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1.
Pan Afr Med J ; 47: 46, 2024.
Article in English | MEDLINE | ID: mdl-38681104

ABSTRACT

COVID-19 vaccination side effects have been increasingly reported, including new-onset autoimmune diseases such as chronic arthritis, thrombocytopenia, Guillain-Barré syndrome (GBS), and more recently chronic inflammatory demyelinating polyneuropathies (CIDP). Molecular mimicry and vaccine adjuvants appear to be important contributors to immune-mediated neuropathies. However, whether the link between the COVID-19 vaccine and these autoimmune disorders is coincidental or causal remains uncertain. We describe the ever-reported case of acute-onset CIDP following the Oxford/AstraZeneca vaccine in Tunisia. The patient is a 41-year-old man who presented with acute, worsening weakness of the four limbs. The symptoms appeared 15 days after his first dose of the AstraZeneca vaccine. The diagnosis of GBS was initially confirmed according to the clinical features, the albumino-cytological dissociation in the cerebrospinal fluid (CSF), and the electroneuromyography (ENMG) findings. Serum workup for all known infections associated with immune-mediated neuropathy was negative. The patient was treated with plasma exchange without initial improvement followed by aggravation of the symptomatology after an interval of four and a half months. Control ENMG showed signs of CIDP meeting the European Academy of Neurology/Peripheral Nerve Society (EAN/PNS) criteria of 2021. The patient was treated with maintenance intravenous immunoglobulin and oral corticosteroids. Neurological examination 3 months after discharge showed partial improvement. Worldwide, cases of demyelinating polyneuropathies post-COVID-19 vaccination are increasingly reported. The acute onset of CIDP might lead to a misdiagnosis of GBS. Awareness of this complication and distinction from GBS enables early relay with maintenance treatment to prevent relapses and severe complications. Post-COVID neuropathies are found to be more frequently linked to the AstraZeneca vaccine, however, temporal association does not confirm causal association.


Subject(s)
COVID-19 Vaccines , Polyradiculoneuropathy, Chronic Inflammatory Demyelinating , Adult , Humans , Male , ChAdOx1 nCoV-19 , COVID-19/prevention & control , COVID-19 Vaccines/adverse effects , Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/chemically induced , Tunisia
3.
Neurol Sci ; 43(2): 755-761, 2022 Feb.
Article in English | MEDLINE | ID: mdl-34796417

ABSTRACT

BACKGROUND: Since the SARS-CoV-2 pandemic has started in December 2019, millions of people have been infected all over the world. Vaccination is the most efficient tool to end this pandemic, but vaccine surveillance is necessary to identify side effects. Some studies have shown that neurological complications after COVID-19 vaccination are rare and dominated by demyelinating disease. CASE PRESENTATION: We present a case of a 67-year-old man who presented 7 days following his first dose of Pfizer-BioNTech COVID-19 vaccine a rapidly progressive ascending muscle weakness. The diagnosis of Guillain-Barré syndrome (GBS) was confirmed according to the clinical features, the albumino-cytological dissociation in the cerebrospinal fluid, and the electroneuromyography findings. The workup for all known infections associated with immune-mediated GBS was negative. The patient received treatment with intravenous immunoglobulin. Neurological examination 1 month after discharge showed full recovery and he regained his baseline functional status. CONCLUSIONS: As far as we know, this is the first reported case in Tunisia. Although extremely rare, neurologists should remain vigilant for acute inflammatory demyelinating polyradiculoneuropathy after COVID-19 vaccination.


Subject(s)
COVID-19 , Guillain-Barre Syndrome , Aged , BNT162 Vaccine , COVID-19 Vaccines , Guillain-Barre Syndrome/chemically induced , Humans , Male , SARS-CoV-2
4.
J Spinal Cord Med ; 44(2): 334-338, 2021 03.
Article in English | MEDLINE | ID: mdl-31013469

ABSTRACT

CONTEXT: After primary infection, varicella zoster virus (VZV) becomes latent in ganglionic neurons. If immunity declines, VZV is reactivated and can spread to the dermatome depending from this ganglion and in some cases to the spinal cord. Myelopathy is rare and may develop in the absence of skin rash making the diagnosis very difficult. FINDINGS: From 1994 to 2014, we collected five observations of clinically and laboratory confirmed zoster myelopathy. The age of our patients ranged from 14 to 78. They did not have any significant past medical history. Four patients had a history of radicular rash. After 3 weeks (4-45 days), patients presented paraparesis, sensory loss, and sphincter dysfunction. Cerebrospinal fluid (CSF) analysis revealed an elevated protein level (5/5cases) and pleocytosis (2/5 cases). Spinal cord magnetic resonance imaging (MRI) demonstrated T2 hyper intense lesions with swelling and contrast enhancement. The diagnosis was supported by laboratory evidence, including the detection of VZV antibodies in the CSF. All patients received intravenous acyclovir and two patients received IV methylprednisolone. A marked improvement was observed in most of the patients within 2 months. CONCLUSION /CLINICAL RELEVANCE: Based on our patients and on previous reports, we highlight the possibility of the occurrence of VZV myelopathy in immunocompetent subjects. The diagnosis must be evoked even in the absence of typical skin lesions. In this case, spinal cord MRI and virological tests are useful tools for the diagnosis. We also emphasize on the importance of accurate diagnosis to enable the specific treatment and ameliorate the outcome.


Subject(s)
Herpes Zoster , Spinal Cord Diseases , Spinal Cord Injuries , Acyclovir , Herpes Zoster/complications , Herpes Zoster/diagnosis , Herpes Zoster/drug therapy , Herpesvirus 3, Human , Humans , Spinal Cord Diseases/diagnosis
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