Complex Catatonia in the Wake of COVID-19: A Case Series Exploration

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The onset of the COVID-19 pandemic marked a critical juncture in global health, unveiling a spectrum of neuropsychiatric complications that transcended the primary respiratory symptoms associated with the virus. Among these, the manifestation of catatonia, a complex neurobehavioral syndrome, has raised significant concerns and prompted in-depth investigations into its correlation with SARS-CoV-2 infection. This article presents a detailed examination of three distinct cases where COVID-19 infection precipitated severe catatonic states, exploring the intricate interplay between the virus and pre-existing psychiatric conditions, and providing insights into the potential neurobiological mechanisms at play.

Case Study: Patient F.B.

F.B., a 51-year-old white woman with a longstanding history of bipolar disorder type I, comorbid with obsessive-compulsive symptoms and panic-agoraphobic traits, represents a prototypical case of psychiatric vulnerability exacerbated by COVID-19. Her psychiatric journey began at 16 with depressive episodes, escalating to frequent manic episodes with psychotic symptoms and necessitating multiple hospitalizations. Her treatment history is extensive, including various mood stabilizers and antipsychotic medications, notably clozapine for treatment-resistant bipolar disorder. F.B. also underwent four electroconvulsive therapy (ECT) cycles, one prompted by neuroleptic malignant syndrome (NMS).

Her medical background was further complicated by a familial predisposition to mental illness, hypothyroidism, uterine leiomyomatosis, and osteoarticular conditions. The intersection of these medical and psychiatric dimensions took a dramatic turn in November 2020 when F.B. contracted COVID-19, leading to hospitalization for interstitial pneumonia. Post-discharge, she experienced severe cognitive and motor deterioration, culminating in a psychiatric transfer for profound catatonia, characterized by mutism, psychomotor arrest, and a loss of daily living activities, scoring 24 on the Bush Francis Catatonia Rating Scale (BFCRS).

Despite normal vital signs and resolving respiratory symptoms, her SARS-CoV-2 positivity persisted, complicating her treatment. Her pharmacological regimen was adjusted in response to her condition, but her mental state rapidly deteriorated, necessitating intensive medical and neurological intervention. Complications such as pulmonary embolism and status epilepticus further obscured the clinical picture, leading to a challenging diagnostic and therapeutic process.

Ultimately, a month post-COVID-19 infection, F.B. underwent ECT, resulting in significant improvement. However, the lingering effects on her daily functioning underscored the profound impact of the catatonic episode. Her case highlights the intricate challenges in managing psychiatric patients with COVID-19, particularly when catatonia is involved, necessitating a careful balance between infectious disease management and psychiatric care.

Case Study: Patient G.S.

G.S., a 54-year-old white woman with no prior psychiatric history, faced a stark transition during the pandemic, shifting from her role as an occupational therapist to a state of extended social isolation. This drastic change, coupled with a pauci-symptomatic COVID-19 infection, triggered a severe psychiatric downturn, manifesting as psychotic depression with catatonic features. Initially, her symptoms were managed with antipsychotics and benzodiazepines, but the treatment inadvertently escalated her catatonic state, necessitating a reevaluation of her therapeutic approach.

The psychological strain of the pandemic, accentuated by her obsessive-compulsive traits, precipitated a profound psychiatric crisis. Despite initial improvements with lorazepam and gabapentin, G.S.’s cognitive and emotional state remained fragile, culminating in a recurrent catatonic state resistant to conventional treatments. This necessitated the use of ECT, which ultimately led to a remission of her symptoms, illustrating the potential efficacy of ECT in managing catatonia post-COVID-19.

G.S.’s experience underscores the psychological toll of the pandemic, particularly in individuals with pre-existing psychiatric vulnerabilities. Her case emphasizes the necessity for a nuanced understanding of the psychiatric sequelae of COVID-19 and the importance of tailored treatment approaches to address the complex interplay of psychiatric and COVID-19-related symptoms.

Case Study: Patient F.Z.

F.Z., a 34-year-old white woman with a clear medical history, experienced a sudden psychiatric decline following COVID-19 vaccination and subsequent infection. Initially presenting with anosmia and dysgeusia, her condition rapidly evolved into a severe catatonic state with both excited and inhibited features. Despite aggressive treatment with lorazepam and valproic acid, her condition deteriorated, leading to intensive care and a coma diagnosis.

The discovery of an ovarian teratoma and the presence of anti-NMDAR antibodies suggested a paraneoplastic syndrome, prompting surgical intervention. The subsequent remission of catatonia post-surgery highlights the potential for complex and atypical presentations of catatonia in the context of COVID-19, necessitating a broad diagnostic lens and an integrated treatment approach.

