The bacterium responsible for Lyme disease, Borrelia burgdorferi, can affect the brain and the entire central nervous system (CNS). This serious complication occurs when the infection spreads beyond the initial bite site and enters the nervous system, a condition medically termed neuroborreliosis. The neurological involvement can develop weeks to months after the initial infection, sometimes when early, localized symptoms were missed. Timely treatment is important for a positive outcome.
Defining Neuroborreliosis
Neuroborreliosis is the specific medical term used to describe the infection of the nervous system by the Borrelia burgdorferi spirochete. This complication typically arises during the disseminated, or second, stage of Lyme disease, weeks to months after the initial tick bite. The spirochete travels through the bloodstream to reach the central nervous system, which includes the brain and spinal cord.
The bacteria must cross the blood-brain barrier, a highly selective membrane that separates the circulating blood from the CNS. Once inside the CNS, the spirochetes trigger an inflammatory response involving cells like microglia and astrocytes. This response releases inflammatory mediators and can lead to swelling and cerebral edema, which is the underlying cause of the neurological symptoms.
Neurological and Psychiatric Manifestations
The symptoms of acute neuroborreliosis are diverse and can affect both the central and peripheral nervous systems.
Physical Symptoms
One common presentation is radiculoneuritis, the inflammation of the spinal nerve roots. This manifests as severe, shooting or lancinating pain, often worse at night, along with sensations like numbness or tingling in the arms or legs.
A hallmark sign is cranial nerve palsy, which is particularly noticeable when it affects the facial nerve. This results in weakness or paralysis on one or both sides of the face, commonly referred to as Bell’s palsy. Other cranial nerves can be involved, leading to issues like double vision or hearing loss.
Involvement of the meninges, the membranes surrounding the brain and spinal cord, can lead to lymphocytic meningitis. This condition often presents with a severe headache, a stiff neck, and increased sensitivity to light. In rare instances, the infection can cause inflammation of the brain tissue itself, known as meningoencephalitis.
Cognitive and Psychiatric Symptoms
Neuroborreliosis can also manifest with cognitive and psychiatric symptoms. Patients may report a mild encephalopathy, experiencing “brain fog,” which includes memory problems and difficulty concentrating.
Psychiatric symptoms that can develop acutely include increased anxiety, sudden mood swings, irritability, and depression. These neuropsychiatric presentations are caused by the infection’s inflammatory impact on brain function.
Diagnostic Procedures and Treatment Protocols
Confirming a diagnosis of neuroborreliosis requires more than the standard blood tests used for early Lyme disease. Since the infection is contained within the nervous system, clinicians often perform a lumbar puncture (spinal tap) to collect cerebrospinal fluid (CSF). This fluid is then analyzed for inflammatory markers and evidence of local antibody production.
The detection of Borrelia-specific intrathecal antibody synthesis in the CSF is considered a definitive diagnostic indicator for CNS infection. Imaging, such as a magnetic resonance imaging (MRI) scan, may also be used to visualize inflammation or rule out other neurological conditions.
The treatment protocol involves administering antibiotics that can effectively penetrate the central nervous system. For acute neuroborreliosis, intravenous (IV) antibiotics, such as ceftriaxone, are the preferred treatment method. Oral antibiotics like high-dose doxycycline are also effective for many patients due to their ability to adequately cross the blood-brain barrier. The standard duration for this antibiotic therapy is typically 14 days for early neuroborreliosis.
Understanding Post-Treatment Lyme Disease Syndrome
Patients may continue to experience non-specific symptoms even after completing the recommended course of antibiotic treatment. This residual condition is termed Post-Treatment Lyme Disease Syndrome (PTLDS). PTLDS is defined by persistent symptoms—most commonly fatigue, widespread pain, and neurocognitive difficulties—that last for six months or longer after the completion of standard antibiotic therapy.
It is important to distinguish PTLDS from an active, ongoing nervous system infection, as the symptoms are not believed to be caused by persistent live bacteria. Current theories suggest that PTLDS may result from residual damage to the nervous system, an ongoing autoimmune response, or chronic neuroinflammation. These persistent symptoms are managed through symptomatic treatments, focusing on pain relief and cognitive rehabilitation, rather than prolonged courses of antibiotics.