• Neurologic complications as result of COVID-19
  • Pedram Ghaderi,1 Tannaz Haghgouie,2,*
    1. University of Tabriz, Faculty of Veterinary Medicine, Department of Basic Sciences, Division of Pharmacology and Toxicology
    2. University of Tabriz, Faculty of Veterinary Medicine, Department of Basic Sciences, Division of Pharmacology and Toxicology


  • Introduction: Since the emergence of severe acute respiratory syndrome coronavirus two (SARS-CoV-two) spread rapidly around the world. As respiratory complication is the primarily reported manifestation though rare, yet serious neurological complications are being frequently reported in the literature. selected coronavirus disease cases (COVID-nineteen) manifested neurologic complications. COVID-nineteen infection cause or even present with different neurological features including Encephalopathy, impaired consciousness, agitation, seizure, headache, anosmia, and neurodegenerative diseases. In this paper we provide a brief review of observed neurological manifestations associated with COVID-nineteen
  • Methods: We searched Pubmed , Google Scholar, ncbi using the keywords; “seizures”, SARS COV two’’, “COVID-nineteen” and "Encephalopathy". Search was limited to the English language manuscript only from twenty twenty to twenty twenty one. We identified two hundred twenty four research articles describing neurological complications in SARS-COV- two
  • Results: During the study period, 6147 people had confirmed COVID-19 in Fars province, Iran; 110 people died from the illness (case fatality rate 1.79%). During this time period, five people had seizures (seizure rate 0.08%). In four patients, seizure was one of the presenting manifestations, and in one person, it happened during the course of hospital admission. Two patients had status epilepticus. All patients experienced hypoxemia and four of them needed respirator. Two patients had related metabolic de- rangements and one had cerebrospinal fluid (CSF) lymphocytic pleocytosis. Brain imaging was abnormal in three patients. Four patients died. In a study conducted on 13 patients, Electroencephalography was obtained in eleven patients. Three patients had generalized slowing, and six patients showed focal areas of status epilepticus including the temporal lobe, frontotemporal regions and the centro-parietal regions Computed tomography (CT) head scan and magnetic resonance imaging (MRI) brain were obtained in all thirteen patients. One patient had MRI evidence of ventriculitis and encephalitis while one patient had MRI evidence of multiple, non-enhancing demyelinating lesions. In the remaining eleven patients, imaging studies showed no acute changes. Eight out of 13 patients underwent lumbar puncture. CSF COVID-PCR was reported positive in one patient though the nasopharyngeal swab was reported negative. Six patients had negative CSF PCRs or were in institutions which could not test the CSF for COVID PCR. Three patients had elevated lymphocytes, one had elevated protein with otherwise normal CSF findings, and the 3 patients had no specific CSF findings. Lumbar puncture was not performed in 6 patients. There are several theorized pathways for SARS- COV-2 to enter the CNS. One of the chief targets of the SARS- COV-2 is the Angiotensin-converting-enzyme-2 (ACE-2) receptor cells. ACE-2 receptors are located on cells throughout the body, including the cardio-respiratory neurons of the brainstem, glial cells, basal ganglia, motor cortex, raphe, and endothelial cells of the brain. Once in the bloodstream, SARS-COV-2 can travel to infect the endothelial cells of the blood-brain barrier and then accumulate in the various ACE 2 heavy brain regions causing direct infection with neurological sequelae. A second route through which the SARS- COV-2 is theorized to enter the CNS is the olfactory nerve via the nasal cavity. It has been demonstrated that within seven days of infection, SARS-COV-2 can reach the CSF and brain through the olfactory nerve causing inflammation and demyelinating reactions with potential subsequent seizures. Removal of the olfactory bulb in mice has shown to restrict invasion of SARS-COV-2 into the CNS. Moreover, SARS-CoV-2 infection leads to a cerebral vascular injury that increases the risk of chronic brain damage, because of the collective damaging effect of multifocal cerebral or haemorrhage, endothelial and BBB dysfunction, and upregulation of pro-inflammatory cytokines within the brain In adults, post-viral anosmia is one of the major reasons for olfactory dysfunction in COVID-19, identified in up to 40% of infected patients. A study from Italy reports that around 33.9% of infected patients have either disturbance in taste or the olfactory system, whereas around 18.3% of infected patients experienced both disturbances. Anosmia was also reported as the first symptom in about 83% of infected patients.
  • Conclusion: The global problem of COVID-nineteen affected millions of human lives with a high infectivity rate. The major proportion of SARS-CoV-two infected patients showed more frequent respiratory disorders compared to neurological manifestations.Clinical, diagnostic, and epidemiological studies during acute and recovery phases are required for better diagnosis and management of the patients with COVID-nineteen
  • Keywords: COVID, Neurologic complications, Seizure, Encephalopathy