Cases of rapid onset of encephalitis with diffuse corticospinal tract signs have been reported in conjunction with COVID-19 (4, 5). Neurological symptoms in COVID-19 patients include a few cases of catatonia (6–8), mutism (9), and autonomic dysfunction (10). Several forms of autoimmunity after COVID-19 are emerging (11), and this coronavirus may join other neurotropic viruses as a risk factor for autoimmune encephalitis.
Malignant catatonia is a more severe form of the catatonia spectrum but perhaps less recognized than the typical form with immobility, waxy flexibility, and stupor (12, 13). Neurologists in this case preferably used the term “acute encephalopathy,” and the problem of divergent nomenclature between specializations in cases of acute, global disturbance in cognition is a current topic of discussion (14). A recent review identified 124 cases of catatonia in conjunction with infections, of which 38% were viral and co-occurred with several autoimmune conditions, especially NMDAR encephalitis (15). The neurological symptom presentation in our case indicated the involvement of the corticospinal tracts and is congruent with pathological function in supratentorial structures and intact brainstem. The hallucinations and simultanagnosia appeared and regressed together, suggesting a common mechanism. Simultanagnosia and prosopagnosia indicate right hemisphere involvement, specifically the right posterior cortical network (16). Prosopagnosia is common after viral encephalitis (17). Although the MRI showed no evidence of structural damage, [18F]FDG PET findings in the striatum are consistent with increased metabolism in local neurons, glial cells, or both. Striatal hypermetabolism has previously been reported for autoimmune encephalitis caused by antibodies against NMDAR and the voltage-gated potassium channel complex, as well as in IgG4-related disease (18–23). The staining, clinical presentation, and radiology in our case are consistent with a synaptic target highly present in the striatum, where binding leads to loss of inhibition with increased metabolism in local neurons, glial cells, or both.
We conclude that malignant catatonia with potentially life-threatening autonomic instability can occur in patients with COVID-19. In our patient, this condition responded to treatment with dramatic improvement and with minimal evidence of structural brain damage. The treatment reduced autoreactive IgG in both serum and CSF but may also have other actions (24). In patients presenting with agitation, changes in behavior and speech, and autonomic instability in the weeks after infection with SARS-CoV-2, these symptoms should be recognized as a potential autoimmune manifestation of COVID-19. We are not aware of other types of encephalitis with such distinct pyramidal tract symptoms and raise the possibility that this may be a novel form of autoimmune encephalitis induced by infection with SARS-CoV-2.
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Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Department of Neuroscience, Karolinska Institute, Stockholm (Mulder); Department of Neuroscience, Neurology (Feresiadou, Virhammar, Kumlien), Department of Surgical Sciences, Radiology (Fällmar), Department of Surgical Sciences, Anesthesia and Intensive Care (Frithiof), Department of Neuroscience, Psychiatry (Rasmusson, Cunningham), and Department of Neuroscience, Neurosurgery (Rostami), Uppsala University, Uppsala, Sweden.
Supported by the Swedish Research Council, Bissen Brainwalk, and the Medical Training and Research Agreement from Uppsala University.The authors report no financial relationships with commercial interests.
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