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Severe acute respiratory syndrome coronavirus 2, the source of COVID-19, causes numerous clinical findings including respiratory and gastrointestinal findings. Evidence is now growing for increasing neurological symptoms. This is thought to be from direct in-situ effects in the olfactory bulb caused by the virus. Angiotensin-converting enzyme 2 receptors likely serve as a key receptor for cell entry for most coronaviridae as they are present in multiple organ tissues in the body, notably neurons, and in type 2 alveolar cells in the lung. Hematogenous spread to the nervous system has been described, with viral transmission along neuronal synapses in a retrograde fashion. The penetration of the virus to the central nervous system (CNS) allows for the resulting intracranial cytokine storm, which can result in a myriad of CNS complications. There have been reported cases of associated cerebrovascular accidents with large vessel occlusions, cerebral venous sinus thrombosis, posterior reversible encephalopathy syndrome, meningoencephalitis, acute necrotizing encephalopathy, epilepsy, and myasthenia gravis. Peripheral nervous system effects such as hyposmia, hypogeusia, ophthalmoparesis, Guillain-Barré syndrome, and motor peripheral neuropathy have also been reported. In this review, we update the clinical manifestations of COVID-19 concentrating on the neurological associations that have been described, including broad ranges in both central and peripheral nervous systems.

We report a case of classic HSE with early neurological relapse 7 days after onset of acyclovir treatment secondary to cerebral venous thrombosis (CVT). The development of CVT after meningoencephalitis has been described with neurotropic viruses such as HSV, HIV, or enteroviruses and also bacterial or fungal agents. CVT is probably the consequence of the inflammation secondary to these infections. A diagnosis of CVT, although rarely described, should be systematically suspected in patients with HSE who present no or only moderate improvement, or early relapse of symptoms despite adapted acyclovir treatment.

We present the case of a 23 year old with acute onset left hemiparesis and meningeal irritation, associated with recent history of chickenpox 15 days prior. Varicella-IgG and IgM was positive in the CSF and blood along with reduced serum/CSF ratios of VZV immunoglobulins. MRV showed thrombosis (CVT) of superior sagittal, transverse, right sigmoid sinuses with haemorrhagic infarct in right frontoparietal region. Patient responded well to intravenous heparin, Acyclovir and oral anticoagulant therapy., (© Journal of the Association of Physicians of India 2011.)

Japanese encephalitis (JE) is a potentially serious form of viral encephalitis with varied clinicoradiological manifestations. We report the case of a 19-year-old girl admitted with headache, vomiting and altered sensorium in the absence of fever, whose cerebrospinal fluid analysis showed lymphocytic pleocytosis with significant protein content and positive serum IgM JE antibodies. MRI with venography revealed bilateral thalamic haemorrhage and cerebral venous sinus thrombosis. Although thalamic hypodensities are a well-described feature, thalamic haemorrhage and cerebral venous thrombosis are distinctly rare in JE. This report highlights the role of imaging in cases of encephalitis in general and JE in particular, in the early detection of uncommon manifestations that may complicate these diseases., (2015 BMJ Publishing Group Ltd.)

Cytomegalovirus (CMV)-associated thrombosis has been reported many times in the medical literature, and most patients had deep vein thrombosis and/or pulmonary embolism. CMV-associated cerebral sinus vein thrombosis has been reported only twice. We present an immunocompetent patient with CMV-associated cerebral sinus vein thrombosis and no other thrombosis risk factors. This is another example of the pro-thrombotic features of CMV. Physicians should be alert for symptoms and signs of acute CMV infection in patients with thrombosis., (Copyright © 2012 Wiley Periodicals, Inc.)

Varicella zoster virus (VZV) has been known to cause cerebral arterial vasculopathy and an acquired antibody-mediated coagulopathy associated with purpura fulminans and generalized thromboembolism. There are no published reports of cerebral venous sinus thrombosis (CVST) associated with primary VZV infection. We report 2 cases that highlight an unusual presentation of VZV infection: CVST with primary varicella infection. One patient had extensive CVST with coexistent middle cerebral artery involvement. Primary VZV infection can be associated with thrombosis of cerebral arteries and venous sinuses., (Copyright © 2012 National Stroke Association. Published by Elsevier Inc. All rights reserved.)