From nerve to brainstem: isolated cranial neuritis as a sentinel sign of listeria rhombencephalitis case report and focused narrative review

We report a case of rhombencephalitis caused by Listeria monocytogenes (LM), initially presenting as additive cranial multineuritis without overt signs of systemic infection. We also conducted a focused review of the literature and identified 26 similar cases reported between 1979 and 2026. LM can involve the central nervous system either as meningitis or as rhombencephalitis, which differ substantially in clinical presentation. In particular, some cases of rhombencephalitis may present with a non-diagnostic lumbar puncture and lack systemic features such as fever or elevated inflammatory markers, potentially leading to misdiagnosis as immune-mediated disorders. In this context, delayed diagnosis and the use of immunosuppressive therapy without concurrent antibiotic coverage may contribute to poor outcomes. Increasing clinical and radiological observations, supported by experimental models and neuropathological studies in humans and animals, suggest that retrograde intra-axonal migration along cranial nerves may represent one potential mechanism by which LM reaches the brainstem in selected cases of rhombencephalitis, alongside the established pathway of hematogenous dissemination. This hypothesis may help explain observations such as the frequent asymmetry of neurological deficits and the inconsistent presence of fever and systemic inflammatory markers in some patients. Postmortem findings in both human and animal studies have described a caudo-rostral distribution of brainstem involvement, with microabscesses affecting cranial nerve nuclei and tracts, supporting the biological plausibility of neural dissemination. Experimental and veterinary studies have also raised the possibility of oral mucosal entry, although the relevance of this mechanism in human disease remains uncertain. These findings support the need to consider LM rhombencephalitis in selected patients presenting with progressive cranial neuritis, particularly when accompanied by brainstem symptoms or radiologic abnormalities, even in the absence of classical signs of infection. However, these observations should be interpreted with caution, and the proposed mechanisms remain hypothesis-generating, warranting further validation in prospective studies.