Title : Diagnostic challenge in post-influenza acute flaccid paralysis in a 48-year-old female: GBS vs viral myositis
Abstract:
Introduction: Acute flaccid paralysis (AFP) is characterised by the rapid onset of flaccid limb weakness and encompasses a broad range of etiologies. In adults, GBS – an immune-mediated polyradiculoneuropathy often triggered by infection – is the most common cause of AFP. GBS typically presents as an ascending paralysis and can be predominantly motor, with minimal sensory involvement. However, post-viral myositis is another vital differential to consider. Viral myositis is typically seen in children, but it can also occur in adults, usually following an influenza infection, and manifest as acute muscle weakness accompanied by myalgia. This clinical overlap between GBS and viral myositis in a post-influenza setting poses a diagnostic challenge.
Case Summary: A 48-year-old woman developed acute, symmetric flaccid paralysis of both legs shortly after an influenza A infection. The weakness was severe enough to render her unable to walk. Notably, she had no sensory loss in the lower limbs and no autonomic dysfunction. Deep tendon reflexes were markedly diminished at the knees and ankles. Laboratory evaluation showed a mild elevation of serum CK, and MRI of the spine was normal (no evidence of myelitis or cord lesion). Nerve conduction studies revealed demyelinating polyneuropathy affecting the lower limbs. Cerebrospinal fluid analysis demonstrated elevated protein with normal cell count (albuminocytologic dissociation). These findings were consistent with acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the classic form of GBS.
Diagnostic Challenge: This case highlights how an acute post-infectious paralysis can blur the line between neuropathic and myopathic etiologies. The patient’s isolated motor deficits without sensory or autonomic involvement were atypical for classic GBS but compatible with a motor variant of GBS as well as a viral myositis. The mildly elevated CK initially suggested a muscle pathology; however, GBS is known to sometimes present with mild CK elevations due to denervation injury. Furthermore, the post-influenza timing was consistent with either diagnosis. Close multidisciplinary evaluation and targeted testing were crucial. Ultimately, the demyelinating features on NCS and the hallmark albuminocytologic dissociation on CSF confirmed GBS as the correct diagnosis, with the CK rise interpreted as secondary to neuropathic muscle damage.
Outcome and Conclusion: The patient was treated with intravenous immunoglobulin (IVIG) and empiric corticosteroids, and she made a full recovery. This case emphasises the need for a comprehensive diagnostic approach to atypical AFP presentations. Even as GBS remains the prime suspect in adults, clinicians should keep viral myositis in mind as a rare post-influenza mimic of GBS. Early recognition and appropriate therapy in such cases are critical and can lead to excellent outcomes, as illustrated by this patient’s recovery.
