Volume 32, Issue 1 (3-2025)                   RJMS 2025, 32(1): 1-8 | Back to browse issues page

Research code: 1404-3-70-35268
Ethics code: IR.IUMS.REC.1404.722
Clinical trials code: 1


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Hadipour K, Vafaee shahi M. Dental Infection as a Trigger for Guillain-Barré Syndrome in a 7-Year-Old Girl: An Educational Case. RJMS 2025; 32 (1) :1-8
URL: http://rjms.iums.ac.ir/article-1-9192-en.html
1- Pediatrician, Assistant Professor of pediatrics, Firoozabadi Hospital, Iran University of Medical Sciences, Tehran, Iran
2- Pediatric Neurology Subspecialist, Associate Professor, Department of Pediatrics, Hazrat Ali Asghar Hospital, Iran University of Medical Sciences, Tehran, Iran , Dr.vafaeeshahi@yahoo.com
Abstract:   (523 Views)
Background & Aims: Guillain-Barré Syndrome (GBS) is the most common cause of acute flaccid paralysis in children worldwide. While respiratory and gastrointestinal infections are well-established triggers, atypical infectious sources remain underrecognized. Additionally, the interplay between psychological stress and autoimmune demyelination has received limited attention in pediatric populations. This case report presents a rare instance of GBS triggered by a dental infection in a 7-year-old girl, emphasizing the diagnostic challenges posed by confounding psychiatric manifestations and the importance of a multidisciplinary approach.
Case Presentation: A previously healthy 7-year-old girl presented to the emergency department with non-specific symptoms including headache, generalized weakness, lethargy, and myalgia. She had a history of tooth extraction one month prior due to dental pain. Initially suspected of having a dental abscess, she received antibiotics and was discharged. However, four days later, she returned with worsening symptoms: inability to walk, dysarthria, neck pain, and parental-reported episodes of "staring spells." Vital signs showed tachycardia (HR 140 bpm), while inflammatory markers were normal (CRP <1, ESR=7). Initial laboratory findings revealed neutropenia (ANC ≈ 1275). CT of the neck reported a small suprasternal soft tissue density, which was not confirmed on subsequent ultrasonography; only non-specific reactive lymph nodes were noted. MRI of the brain and spine was unremarkable. Psychiatric consultation diagnosed Adjustment Disorder with Anxiety, and olanzapine was initiated. The diagnostic breakthrough came from EMG/NCV studies, which revealed acute demyelinating sensorimotor polyneuropathy, confirming the diagnosis of GBS. Prior to this, empirical antibiotic therapy had been continued for a presumed deep dental infection. Following the EMG/NCV results, management was redirected toward GBS-specific treatment.
Discussion: This case highlights several important clinical and pathophysiological points. First, it demonstrates that dental infections—although uncommon—can serve as effective triggers for GBS, likely through molecular mimicry between bacterial antigens and myelin gangliosides. This expands the spectrum of infectious agents that clinicians should consider when evaluating pediatric patients with acute weakness. Second, the patient had a history of severe psychological stress preceding symptom onset, which may have exacerbated disease severity through hypothalamic-pituitary-adrenal (HPA) axis activation and cortisol-mediated immune dysregulation. Third, the coexistence of an Adjustment Disorder with Anxiety illustrates that psychiatric symptoms can act both as a trigger for, and a consequence of, autoimmune neurological disease. This overlapping presentation created significant diagnostic confusion, reinforcing the need for thorough neurological evaluation—including EMG/NCV—even when psychiatric or confounding radiological findings are present. The absence of ankle reflexes (areflexia) proved to be a crucial clinical clue in guiding the diagnosis. The patient showed gradual improvement during follow-up, with eventual return of deep tendon reflexes, indicating progressive neurological recovery.
Conclusion: This report serves as an educational reminder that GBS should remain on the differential diagnosis for any child presenting with acute progressive weakness, regardless of whether the antecedent event is a common respiratory infection or an atypical source such as a dental infection. Moreover, the role of psychological stress as a disease-modifying factor warrants further investigation. The case underscores the importance of multidisciplinary collaboration—involving infectious disease specialists, neurologists, and psychiatrists—in managing complex pediatric cases where physical and psychiatric symptoms coexist.
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Type of Study: case report | Subject: Pediatric Neurology

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