ArticleCureus2025
Transient Quadriplegia With Albuminocytologic Dissociation: A Unique Presentation of Suspected Guillain-Barré Syndrome.
Article in Cureus, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
Guillan-Barré syndrome (GBS) is an autoimmune-mediated process that typically causes a progressive ascending paralysis that can lead to persistence of symptoms, permanent paralysis, and even death. While most cases follow a classical course with gradual progression of symptoms until eventual plateau, atypical and rapid onset clinical presentations can complicate differential diagnosis and diagnostic certainty, leading to late diagnosis by clinicians. A 35-year-old male with a history of intravenous (IV) methamphetamine use presented with a sudden onset and complete motor and sensory triplegia of the bilateral legs and left arm upon waking, which resolved shortly after hospital admission. After transfer for neurological referral, his only complaint of distal extremity paresthesia improved daily until hospital day 3, in which he experienced acute quadriplegia with complete sensory and motor loss, prompting stroke protocol activation. Neuroimaging was unremarkable, but cerebrospinal fluid (CSF) analysis revealed elevated protein (87.3 mg/dL) with albuminocytologic dissociation (ACD). The patient was subsequently initiated on intravenous immunoglobulin (IVIg); however, his symptoms had almost completely resolved prior to the initiation of this treatment. He ultimately experienced full recovery without residual deficits. This case highlights a rare and diagnostically challenging presentation of suspected GBS, marked by transient and recurrent neurologic deficits rather than the classic monophasic presentation. Such presentations may be mistaken for functional disorders or overlooked entirely, delaying appropriate neurological evaluation. Despite rapid resolution of symptoms and other possible underlying etiologies in this case, hallmark CSF findings of elevated protein and ACD supported the diagnosis. This underscores the importance of maintaining a high index of suspicion for GBS in patients with unexplained neurological deficits, especially in the context of a recent illness. Early recognition remains critical to guide management and prevent severe complications.
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