Three of them had a preceding anosmia or ageusia
Three of them had a preceding anosmia or ageusia. prodromic symptoms. However, it is likely that there is a connection between the severity of the respiratory syndrome and further neurological consequences. Keywords: COVID\19, Guillain\Barr syndrome, SARS\CoV2 1.?BACKGROUND AND AIMS There is an emerging evidence that SARS\CoV\2 (coronavirus\2) contamination could be associated with neurological complications, including febril seizures, headache, dizziness, myalgia, as well with encephalopathy, encephalitis, stroke, and acute peripheral nerve diseases.1, 2 Neurotropic characteristics of coronavirus have been described in humans. It enters the CNS through the olfactory bulb due to a nasal contamination, causing inflammation and demyelination which may lead to transitory loss of smell and taste, occasionally without fever and common respiratory or gastrointestinal symptoms in infected patients. 1 According to Helms et al., 58 of 64 patients with acute respiratory distress syndrome (ARDS) due to Covid\19 (coronavirus disease 2019), had neurological symptoms caused by encephalopathy with agitation, confusion, dysexecutive syndrome, ataxia, and corticospinal tract indicators. MRI of two patients showed single acute ischemic strokes. 2 Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) is usually a common form of Guillain\Barr syndrome (GBS) characterized by ascending flaccid symmetrical limb paralysis with areflexia, sensory symptoms and often involvement of the cranial nerves. Common electrodiagnostic features include indicators of segmental demyelination as temporal dispersion of the compound muscle action potentials (CMAP) and sensory potentials, prolonged distal motor latencies and reduced conduction velocity in the demyelinative range as well as conduction blocks and absent or prolonged F\waves. 3 A few patients with demyelinating and axonal type of Guillain\Barr syndrome have been reported recently, the onset of neurological symptoms occurred 5 to 10?days after the diagnosis of COVID\19 with respiratory symptoms.4, 5, 6, 7, 8 2.?CASE REPORT The 54\12 months\aged, Caucasian female patient with an uneventful medical history was admitted to our neurological department in April 2020 with an acute, proximally pronounced, moderate, symmetric paraparesis (Medical Research Council/MRC/scale was 3/5 proximal and 4/5 distal in the lower extremities). Areflexia, numbness, and tingling of all extremities were also found, with initial maintained Emicerfont gain ability. These symptoms began 3?weeks following a positive reverse\transcriptase\polymerase\chain\reaction (PCR) oropharyngeal test for COVID\19 and were progressing already for 10?days at admission. The test was performed because of her contact to a coronavirus\positive person. She did not experience fever, respiratory or gastrointestinal symptoms, but reported about a transient loss of smell and taste 2?weeks before the GBS symptoms occurred. The altered Erasmus Guillain\Barr Syndrome outcome score (mEGOS) was 3/9 at admission and 1/12 at day 7 of hospitalization pointing to a favorable outcome. The general physical examination was normal, she had no fever and a new CD7 PCR\oropharyngeal test was unfavorable. Cerebrospinal fluid (CSF) assessment showed an albuminocytologic Emicerfont dissociation with increased protein level (140?g/L) and normal cell count, immunoassay, and Lyme\serology were negative. SARS\Cov\2 RNA was not tested in CSF. Standard laboratory assessments (complete blood count, CRP, serum glucose, creatinin, sodium and potassium level, TSH, creatine kinase, and urine test) and special blood assessments (serology, HbA1c, ANA, anti\DNA, c\ANCA, p\ANCA, HIV, serum vitamin B12\level, and serum protein electrophoresis) were also within the normal range. MRI of the cervical spine and the chest x\ray examination did not show pathological findings. Electrophysiological studies were performed using a Nicolet Viking EMG device. The Emicerfont first electrophysiological evaluation (at admission) showed significantly prolonged distal motor latencies and temporal dispersion of the CMAP of the common peroneal nerve bilaterally (recorded from the extensor digitorum brevis muscle; Figure ?Physique1).1). Stimulation of the tibial nerves at the ankle elicited normal F\wave latencies with pathological intermediate latency responses (complex A\waves) on both sides (Physique ?(Figure2).2). Motor nerve conduction studies of the tibial, median and ulnar nerves and sensory nerve conduction studies of the median, ulnar, and sural nerves were normal on both sides. Electromyography (EMG) showed no denervation indicators. An acute inflammatory demyelinating polyradiculoneuropathy was diagnosed. Open in a separate window Physique 1 Motor conduction study of the peroneal nerves with significantly prolonged distal motor.