declare no competing interests.