# A Rare Presentation of Guillain-Barré Syndrome: A Case Report and Literature Review

**Authors:** Ivonne De la Hoz, Grayson White, Mohamad Sharbatji

PMC · DOI: 10.7759/cureus.95310 · Cureus · 2025-10-24

## TL;DR

A 36-year-old man presented with a rare and complex form of Guillain-Barré Syndrome, showing unique symptoms and a challenging diagnostic journey.

## Contribution

This case report highlights a rare clinical presentation of GBS combining features of classic and variant forms, emphasizing diagnostic challenges.

## Key findings

- The patient exhibited ataxia, facial diplegia, paresthesia, and ascending weakness, indicating a complex GBS variant.
- Early treatment with IVIG led to stabilization and gradual improvement without respiratory compromise.
- The case underscores the importance of prompt diagnosis and monitoring in managing life-threatening GBS.

## Abstract

Guillain-Barré syndrome (GBS) is a term that includes a group of autoimmune-mediated peripheral neuropathies affecting varying nerve distributions, typically characterized by an acute onset of areflexic paralysis with albumino-cytologic dissociation. Given the wide range of subtypes and clinical presentations, GBS can be difficult to diagnose; however, the life-threatening nature of the disorder makes prompt diagnosis and treatment a top priority.

A 36-year-old athletic young male with a history of recent upper respiratory infection presented to the emergency department complaining of difficulty walking. He initially developed numbness in his genital and perianal area, followed by tingling in his hands and feet, and then difficulty walking due to unsteadiness, which ultimately prompted him to seek medical attention. His blood pressure was 142/85 mmHg, and his heart rate was 58 bpm. The initial physical exam revealed hyporeflexia and ataxic gait, while no deficits were observed in the cranial nerves, and the motor strength was intact in all four extremities. The following day, right-sided facial paralysis and proximal lower extremity weakness (able to move against only minimal resistance) were noted. Due to a strong suspicion of GBS, a five-day course of intravenous immunoglobulin (IVIG) was started. By the following day, the patient showed areflexia with worsening proximal lower extremity weakness and proximal upper extremity weakness. Cerebrospinal fluid (CSF) analysis showed albumin-cytologic dissociation. The total protein was elevated while the cell count was normal, findings consistent with GBS. By hospital day four, facial diplegia was evident, though notably, without any oculomotor involvement. In addition, he had developed dysarthria and dysphagia. The weakness in the lower extremities continued to progress, ultimately restricting movement only to instances when gravity was counterbalanced. Fortunately, the patient did not exhibit any signs of respiratory compromise, and both vital capacity (VC) and negative inspiratory force (NIF), which were carefully monitored, remained within normal limits. Upon completion of the IVIG course, the patient did not show any new neurologic deficits; instead started to show slow improvement in motor function. He continued to engage in intensive physical and occupational therapy and was eventually discharged to an inpatient rehab facility, where gradual improvement continued.

This patient exhibited a unique constellation of symptoms, combining features of classic GBS and rarer variants, posing a true diagnostic challenge. This case was marked by ataxia, facial diplegia, and paresthesia, in addition to the hallmark ascending weakness, highlighting the clinical complexity. GBS is a life-threatening condition; therefore, early recognition is crucial. Patients need close cardiac and respiratory monitoring as they are at risk for autonomic dysfunction and respiratory compromise. Treatment options include plasmapheresis and IVIG, and both therapies are equivalent and should be started rapidly.

## Linked entities

- **Diseases:** Guillain-Barré Syndrome (MONDO:0016218)

## Full-text entities

- **Genes:** ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** areflexia (MESH:D000071699), autonomic dysfunction (MESH:D001342), neurologic deficits (MESH:D009461), facial paralysis (MESH:D005158), dysphagia (MESH:D003680), respiratory compromise (MESH:D012131), autoimmune-mediated peripheral neuropathies (MESH:D010523), areflexic paralysis (MESH:D010243), hyporeflexia (MESH:D012021), respiratory infection (MESH:D012141), proximal upper extremity weakness (MESH:D018908), paresthesia (MESH:D010292), facial diplegia (MESH:C531747), GBS (MESH:D020275), ataxia (MESH:D001259), dysarthria (MESH:D004401), ataxic (MESH:D001039), proximal lower extremity weakness (MESH:D020335), numbness (MESH:D006987)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

12 references — full list in the complete paper: https://tomesphere.com/paper/PMC12640570/full.md

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Source: https://tomesphere.com/paper/PMC12640570