Lyme disease, caused by the bacterium Borrelia burgdorferi, is an infection primarily transmitted through the bite of infected ticks. While often associated with skin rashes and joint pain, this spirochete is capable of spreading throughout the body, including the nervous system. When the bacteria reaches the brain and spinal cord, it causes a condition known as Neuroborreliosis. This neurological involvement confirms that Lyme disease can indeed affect the brain, requiring specialized diagnostic and treatment approaches.
How the Bacteria Infects the Central Nervous System
The movement of Borrelia burgdorferi from the bloodstream into the central nervous system (CNS) requires it to bypass a highly selective protective layer called the Blood-Brain Barrier (BBB). This barrier is composed of tightly packed endothelial cells that normally prevent most pathogens from entering the delicate brain tissue. The spiral shape of the Borrelia bacteria is thought to play a facilitating role in this invasion process.
The bacteria adhere to the endothelial cells of the BBB, potentially inducing enzymes known as matrix metalloproteinases. This action may cause a focal degradation of the tight junction proteins, allowing the spirochete to slip between the cells in a process called paracellular transmigration. Once inside the CNS space, the bacteria trigger a rapid inflammatory response. This immune reaction can result in inflammation of the meninges, leading to conditions like meningitis or encephalitis.
Distinct Neurological and Cognitive Manifestations
Infection of the nervous system by Borrelia burgdorferi can produce a wide array of specific neurological and cognitive symptoms. Among the most common neurological deficits is cranial nerve palsy, frequently seen as facial drooping or weakness, similar to Bell’s palsy. This occurs when the infection directly inflames the seventh cranial nerve, which controls facial movement.
The infection can also cause inflammation of the nerve roots, a condition known as radiculoneuritis. This often presents as severe nerve pain, numbness, or tingling sensations (peripheral neuropathy) that can radiate across the body. Signs of meningitis, such as a severe headache and a stiff neck, may also be present due to the inflammation of the meninges.
The effects on the brain parenchyma manifest as encephalopathy, a generalized disturbance of brain function. Patients frequently report cognitive issues, often described as “brain fog,” including difficulty concentrating and memory loss. Mood disturbances such as anxiety and depression are commonly reported and are considered direct consequences of the infection’s impact on the central nervous system.
Specific Diagnosis and Treatment Protocols
Diagnosing Neuroborreliosis requires more than a standard blood test, as general antibody levels in the blood do not confirm that the infection has penetrated the CNS. The definitive diagnostic procedure involves a Lumbar Puncture (spinal tap) to collect Cerebrospinal Fluid (CSF). This fluid is then analyzed for signs of inflammation, such as an elevated white blood cell count (pleocytosis).
The most specific confirmation is the detection of intrathecal antibody production. This is confirmed by calculating the Borrelia-specific antibody index (AI), which compares the level of Borrelia antibodies in the CSF to the level in the blood serum. A positive index indicates that the immune system is actively producing antibodies within the central nervous system, confirming an active infection. Imaging studies, such as Magnetic Resonance Imaging (MRI), may be used to exclude other potential causes or show enhancement of the inflamed cranial nerves.
Treatment must be specialized due to the difficulty of getting standard oral antibiotics across the Blood-Brain Barrier in sufficient concentration. Therefore, intravenous (IV) antibiotics are the preferred method of treatment. Commonly used IV medications include ceftriaxone, cefotaxime, or penicillin G. The typical treatment duration for early Neuroborreliosis is a 14-day course of IV therapy, which may be extended to 21 days for later or more complex neurological involvement.