International journal of psychiatry in medicine · 2023
Parainfectious autoimmune encephalitis related to SARS-CoV-2 infection, presenting with catatonia.
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Aktan Suzgun Merve, Kochan Kızılkılıc Esra, Ucar Bostan Busra, Tutuncu Melih, Kızıltan Gunes
Аннотация
OBJECTIVE: SARS-CoV-2 infection commonly affects both the central and peripheral nervous systems, resulting in a variety of neurological and psychiatric symptoms. Whereas the effects of SARS-CoV-2 on neuronal structures in the short and long-term are still controversial, neurological involvement secondary to SARS-CoV- 2 is heterogeneous in terms of clinical presentation, treatment response, and prognosis.
METHOD: A case of autoimmune encephalitis developing after SARS-CoV-2 is described in this article.
RESULTS: The patient was admitted to the clinic with classical signs of catatonia and encephalopathy. The emergence of neuropsychiatric problems after the relief of SARS-CoV-2 symptoms suggests that symptoms were primarily related to immune processes. This patient demonstrated a good clinical response to symptomatic catatonia treatment and immune-modulatory agents and recovered both physically and cognitively without sequelae.
CONCLUSION: SARS-CoV-2 infection may involve encephalitic involvement and psychological symptoms (including catatonia) after the infection by triggering autoimmune pathways.
METHOD: A case of autoimmune encephalitis developing after SARS-CoV-2 is described in this article.
RESULTS: The patient was admitted to the clinic with classical signs of catatonia and encephalopathy. The emergence of neuropsychiatric problems after the relief of SARS-CoV-2 symptoms suggests that symptoms were primarily related to immune processes. This patient demonstrated a good clinical response to symptomatic catatonia treatment and immune-modulatory agents and recovered both physically and cognitively without sequelae.
CONCLUSION: SARS-CoV-2 infection may involve encephalitic involvement and psychological symptoms (including catatonia) after the infection by triggering autoimmune pathways.