Lyme disease is caused by the bacterium Borrelia burgdorferi, transmitted to humans through the bite of infected Ixodes ticks. This systemic infection allows the bacteria to spread throughout the body, potentially involving multiple organ systems, including the nervous system. When Borrelia reaches the nervous system, the condition is called Neuroborreliosis. This serious complication includes the potential for the bacteria to affect the spinal cord and its associated structures.
How Lyme Reaches the Nervous System
The Borrelia burgdorferi spirochetes must first disseminate from the site of infection into the bloodstream to reach the nervous system. Once in circulation, the bacteria can penetrate the protective barriers that shield the central nervous system (CNS), which includes the brain and the spinal cord. This entry involves crossing the blood-brain barrier (BBB), which normally separates circulating blood from the CNS.
The mechanism of entry is often linked to localized inflammation, which disrupts the BBB’s integrity. This allows the spirochetes to pass into the cerebrospinal fluid (CSF) and surrounding tissues. This bacterial migration can result in inflammation of the membranes surrounding the CNS, known as lymphocytic meningitis, which often precedes direct involvement of the spinal cord.
Specific Spinal Cord Damage from Lyme
Lyme disease can cause lesions on the spine by triggering inflammatory changes that manifest as visible abnormalities. These lesions are areas of inflammation and tissue reaction caused by the presence of the bacteria or the body’s immune response, not structural injuries like a herniated disc.
The most common form of spinal involvement is Lyme radiculitis, also known as meningoradiculitis, which affects the nerve roots as they exit the spinal cord. This inflammation of the spinal nerve roots is a characteristic presentation of Neuroborreliosis. The swelling and irritation of these peripheral nerve structures can be visualized on magnetic resonance imaging (MRI) as nerve root enhancement following the injection of a contrast agent. This enhancement reflects the breakdown of the blood-nerve barrier due to the inflammatory process.
A less frequent manifestation is Lyme myelitis, which is the direct inflammation of the spinal cord tissue itself. In myelitis, the inflammatory process leads to visible lesions within the spinal cord parenchyma, often appearing as areas of high signal intensity on T2-weighted MRI scans. These lesions can be longitudinally extensive, meaning they cover a significant length of the spinal cord, and are indicative of transverse myelitis caused by the infection. The damage in myelitis results from the inflammatory cascade, which may include a direct effect of the spirochetes or secondary effects like small vessel inflammation (vasculitis).
Neurological Symptoms Associated with Spinal Involvement
The inflammatory damage to the spinal nerve roots and the spinal cord results in a distinct set of neurological symptoms. Lyme radiculitis is characterized by severe, intense pain that follows the distribution of the affected spinal nerves. This radicular pain often has a burning or shooting quality and is commonly reported to be worse during the night, sometimes significantly disrupting sleep.
Beyond pain, the inflammation of the nerve roots can lead to sensory disturbances, such as tingling, numbness, or a pins-and-needles sensation (paresthesia), in the limbs or torso. Motor deficits can also develop if the motor nerve fibers are involved, resulting in muscle weakness or even paralysis in the area supplied by the affected spinal nerves. A common example of this motor deficit is foot drop, where the patient has difficulty lifting the front part of the foot.
In Lyme myelitis, where the spinal cord itself is inflamed, the symptoms are often more severe and widespread. Patients may experience weakness in multiple limbs, difficulty with gait, and disturbances in bowel or bladder function. The presence of these specific radicular or myelitic symptoms provides a strong clinical suspicion for spinal Neuroborreliosis.
Diagnosis and Treatment of Severe Neuroborreliosis
The diagnosis of spinal Neuroborreliosis requires more than just a positive blood test for Lyme antibodies, as the central nervous system must be confirmed as the site of infection. The definitive method for confirming CNS involvement is a lumbar puncture, or spinal tap, to analyze the cerebrospinal fluid (CSF). This procedure allows clinicians to detect the presence of inflammatory changes and, most importantly, evidence of intrathecal antibody synthesis. Intrathecal synthesis means the patient’s immune system is producing antibodies against Borrelia directly inside the CNS, which is the most reliable indicator of active Neuroborreliosis.
Magnetic Resonance Imaging (MRI) is also utilized to support the diagnosis by visualizing the characteristic signs of inflammation, such as nerve root enhancement in radiculitis or T2 hyperintense lesions within the spinal cord in myelitis. However, the imaging findings alone are not sufficient for a diagnosis, as they can be non-specific and sometimes the MRI appears normal despite the presence of Neuroborreliosis.
Once a diagnosis of established Neuroborreliosis is confirmed, the standard treatment involves a course of intravenous (IV) antibiotics. Medications such as Ceftriaxone are administered directly into the bloodstream for a period of 14 to 21 days. IV administration is favored over oral antibiotics for severe neurological presentations because it ensures sufficient concentration of the drug reaches the CNS to eradicate the infection. Early and appropriate antibiotic treatment is associated with a favorable prognosis, with most patients seeing improvement or complete resolution of their neurological symptoms.