COVID-19-Associated Guillain-Barre Syndrome: Atypical Para-infectious Profile, Symptom Overlap, and Increased Risk of Severe Neurological Complications.


The concurrence of COVID-19 with Guillain-Barre syndrome (GBS) can increase the likelihood of neuromuscular respiratory failure, autonomic dysfunction, and other life-threatening symptoms. Currently, very little is known about the underlying mechanisms, clinical course, and prognostic implications of comorbid COVID-19 in patients with GBS. We reviewed COVID-19-associated GBS case reports published since the outbreak of the pandemic, with a database search up to August 2020, including a manual search of the reference lists for additional relevant cases. Fifty-one (51) case reports of COVID-19 patients (aged 23-84 years) diagnosed with GBS in 11 different countries were included in this review. The results revealed atypical manifestations of GBS, including para-infectious profiles and onset of GBS without antecedent COVID-19 symptoms. Although all tested patients had signs of neuroinflammation, none had SARS-CoV-2 in the cerebrospinal fluid (CSF), and only four (4) patients had antiganglioside antibodies. The majority had a 1- to 10-day time interval between the onset of COVID-19 and GBS symptoms, and many had a poor outcome, with 20 out of the 51 (39.2%) requiring mechanical ventilation, and two deaths within 12 to 24 h. The atypical manifestations of COVID-19-associated GBS, especially the para-infectious profile and short time interval between the onset of the COVID-19 and GBS symptoms, increase the likelihood of symptom overlap, which can complicate the treatment and result in worsened disease progression and/or higher mortality rates. Inclusion of a neurological assessment during diagnosis of COVID-19 might facilitate timely identification and effective management of the GBS symptoms and improve treatment outcome.





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Publication Info

Kajumba, Mayanja M, Brad J Kolls, Deborah C Koltai, Mark Kaddumukasa, Martin Kaddumukasa and Daniel T Laskowitz (2020). COVID-19-Associated Guillain-Barre Syndrome: Atypical Para-infectious Profile, Symptom Overlap, and Increased Risk of Severe Neurological Complications. SN comprehensive clinical medicine, 2(12). pp. 1–13. 10.1007/s42399-020-00646-w Retrieved from

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Bradley Jason Kolls

Associate Professor of Neurology

As a neurointensivist, I am interested in improving our ability to monitor brain function and impact of therapy on our patients in the critical care setting. To this end I am developing new approaches to patient monitoring that will integrate patient physiologic monitoring with brain activity recorded by electroencephalography (EEG). On the basic science side I am interested in the central nervous system's response to injury. Although much attention has been focused on closed head injury as of late, stroke and brain hemorrhage are just as common in the civilian population and pose many of the same clinical challenges as traumatic brain injury. Using mouse models of clinically relevant brain injury, including models of stroke, subarachnoid hemorrhage, lobar hemorrhage, closed head injury and penetrating brain injury, we can explore the key molecular events that lead to edema, secondary brain injury, hyperexcitability and epilepsy, and other sequelae which contribute to poor patient recovery, and significant morbidity following brain injury. By investigating the underlying mechanisms that contribute to these adaptive changes using electrophysiology and molecular biology approaches we can then find ways to prevent them from becoming maladaptive and develop new therapies for our patients with head injuries.


Deborah Koltai

Associate Professor in Psychiatry and Behavioral Sciences
  1. Investigation of factors related to care of epilepsy patients in Uganda, Africa to inform capacity building and infrastructure strengthening efforts. Studies have involved a pursuit of understanding the cultural context and its impact on health care delivery and utilization.

    2) Development and psychometric validation of neuropsychological and behavioral instruments.

    3) The effect of psychological interventions on the abilities and adjustment of dementia patients and those at-risk for developing neurodegenerative illnesses such as Alzheimer's disease. Interventions include modified cognitive (mnemonic; organizational) strategies, and traditional psychotherapy (dynamic and behavioral). 

Daniel Todd Laskowitz

Professor of Neurology

Our laboratory uses molecular biology, cell culture, and animal modeling techniques to examine the CNS response to acute injury. In particular, our laboratory examines the role of microglial activation and the endogenous CNS inflammatory response in exacerbating secondary injury following acute brain insult. Much of the in vitro work in this laboratory is dedicated to elucidating cellular responses to injury with the ultimate goal of exploring new therapeutic interventions in the clinical setting of stroke, intracranial hemorrhage, and closed head injury.

In conjunction with the Multidisciplinary Neuroprotection Laboratories, we also focus on clinically relevant small animal models of acute CNS injury. For example, we have recently characterized murine models of closed head injury, subarachnoid hemorrhage, intracranial hemorrhage and perinatal hypoxia-ischemia, in addition to the standard rodent models of focal stroke and transient forebrain ischemia. Recently we have adapted several of these models from the rat to the mouse to take advantage of murine transgenic technology. The objective of these studies are two-fold: to gain better insight into the cellular responses and pathophysiology of acute brain injury, and to test novel therapeutic strategies for clinical translation. In both cell culture systems and animal models, our primary focus is on examining the role of oxidative stress and inflammatory mechanism in mediating brain injury following acute brain insult, and examining the neuroprotective effects of endogenous apolipoprotein E in the injured mammalian central nervous system.

Our laboratory is committed to translational research, and has several active clinical research protocols, which are designed to bring the research performed in the Multidisciplinary Research Laboratories to the clinical arena. These protocols are centered around patients following stroke and acute brain injury, and are primarily based out of the Emergency Room and Neurocritical Care Unit. For example, we are currently examining the role of inflammatory mediators for use as a point-of-care diagnostic marker following stroke, intracranial hemorrhage, and closed head injury. We have recently translated a novel apoE mimetic from the preclinical setting to a multi center Phase 2 trial evaluating efficacy in intracranial hemorrhage. We are also examining the functional role of different polymorphisms of of inflammatory cytokines in the setting of acute brain injury and neurological dysfunction following cardiopulmonary bypass.

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