Guillain-Barré Syndrome Secondary to Herpes Zoster: A Rare Case Report of Death and Literature Review

The reactivation of the varicella-zoster virus infection is the cause of herpes zoster (HZ) [1‒3]. The virus remains in a latency state in the cranial nerve ganglia or dorsal root following varicella [4]. The reactivation of the varicella-zoster virus causes a characteristic prodromal dermatomal pain and unilateral vesicular rash [5]. Postherpetic neuralgia is the most common and feared complication of shingles, while other complications such as meningoencephalitis, myelitis, cranial nerve palsies, vasculopathy, retinopathy, ulcers, hepatitis are less common [5‒7]. Guillain-Barré syndrome (GBS) is a rare neurological complication after varicella and HZ [8, 9]. Fatal cases are extremely rare. This article describes a patient who developed GBS following HZ finally resulting in death. A review of the literature is presented.

A 68-year-old Chinese male patient, without any significant medical and surgical prior history, suffered from HZ on the right side of the face. There was no drug intake. The HZ lesions had significantly improved since the initiation of an oral antiviral treatment with aciclovir, but pain sensations persisted. During the first 3 days of the induction of symptoms, the early therapeutic intervention with antiviral drugs was not applied to this patient. One month later, the patient was admitted for progressive numbness of the extremities. At the time of admission, scabbing was observed on the right side of the face. Neurological examination revealed muscle weakness in all four limbs. Deep tendon reflexes were absent. Computed tomography and magnetic resonance imaging of the brain showed lacunar infarction. The patient was treated with intravenous 0.5 g/d N-acetyl-L-glutamine and oral 100 mg/d aspirin. The muscle weakness in all extremities worsened every day and he was unable to walk. On the 4th day of admission, the patient was transferred to the intensive care unit due to severe respiratory failure. Cerebrospinal fluid (CSF) analysis showed no cells, 1.99 g/L protein, and a Pandy test (2+). Serum antibody tests were all negative. GBS was diagnosed due to suggestive clinical presentation and the typical CSF albuminocytological dissociation [10, 11]. Therefore, a plasmapheresis was indicated [12]. On the 5th day, invasive mechanical ventilation was used to provide respiration assistance. Airway suctioning was performed because the patient was unable to effectively move phlegm from the respiratory tract. During the ventilator therapy, however, his general symptoms still progressed. Unfortunately, the patient suffered from a sudden high fever on the 18th day and was declared clinically dead due to cardiopulmonary failure on the 19th day.

GBS is a rare dangerous immune-mediated neuropathy that develops after an infection with an annual incidence of 1.3–2 per 100,000 worldwide [13, 14]. Clinical symptoms include numbness, tingling, and weakness caused by the autoimmune destruction of the peripheral nervous system. GBS is characterized by symmetrical progressive weakness of limbs, diminished tendon reflexes, and involvement of cranial nerves [15, 16]. The present case showed the classical clinical features and CSF results, fully consistent with GBS.

GBS is a rare complication of HZ. A review included 39 patients with shingle-induced GBS. Clinical features are presented in Table 1. The 39 patients included 30 males and 9 females, with a median age of 50. HZ was most frequent on the trunk (31.58%), followed by the head and face area (36.84%). Patients between 30 and 60 years (48.72%) were the most common. GBS developed 2 weeks following HZ in 71% of the cases. The most common clinical signs were decreased tendon reflexes and numbness of the extremities. Most patients had a high CSF protein concentration (80.56%) with a normal cellular count (89.66%). Notably, after 1 year, 2 patients (10.53%) died; both were male patients with HZ of the cephalic extremity, similar to the present case. There was no association between GBS and the anatomical site of HZ. GBS might occur rather immediately following HZ or have a late appearance.

In conclusion, in patients presenting GBS symptoms like decreased tendon reflexes and numbness in the extremities, HZ should be searched for in the anamnesis and should be tested immediately for CSF and serum antibodies. A higher risk of death seems to be present in male patients aged 30–60 with head and facial HZ with GBS.

The CARE Checklist has been completed by the authors for this case report, attached as online supplementary material (for all online suppl. material, see https://doi.org/10.1159/000544954).

The authors would like to thank the patient and his spouse who participated in this study.

The present study was reviewed by the Medical Ethics Committee of the Affiliated Hospital of Jining Medical University (Jining, China; Approval No. 2022C261). Written informed consent was obtained from the patient’s next of kin for publication of the details of their medical case and any accompanying images.

The authors declared that they had no competing interests.

This research was funded by Research and Development Fund of Jining (2023YXNS064).

Jingyu Wang was responsible for writing the manuscript. Bin Lu was responsible for the subsequent revision of the manuscript. Xinyi Hou was responsible for collecting case data. Jin Zhang and Bo Ren were responsible for searching the literature and making forms. All authors contributed to the results of the study, accept public responsibility for the corresponding parts of the study, agree to take responsibility for all aspects of the study to ensure the accuracy and completeness of this thesis, and have read and approved the final manuscript.

The data that support the findings of this study are not publicly available due to privacy reasons but are available from the corresponding author upon reasonable request.