Onset of Covid-19 with impaired consciousness and ataxia: a case report
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LETTER TO THE EDITORS
Onset of Covid‑19 with impaired consciousness and ataxia: a case report R. Balestrino1 · M. Rizzone1 · M. Zibetti1 · A. Romagnolo1 · C. A. Artusi1 · E. Montanaro1 · L. Lopiano1 Received: 24 April 2020 / Revised: 27 April 2020 / Accepted: 29 April 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
COVID-19 is an infectious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) [1]. To date, the major concerns about the SARS-CoV2 infection are pulmonary complications [2]; however, neurological manifestations, as dizziness, headache, taste and smell impairment are frequent [3, 4]; cerebrovascular diseases, impaired consciousness, muscle injury, polyradiculoneuropathy and epilepsy have also been reported [3, 5]. Moreover, the presence of SARS-CoV-2 RNA had been identified in cerebrospinal fluid in a patient with encephalitis [6]. Neurological manifestations mostly occur early in the illness and may be the presenting features of COVID-19 [3–6]. Several mechanisms have been proposed to explain the neuro-invasive potential of the virus, especially its affinity for ACE2 and previous demonstration of neuro-invasivity in other coronaviruses; indirect mechanism might contribute to the neurological damage as well [7]. Here, we present a case of COVID-19 occurring together with neurological symptoms. The patient is a 73-year-old Caucasian male, in treatment for hypertension (Atenolol/ Chlortalidone) and type 2 diabetes (Metformin), without previous neurological history, cognitively intact and professionally active. On the 23rd of February 2020, the patients gradually developed asthenia, gait ataxia, confusion and drowsiness; after 3 days lipothymia and urinary incontinence occurred. The following day, due to the worsening of drowsiness and confusion the patient was admitted to the Emergency Room (ER); at admission, body temperature was 38.6 °C, oxygen saturation was 98% in air; the neurological examination found confusion, balance impairment and gait ataxia; no meningeal signs were present. The EEG (awake, closed eyes) showed a reactive, unstable and symmetrical background alpha activity in posterior regions; * L. Lopiano [email protected] 1
Dipartimento di Neuroscienze, Universita degli Studi di Torino, Turin, Italy
the main features of the record were sporadic, low-voltage, focal polymorph delta elements in the anterior-frontal left cortex and sporadic spikes without clear epileptic correlate in the frontotemporal lobe, predominantly on the left; hyperventilation and intermittent photic stimulation did not modify the activity. Brain CT scan was negative for acute or chronic disease, chest X-ray and abdominal US were negative; in blood tests, C-reactive protein (CRP) was elevated (66 mg/L), white blood cells count (5.39 10^9/l), neutrophils count (2.87 10^9/l), creatine kinase, lactate dehydrogenase, procalcitonin were normal; urinary stick was mildly positive for protein (1 +). After the administration of paracetamol and the resolution of fever, the
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