Lyme disease is an infection transmitted by ticks carrying the bacterium Borrelia burgdorferi. While often known for the characteristic skin rash and joint pain, the infection can affect various organ systems, including the nervous system. This complication, known as Neuroborreliosis, can cause significant neurological symptoms that often prompt a magnetic resonance imaging (MRI) scan of the brain. Understanding the mechanisms of the infection and the nature of these imaging findings addresses the question of whether Lyme disease can cause visible brain lesions on an MRI.
Neuroborreliosis: The Link Between Lyme and the Central Nervous System
The neurological manifestation of Lyme disease is termed Neuroborreliosis (LNB), which occurs when the Borrelia spirochete invades the peripheral or central nervous system. The bacteria must first cross the blood-brain barrier (BBB), triggering an inflammatory response within the brain and spinal cord tissue, known as neuroinflammation. This process can lead to symptoms like lymphocytic meningitis, cranial neuritis (often facial nerve palsy), or encephalopathy, such as cognitive difficulties. These symptoms typically lead a physician to order a brain MRI to look for structural causes.
Understanding Brain Lesions on MRI
When a brain MRI is performed, a “lesion” refers to any area of abnormal tissue appearance on the scan. The lesions most frequently observed in suspected Neuroborreliosis are small, bright spots known as white matter hyperintensities, best visualized on T2-weighted and Fluid-Attenuated Inversion Recovery (FLAIR) MRI sequences. These hyperintensities represent non-specific foci of inflammation, demyelination, or microvascular changes within the white matter.
These lesions are often located in the subcortical and periventricular regions. While they can be a feature of Neuroborreliosis, these white matter lesions are highly non-specific and are commonly seen in many other conditions, including migraine, aging, and other inflammatory or vascular diseases. Their presence alone is insufficient for a definitive diagnosis of LNB.
In rare cases, LNB can cause more distinct findings, such as contrast enhancement of cranial nerves, meningitis, or a stroke-like appearance due to cerebral vasculitis. The most common white matter lesions are often indistinguishable from those found in a healthy population. Furthermore, the brain MRI may be completely normal in confirmed cases of Neuroborreliosis, especially in early stages.
Diagnosis and Clinical Significance
A definitive diagnosis of Neuroborreliosis requires clinical symptoms, a history of possible tick exposure, and specific laboratory evidence. MRI findings, including the presence or absence of lesions, primarily serve to rule out other neurological conditions, such as multiple sclerosis or brain tumors, in the differential diagnosis. The lesions only gain clinical significance when they align with the patient’s specific neurological presentation and confirmatory testing.
The most specific laboratory method for confirming LNB is the analysis of cerebrospinal fluid (CSF), which is obtained via a lumbar puncture, or spinal tap. This fluid is tested for an inflammatory change known as pleocytosis (an elevated white blood cell count) and to detect the intrathecal production of antibodies specific to Borrelia burgdorferi.
Intrathecal antibody production means that the immune system is actively creating Lyme-specific antibodies within the CNS, which is a strong indicator of an active Neuroborreliosis infection. This finding is generally more reliable than standard serology (ELISA and Western Blot) alone. While the absence of intrathecal antibodies does not completely exclude the diagnosis, their presence provides definitive confirmation.
Treatment and Recovery
The standard treatment for confirmed Neuroborreliosis involves a course of antibiotics aimed at eradicating the Borrelia bacteria to halt the underlying inflammation. For central nervous system involvement, intravenous (IV) antibiotics are typically used because they achieve higher concentrations within the brain and CSF. The preferred IV antibiotic is often ceftriaxone, administered for 14 to 21 days.
Oral doxycycline can also be an effective treatment option for some manifestations of Neuroborreliosis, as it demonstrates good penetration into the central nervous system. The goal of this treatment is clinical improvement, measured by the resolution or reduction of the patient’s neurological symptoms.
The outcome for the brain lesions can vary; they may partially or completely resolve following successful antibiotic treatment, or they may persist on subsequent MRI scans. The persistence of these small white matter changes after treatment does not necessarily indicate a failure of therapy or ongoing active infection. The primary measure of success is the patient’s clinical recovery and the normalization of CSF markers.