Neurobiological Mechanisms and COVID-19-Induced Catatonia

The cases of F.B., G.S., and F.Z. illuminate the diverse and complex manifestations of catatonia in the context of COVID-19, suggesting multifactorial etiologies involving psychiatric, neurological, and immunological factors. The role of COVID-19 in exacerbating or triggering catatonic states is increasingly recognized, with implications for the neurobiological understanding of catatonia.

The interaction between COVID-19 and pre-existing psychiatric conditions, the impact of the virus on neural pathways, and the potential for post-infectious autoimmune responses provide a fertile ground for exploring the pathophysiology of catatonia. These case studies contribute to the growing body of evidence linking COVID-19 with acute and persistent neuropsychiatric complications, urging a reevaluation of catatonia within the broader spectrum of COVID-19-related disorders.

Discussion: Unraveling the Complexities of Catatonia in the COVID-19 Era

The elusive nature of catatonia, with its multifaceted presentations and underlying mechanisms, remains a significant challenge in neuropsychiatry. The interplay between dopamine and GABA neurotransmission in the basal ganglia, as supported by robust neuroscientific evidence, is a central theme in the discourse on catatonia (Rogers et al., 2019; Torrico et al., 2021). The emergence of catatonia in association with anti-NMDAR encephalitis and the observed benefits of glutamate antagonist therapy underscore the potential role of glutamatergic dysfunction in catatonic syndromes (Carroll et al., 2007; Dalmau et al., 2007; Vasilevska et al., 2021).

Our case series, involving Caucasian women who developed catatonia post-SARS-CoV-2 infection, underscores the potential for COVID-19 to precipitate or exacerbate catatonic states. The diversity in psychiatric backgrounds, severity of COVID-19 infection, and medical comorbidities among the patients suggests a complex interplay of pathogenic mechanisms leading to catatonia.

Patient 1, with a history of bipolar disorder and previous catatonic episodes, exhibited severe neuroinflammation during her COVID-19 infection, hinting at neuroinflammation as a pivotal factor in her catatonic presentation. The neuroinvasive potential of SARS-CoV-2, coupled with its capacity to induce neuroinflammation and disrupt neurotransmitter systems, offers a plausible explanation for the catatonic symptoms observed (Rogers et al., 2019; Torrico et al., 2021).

Patient 2’s catatonia emerged in the context of thyrotoxicosis and mild COVID-19, with her premorbid obsessive-compulsive traits potentially heightening her vulnerability to psychiatric distress during the pandemic. This case illustrates how individual psychological and biological factors, exacerbated by the pandemic’s stressors, can culminate in catatonia.

Patient 3’s case, marked by the absence of prior psychiatric history and the presence of anti-NMDAR antibodies, points to a paraneoplastic syndrome induced by COVID-19. The association of anti-NMDAR encephalitis with catatonia, particularly in the context of ovarian teratoma, highlights the intricate connection between immune-mediated neurological disorders and catatonia (Dalmau et al., 2007; Kayser and Dalmau, 2016).

The pathogenesis of catatonia in these cases likely involves a combination of direct neurotoxic effects of the virus, neuroinflammatory responses, and the perturbation of neurotransmitter systems. The “cytokine storm” observed in severe COVID-19 cases may exacerbate these effects, leading to neuropsychiatric manifestations, including catatonia (Troyer et al., 2020; Kumar et al., 2021).

The response to treatment in our cases, particularly the limited efficacy of benzodiazepines and the subsequent improvement with ECT, emphasizes the need for tailored therapeutic strategies in COVID-19-associated catatonia. This aligns with emerging evidence suggesting the potential of NMDAR antagonists like amantadine or memantine in treating refractory cases, possibly by modulating the interaction between COVID-19 and neurotransmitter systems (Oh et al., 2022; Hasanagic and Serdarevic, 2020).

In conclusion, the intricate web of factors contributing to catatonia in the context of COVID-19 underscores the importance of a comprehensive diagnostic and therapeutic approach. Early recognition and intervention in catatonic states, particularly in the backdrop of COVID-19, are crucial for improving patient outcomes. The ongoing pandemic mandates a vigilant monitoring of neuropsychiatric symptoms and a readiness to adapt treatment modalities to the evolving understanding of COVID-19’s neuropsychiatric impact.


reference link :https://www.sciencedirect.com/science/article/pii/S277302122400018X

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