Serial Changes in Magnetic Resonance Imaging During the Acute Phase of Neurosyphilis With Trigeminal Nerve Palsy

TL;DR

This case study describes the MRI changes in a patient with neurosyphilis presenting with trigeminal nerve palsy and highlights the importance of early diagnosis for effective treatment.

Contribution

The study presents a rare case of neurosyphilis with trigeminal nerve palsy and documents serial MRI changes linked to angiogenic edema from secondary inflammation.

Findings

MRI showed trigeminal nerve swelling followed by pontine hyperintensity with elevated ADC values.

Early diagnosis and treatment led to clinical improvement and MRI resolution.

Abnormal MRI signals suggest angiogenic edema due to secondary inflammation in neurosyphilis.

Abstract

Syphilis cases are increasing worldwide, raising concerns about a potential rise in neurosyphilis. However, neurosyphilis presenting with cranial nerve palsy as the initial symptom remains rare.

A 45-year-old man presented with fever, right-sided headache, and numbness localized to the first branch of the right trigeminal nerve for eight days. Initial brain magnetic resonance imaging (MRI), performed on day eight after symptom onset, revealed enlargement of the right trigeminal nerve. A follow-up MRI on day 15 later demonstrated a hyperintense lesion on the T2-weighted image in the pontine region adjacent to the swollen nerve. The lesion in the pons had an iso-intensity on diffusion-weighted imaging and elevated apparent diffusion coefficient (ADC) values. Cerebrospinal fluid analysis showed an elevated cell count, a positive fluorescent treponemal antibody absorption test, and increased rapid plasma reagin levels, leading to a diagnosis of neurosyphilis. Intravenous penicillin G treatment was initiated on day 15, resulting in an improvement of the patient's fever, headache, and numbness. Additionally, a follow-up brain MRI on day 44 showed reduced trigeminal nerve swelling and resolution of signal changes in the brain parenchyma.

The chronological progression observed on MRI, with signal changes in the adjacent brain parenchyma appearing after trigeminal nerve swelling, and the signal changes in the brain parenchyma accompanied by elevated ADC values, suggest that the abnormal signal changes in neurosyphilis may be linked to angiogenic edema resulting from secondary inflammation. In this case, early diagnosis likely contributed to a favorable therapeutic response. This case further highlights the importance of considering neurosyphilis in the differential diagnosis of patients presenting with trigeminal nerve impairment.

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