Neuroborreliosis – What is it?

Introduction

Neuroborreliosis is a form of Lyme disease caused by the bacterium Borrelia burgdorferi. The bacterium is most frequently transmitted to humans in Europe by tick bites. The most frequent manifestation of Lyme disease is the so-called erythema migrans, a skin rash after a tick bite. However, half of the patients with Lyme disease also develop neuroborreliosis. This can lead to meningitis (inflammation of the meninges) as well as various other neurological complaints.

The causes

Neuroborreliosis is caused by an infection with the bacterium Borrelia burgdorferi. In Europe, the pathogens most often enter the patient’s body through a tick bite. The common wood tick (Ixodes ricinus) is the main carrier of the bacterium.

In contrast to early summer meningoencephalitis (FSME), which can also be caused by tick bites and whose high-risk area is concentrated in southern Germany, borreliosis is widespread throughout Germany. The transmission of the Borrelia from the tick to humans begins at the earliest six hours after the bite of the animal. The longer the tick remains on the patient, the higher is the risk of Borrelia transmission. In addition, if the tick is not removed properly, the pathogens are often transmitted, for example if the tick is squeezed out during the removal.

The symptoms

Neuroborreliosis usually develops only after a few weeks to months after infection with the bacterium Borrelia burgdorferi. Up to 95% of the cases express themselves through meningitis. The affected person often suffers from headaches, fever and neck stiffness.

Nerve roots can also be affected by the inflammatory process, which can manifest itself as paralysis, sensitivity disorders and pain. It is not uncommon for unilateral or bilateral facial paralysis to occur when the facial nerve is affected (facial nerve palsy). In most cases, the symptoms recede within half a year.

In the remaining 5-10% of patients, not only meninges and nerve roots become inflamed, but also the brain and spinal cord. Affected patients develop, for example, gait disorders, dizziness, balance disorders, epileptic seizures, incontinence, hallucinations, speech and hearing difficulties, extreme fatigue or other psychological symptoms. Often concentration and retentiveness are limited. Relatives or acquaintances of the patients sometimes notice a change in their nature. Progressions in which the brain is directly affected are usually more protracted than those in which the meninges alone are involved.