INTRODUCTION: Catatonia is a psychomotor syndrome associated with a range of psychiatric and medical illnesses and can entail increased, decreased, and abnormal psychomotor activity. Catatonia has been associated with over 100 medical conditions, including metabolic, autoimmune, inflammatory, infectious, and neoplastic conditions generally involving diffuse cerebral dysfunction, and numerous substances, including antipsychotics, immunosuppressants, antibiotics, and recreational drugs. Individuals with severe acute illness may be at especially high risk of developing catatonia. Among infectious causes of catatonia, many are known to be neurotropic pathogens; the pathogenesis may be through a direct toxic effect or an immune response.
Coronavirus disease 2019 (COVID-19), the disease caused by severe acute respiratory syndrome coronavirus 2, has contributed to considerable morbidity and mortality in 2020. While respiratory symptoms are predominant in COVID-19, there have been reports of neurologic sequelae, including peripheral nervous system abnormalities such as hypogeusia and hyposmia and central nervous symptoms such as dizziness, headache, stroke, and delirium. The neurotropism of severe acute respiratory syndrome coronavirus 2 is theoretically conferred by the binding of glycoproteins on its surface to the angiotensin-converting enzyme 2, which is present in neurological tissue. The virus may enter the central nervous system from the nares through the cribriform plate or via hematogenous spread across the blood-brain barrier. It is hypothesized that brainstem involvement of the virus may partially contribute to the acute respiratory failure of patients with COVID-19. Although a variety of neuropsychiatric manifestations have been reported, COVID-19 has not previously been associated with catatonia to our knowledge. We present a case of catatonia occurring in the absence of any preexisting neuropsychiatric condition in a patient medically hospitalized for COVID-19.
Caan MP, Lim CT, Howard M
Psychosomatics. 2020 May 27:S0033-3182(20)30162-6. doi: 10.1016/j.psym.2020.05.021.
BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of an ongoing pandemic, with increasing deaths worldwide. To date, documentation of the histopathological features in fatal cases of the disease caused by SARS-CoV-2 (COVID-19) has been scarce due to sparse autopsy performance and incomplete organ sampling. We aimed to provide a clinicopathological report of severe COVID-19 cases by documenting histopathological changes and evidence of SARS-CoV-2 tissue tropism. METHODS: In this case series, patients with a positive antemortem or post-mortem SARS-CoV-2 result were considered eligible for enrolment. Post-mortem examinations were done on 14 people who died with COVID-19 at the King County Medical Examiner's Office (Seattle, WA, USA) and Snohomish County Medical Examiner's Office (Everett, WA, USA) in negative-pressure isolation suites during February and March, 2020. Clinical and laboratory data were reviewed. Tissue examination was done by light microscopy, immunohistochemistry, electron microscopy, and quantitative RT-PCR. FINDINGS: The median age of our cohort was 73·5 years (range 42-84; IQR 67·5-77·25). All patients had clinically significant comorbidities, the most common being hypertension, chronic kidney disease, obstructive sleep apnoea, and metabolic disease including diabetes and obesity. The major pulmonary finding was diffuse alveolar damage in the acute or organising phases, with five patients showing focal pulmonary microthrombi. Coronavirus-like particles were detected in the respiratory system, kidney, and gastrointestinal tract. Lymphocytic myocarditis was observed in one patient with viral RNA detected in the tissue. INTERPRETATION: The primary pathology observed in our cohort was diffuse alveolar damage, with virus located in the pneumocytes and tracheal epithelium. Microthrombi, where observed, were scarce and endotheliitis was not identified. Although other non-pulmonary organs showed susceptibility to infection, their contribution to the pathogenesis of SARS-CoV-2 infection requires further examination. FUNDING: None.
Bradley BT, Maioli H, Johnston R, Chaudhry I, Fink SL, Xu H, Najafian B, Deutsch G, Lacy JM, Williams T, Yarid N, Marshall DA
Lancet. 2020 Aug 1;396(10247):320-332. doi: 10.1016/S0140-6736(20)31305-2. Epub 2020 Jul 16.
No abstract available.
No abstract available.