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A 26-year-old Brazilian man, previously well, developed acute-onset flaccid tetraparesis. He had retired to bed at 11 p.m. without neurological symptoms and had awoken at midnight with weakness in all four limbs and unable to walk. He took no medications, drugs (including nitrous oxide) or alcohol and had no history of intense physical exertion, fever, recent vaccination, recent trauma and loss of sphincter control. The previous night, he had eaten a meal with a higher carbohydrate content than usual. Four months before, he had experienced one episode of sudden lower limb weakness lasting for minutes. He reported persistent tremors in both his hands and feet, along with unintentional weight loss of 45 kg over 6 months. There was no relevant family history.
On examination, he was alert and orientated. Pupils were equal, rounded and reactive to light. Extraocular movements were normal, with no ptosis or fatiguability. Visual fields were intact, and his face was symmetrical. There was weakness in both upper (proximal Medical Research Council grade 2/5 and distal 4/5) and lower limbs (proximal 3/5 and distal 4/5). All four limbs were hypotonic. Deep tendon reflexes were normal and symmetrical. Coordination and sensory systems were normal. He had a tachycardia with a regular rhythm and normal blood pressure.
Question: what are the differential diagnoses for this patient’s flaccid paralysis?
This patient presented an acute-onset symmetrical tetraparesis with hypotonia and normal deep tendon reflexes: an acute flaccid paralysis. Differential diagnoses include myopathies, neuromuscular transmission disorders, neuropathies and acute myelopathies.1
The most common global cause of acquired flaccid paralysis is Guillain-Barré syndrome, a polyradiculoneuropathy. Patients present acute, symmetrical paralysis, usually ascending and …
Contributors All authors contributed significantly to the conception, design, analysis and interpretation of the case report. Each author has reviewed and approved the final version of the manuscript. CRDB contributed to the conception and design of the case report, acquisition of data, drafting of the manuscript and critical revision of the intellectual content. FDDC participated in the acquisition of clinical data, contributed to the drafting and critical revision of the manuscript and provided important intellectual content. LM provided substantial contributions to the analysis and interpretation of pathological findings, critically reviewed and revised the manuscript and approved the final version for submission. MBDC, MdCT and RKS contributed to the literature review and provided critical feedback on the manuscript. RG supervised the entire process, provided guidance in the design and execution of the case report, critically reviewed and revised the manuscript and gave final approval for submission.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed by Arani Nitkunan, London, UK.