ABSTRACT
BACKGROUND: A growing number of Guillain-Barré syndrome (GBS) and Miller Fisher Syndrome (MFS) cases following severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection are reported. Nevertheless, this association is still debated, and pathophysiology remains unclear. METHODS: Between April and December 2020, in three hospitals located in Brussels, Belgium, we examined four patients with GBS following SARS-CoV-2 infection. RESULTS: Neurological onset occurred 3 weeks after SARS-CoV-2 symptoms in all patients. Three patients presented with acute inflammatory demyelinating polyneuropathy (AIDP) and had negative anti-ganglioside testing: two suffered from a severe SARS-CoV-2 infection and had good clinical outcome after intravenous immunoglobulin (IVIG) treatment; one with mild SARS-CoV-2 infection had spontaneously favorable evolution without treatment. The fourth patient had critical SARS-CoV-2 infection and presented acute motor and sensory axonal neuropathy (AMSAN) with clinical features highly suggestive of brainstem involvement, as well as positive anti-ganglioside antibodies (anti-GD1b IgG) and had partial improvement after IVIG. CONCLUSIONS: We report four cases of SARS-CoV-2-associated GBS. The interval of 3 weeks between SARS-CoV-2 symptoms and neurological onset, the clinical improvement after IVIG administration, and the presence of positive anti-ganglioside antibodies in one patient further support the hypothesis of an immune-mediated post-infectious process. Systematic extensive antibody testing might help for a better understanding of physiopathology.
Subject(s)
COVID-19 , Guillain-Barre Syndrome , Miller Fisher Syndrome , COVID-19/complications , Gangliosides , Guillain-Barre Syndrome/complications , Guillain-Barre Syndrome/etiology , Humans , Immunoglobulins, Intravenous/therapeutic use , Miller Fisher Syndrome/complications , Miller Fisher Syndrome/drug therapy , SARS-CoV-2ABSTRACT
Among patients with multiple sclerosis (MS), the impairment of exercise tolerance is closely related to disability. Maximal oxygen uptake (VO2max ) is the gold standard to assess exercise tolerance in healthy subjects (HS). Among patients with MS, the accuracy of VO2max measurement is often impaired because the patients are unable to reach the maximal exercise intensity due to interdependent factors linked to the disease (such as pathological fatigue, pain, lack of exercise habit, and lack of mobility). This study assesses the accuracy of simplified indices for assessing exercise tolerance, which are more suitable in patients with MS. They are simple in the way they are either measurable during submaximal exercise (oxygen uptake efficiency slopes (OUES), physical working capacity at 75% of maximal heart rate (PWC75% ), oxygen consumption at a respiratory exchange ratio of 1 (VO2 @RER1)) or not based on gas exchange analysis (peak work rate (PWR)-based predictive equation and PWC75% ). All indices were significantly lower in the MS group compared to the HS group (P < .001). OUES appeared highly correlated (r > .70, P < .001) with VO2peak , in both groups, without difference between groups. PWR-based prediction of VO2peak showed a standard error of the estimate of 315 mL min-1 in HS and 176 mL min-1 in MS. PWC75% did not correlate to VO2peak in neither group. These findings suggest an impairment of exercise tolerance functions in mildly disabled persons with MS, independently from other factors. Submaximal indices involving gas exchange analysis or peakWR-based estimation of VO2peak are usable to accurately assess exercise tolerance.
