Lyme neuroborreliosis
General description
Lyme disease is caused by spirochetes, specifically the Borrelia burgdorferi, within the family Spirochaetaceae. This infectious disease is most prevalent in temperate forested regions of Europe, Asia, northeastern and north-central North America, and along the Pacific coast.
Early infection often presents with migratory erythema, a distinctive red papule at the tick bite site that expands outward in a ring-like pattern. Initial symptoms may include myalgia, arthralgia, headache, fever, chills, and general malaise.
As the infection disseminates, patients may experience a range of symptoms such as severe headaches, stiff neck, rashes beyond the bite site, joint pain and swelling, muscle pain, palpitations, dizziness, shortness of breath, nerve pain, numbness and pain in extremities, as well as inflammation of the brain and spinal cord, leading to memory loss.
In advanced stages, months or years post-infection, symptoms such as skin manifestations, arthritis, and spinal encephalitis may intensify, potentially leading to fatal outcomes.
Cranial neuritis
-
Oculomotor nerve
-
Trigeminal nerve
-
Facial nerve
In Lyme disease, the cranial nerves, particularly the facial nerve, trigeminal nerve, and oculomotor nerve, are often bilaterally affected with contrast enhancement observed in imaging studies.
White matter lesion
-
CerebrumFrontal lobeCerebral white matterSubcortical white matter
-
Corpus callosumSplenium
Occasionally, T2WI reveals hyperintensity in the subcortical white matter of the frontal lobe. T2WI hyperintensity of the splenium of the corpus callosum may also be observed.