“…Notably, these same two patients also displayed increased muscle tone and rigidity. Of note given the motor findings, it has previously been observed that the basal ganglia is particularly sensitive to strongly neurotropic viruses, perhaps related to virally-induced autoimmune inflammatory response to basal ganglia antigens [8].…”
Introduction: Neuropsychiatric manifestations of the coronavirus disease 2019 (COVID-19) have been described, including anosmia, ageusia, headache, paresthesia, encephalitis and encephalopathy. Little is known about the mechanisms by which the virus causes central nervous system (CNS) symptoms, and therefore little guidance is available regarding potential workup or management options. Cases: We present a series of four consecutive cases, seen by our psychiatry consultation service over a one-week period, each of which manifested delirium as a result of infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Discussion: The four cases highlighted here all occurred in older patients with premorbid evidence of cognitive decline. Unique features seen in multiple cases included rigidity, alogia, abulia, and elevated inflammatory markers. In all four cases, a change in mental status was the presenting symptom, and three of the four cases lacked significant respiratory symptoms. In addition to discussing unique features of the cases, we discuss possible pathophysiologic explanations for COVID-19 delirium. Conclusions: Delirium should be recognized as a potential feature of infection with SARS-CoV-2 and may be the only presenting symptom. Based on the high rates of delirium demonstrated in prior studies, hospitals should consider adding mental status changes to the list of testing criteria. Further research is needed to determine if delirium in COVID-19 represents a primary encephalopathy heralding invasion of the CNS by the virus, or a secondary encephalopathy related to systemic inflammatory response or other factors.
“…Notably, these same two patients also displayed increased muscle tone and rigidity. Of note given the motor findings, it has previously been observed that the basal ganglia is particularly sensitive to strongly neurotropic viruses, perhaps related to virally-induced autoimmune inflammatory response to basal ganglia antigens [8].…”
Introduction: Neuropsychiatric manifestations of the coronavirus disease 2019 (COVID-19) have been described, including anosmia, ageusia, headache, paresthesia, encephalitis and encephalopathy. Little is known about the mechanisms by which the virus causes central nervous system (CNS) symptoms, and therefore little guidance is available regarding potential workup or management options. Cases: We present a series of four consecutive cases, seen by our psychiatry consultation service over a one-week period, each of which manifested delirium as a result of infection with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Discussion: The four cases highlighted here all occurred in older patients with premorbid evidence of cognitive decline. Unique features seen in multiple cases included rigidity, alogia, abulia, and elevated inflammatory markers. In all four cases, a change in mental status was the presenting symptom, and three of the four cases lacked significant respiratory symptoms. In addition to discussing unique features of the cases, we discuss possible pathophysiologic explanations for COVID-19 delirium. Conclusions: Delirium should be recognized as a potential feature of infection with SARS-CoV-2 and may be the only presenting symptom. Based on the high rates of delirium demonstrated in prior studies, hospitals should consider adding mental status changes to the list of testing criteria. Further research is needed to determine if delirium in COVID-19 represents a primary encephalopathy heralding invasion of the CNS by the virus, or a secondary encephalopathy related to systemic inflammatory response or other factors.
“…Myoclonus may present in the context of other viral infections, with concomitant encephalopathy/encephalitis or as an isolated postinfectious phenomenon. 5,6 SARS-CoV-2 may theoretically access subcortical structures involved in myoclonus generation via invasion of the olfactory bulb. 1 In our patient, however, clinical course (including the absence of hyposmia), magnetic resonance imaging, and CSF findings argue against a direct pathogenic role of central nervous system viral invasion.…”
Myoclonus has been reported as a possible manifestation of coronavirus disease 2019 (COVID-19), yet its neurophysiology and pathogenesis were poorly investigated. 1-4 We describe a middleaged man with COVID-19 who underwent extensive examinations for his disabling myoclonus. CASE REPORT A 58-year-old hypertensive man with a 1-week history of fever and cough presented to the emergency department with dyspnea. A nasopharyngeal swab tested positive for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The patient was admitted to the intensive care unit after 1 week and placed on invasive mechanical ventilation as a result of respiratory distress. He was treated with hydroxychloroquine, tocilizumab, and remdesivir. Respiratory status quickly improved, thus he was extubated after 5 days, and oxygen therapy was progressively weaned off. Two days after discharge from the intensive care unit, he became markedly agitated. His mental status normalized in 48 hours; however, at this point he developed multifocal myoclonus elicited by action and tactile stimuli, predominant in the right proximal inferior limb muscles, preventing his ability to stand (Video SS1). Cognitive deficits were not observed. Electrolytes and renal and liver function tests were unremarkable. Cerebrospinal fluid (CSF) analysis, performed 8 days after myoclonus onset, demonstrated 5 leukocytes/μL, elevated protein levels (75 mg/dL) and CSF/serum albumin ratio (13.1), and negative SARS-CoV-2 reverse-transcription polymerase chain reaction. Cytokine analyses revealed interleukin-6 at 11.6 pg/mL in CSF (29.3 pg/mL in serum, reference < 5.9) and interleukin-8 at 38 pg/ mL in CSF (11 pg/mL in serum, reference < 70). A serologic panel
The first step in diagnosis is recognizing the movement disorder as chorea [1]. Chorea is characterized by irregu lar, purposeless, arrhythmic, nonstereotyped involuntary movements that flow from one body part to another [2]. These movements can affect any part of the body, although usually brief, can also be of long duration, and can have small or large amplitude. Movements with large amplitude localized proximally in the arms are called "ballismus" [3]. Once the movement disorder has been recognized as chorea, we then recommend classifying the age of onset as either childhood (prior to the age of 16) or adultonset [1]. Multiple causes of chorea exist in both age groups, many of which fit in the definition of rare diseases [4]. Since the most common cause of acute chorea in childhood is Sydenham's chorea and of chronic progressive chorea in adults is Huntington's disease (HD), we recommend these disorders should be tested for, as appropriate, and excluded before proceeding to other diagnostic pathways. The next step is to determine, if possible, whether the chorea is hereditary (genetic) or acquired (nongen etic) in nature. The family history should be carefully and
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