Paternain A1, Villino R2, Riverol M2, Malmierca P1, Soriano I1, Calvo-Imirizaldu M1, García-Eulate R1, Domínguez PD1Patient
22 years, female
A 22-year-old woman was admitted to the emergency room with sudden right peripheral facial palsy. She also referred to progressive and ascending burning pain in the spine for two weeks. After a trip to the mountains one month before, she had developed an erythematous skin lesion that resolved spontaneously.
MRI of the spine showed a diffuse enhancement of all nerve roots after contrast administration, without a significant thickening (Fig. 1). In the brain, bilateral enhancement of the trigeminal nerves in the posterior cranial fossa (Fig. 2) was also appreciated. In addition, there was also an abnormally high signal intensity in FLAIR surrounding the cerebral aqueduct of Sylvius (Fig. 3).
A lumbar puncture was performed, which showed a positive serology for Lyme disease. The patient was treated with intravenous ceftriaxone for two weeks, followed by oral doxycycline for another 2 weeks, having a complete clinical response afterwards.
Lyme disease is an infection caused by the spirochete Borrelia burgdorferi, which is transmitted by ixodid tick and disseminates to secondary organs, including the central nervous system. Its estimated prevalence is about 100-130 cases per 100,000 people in Europe .
The disease process has three stages that can overlap. In stage 1 (20-30 days after the tick bite), patients have flu-like symptoms and an expanding skin lesion (erythema chronicum migrans). Stage 2 (1-4 months after infection) consists of cardiac and neurologic symptoms. Arthritic and chronic neurologic symptoms appear a few years later in stage 3 . Nervous system affectation occurs in up to 15% of untreated patients . The most common neurological manifestations are painful radiculoneuritis and aseptic meningitis. Other symptoms include meningoencephalitis, encephalomyelitis, peripheral neuropathy, cranial nerve palsies and vasculitis [2-5]. The European Federation of Neurological Societies (EFNS) diagnostic criteria for Neuro-Lyme disease are: Compatible neurological symptoms suggestive without other explanations, cerebrospinal fluid pleocytosis and intrathecal antibody production .
The role of MRI in this disease is, firstly, to rule out other causes that can explain the symptoms, and secondly, to assist the follow-up evaluation . A substantial number of MRI will show no alterations, even with neurological symptoms . The most common radiological manifestations are enhancement of meninges, cranial and spinal nerves, as well as non-specific foci of white matter T2 hyperintensity lesions [2,4,5]. Central or slightly anterior and hyperintense in T2WI cervical spinal cord lesion affecting various segments, can also be seen in the few patients who have myelitis as the primary manifestation [4,5].
In conclusion, Lyme borreliosis should be included in the differential diagnosis if compatible MRI findings (white matter lesions, meningeal and nerve enhancement) are seen in an appropriate clinical context [2,4]. It is usually a challenging diagnosis due to the wide spectrum of neurological symptoms and radiological findings, being mandatory a multidisciplinary approach .
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