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Background <p>Polyneuritis cranialis (PNC), a rare variant of Guillain-Barré syndrome (GBS), is usually characterized by ocular and pharyngeal weakness without obvious numbness or weakness of the limbs or ataxia. Horner’s syndrome is extremely rare in patients with PNC. Here, we describe a case of GBS presenting with acute PNC and unilateral Horner syndrome.</p> Case presentation <p>A 53-year-old male presented with headache, abducent paresis, peripheral-type facial palsy, bulbar type dysarthria, decreased gag reflex and tongue palsy. Neurological examination showed Cranial Nerve V, VI, VII, IX, X and XII were affected, and Horner’s syndrome was observed. Cerebrospinal fluid analysis showed albuminocytologic dissociation. Sensorimotor conduction velocity and needle electromyography of limbs were normal. Magnetic resonance imaging of brain was normal. Finally, the patient was diagnosed as PNC combined with Horner’s syndrome. The patient received plasma exchange and intravenous immunoglobulin, which relieved the symptoms rapidly.</p> Conclusion <p>GBS presenting only as Horner syndrome and PNC is a challenge for etiological diagnosis. Clinicians need to know enough to distinguish GBS and its variants from other potential similar diseases.</p>

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Polyneuritis cranialis combined with Horner’s syndrome: a rare variant of Guillain Barré syndrome

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月16日

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  • Xiangtao Nie,
  • Wei He,
  • Wenjing Qi,
  • Yongbo Ma,
  • Geke Zhu,
  • Lei Hao,
  • Xiuming Guo

摘要

Background

Polyneuritis cranialis (PNC), a rare variant of Guillain-Barré syndrome (GBS), is usually characterized by ocular and pharyngeal weakness without obvious numbness or weakness of the limbs or ataxia. Horner’s syndrome is extremely rare in patients with PNC. Here, we describe a case of GBS presenting with acute PNC and unilateral Horner syndrome.

Case presentation

A 53-year-old male presented with headache, abducent paresis, peripheral-type facial palsy, bulbar type dysarthria, decreased gag reflex and tongue palsy. Neurological examination showed Cranial Nerve V, VI, VII, IX, X and XII were affected, and Horner’s syndrome was observed. Cerebrospinal fluid analysis showed albuminocytologic dissociation. Sensorimotor conduction velocity and needle electromyography of limbs were normal. Magnetic resonance imaging of brain was normal. Finally, the patient was diagnosed as PNC combined with Horner’s syndrome. The patient received plasma exchange and intravenous immunoglobulin, which relieved the symptoms rapidly.

Conclusion

GBS presenting only as Horner syndrome and PNC is a challenge for etiological diagnosis. Clinicians need to know enough to distinguish GBS and its variants from other potential similar diseases.