Case Presentation: A 49-year-old male with hyperlipidemia presented with two days of progressive numbness in the right lower limb and groin. Several weeks prior, he experienced back pain radiating to the left upper limb, followed by transient left leg numbness that gradually resolved. He denied recent illness, fever, or exposure to environmental toxins, but reported urinary frequency, constipation, and erectile dysfunction. Neurological examination demonstrated diminished sensation in both legs and the left arm, impaired proprioception, and diffusely decreased reflexes. Laboratory evaluation, including vitamin B12, thyroid function, and Lyme serology, was unremarkable. MRI of the cervical, thoracic, and lumbar spine revealed no evidence of cord or root compression. Cerebrospinal fluid analysis showed albuminocytologic dissociation with a normal cell count, consistent with a demyelinating process. In the context of progressive sensory symptoms, areflexia, and autonomic dysfunction with normal imaging and CSF findings, a diagnosis of the pure sensory variant of GBS was favored. The patient was admitted for close monitoring and initiated on intravenous immunoglobulin therapy.Approximately one month after his initial treatment, he developed a partial recurrence of sensory symptoms ascending to the xiphoid level and received a second course of immunoglobulin therapy. At follow up, he demonstrated marked improvement with only subtle residual hyporeflexia and a mild sensory ataxic gait, although painful distal neuropathy persisted. After an additional two months, he presented with worsening bilateral foot pain and new unilateral band like truncal dysesthesias. Given the change in sensory distribution, a thoracic spine MRI was performed and excluded evolving myelopathy. Despite episodic neuropathic flares and medication related side effects, his motor recovery trajectory continued to improve with physical therapy.
Discussion: Guillain-Barré syndrome (GBS), although often viewed as a single entity, encompasses a spectrum of acute immune mediated polyradiculoneuropathies with distinct clinical and electrophysiological features. While the classic presentation is characterized by ascending motor weakness, areflexia, and varying degrees of sensory involvement, several variants exist and differ in their predominant deficits. Among these, acute sensory large fiber axonopathy-ganglionopathy subtype is a rare, pure sensory form of GBS which presents with sensory disturbances, autonomic dysfunction, and predominant ataxia. The combination of an absence of weakness and normal MRI findings often leads to misattribution to spinal or metabolic etiologies. Cerebrospinal fluid analysis and neurophysiologic studies are critical in distinguishing this variant from dorsal column pathology, sensory neuronopathies, and other peripheral neuropathies. Recurrence of sensory symptoms has been reported and may warrant repeat immunotherapy in select cases.
Conclusions: This case emphasizes the need for heightened clinical suspicion in patients with progressive sensory and autonomic symptoms when common causes are excluded. Early identification through cerebrospinal fluid analysis, antibody testing, and neurophysiologic studies is key to improving outcomes and preventing long term sensory deficits.