Lyme neuroborreliosis is an infection of the nervous system caused by spirochetes of the Borrelia burgdorferi sensulato group. Neurological clinical manifestations usually present a steady evolution and are different in patients from Europe compared to those from America, possibly due to vector agents and different bacterial species. Various diagnostic markers were studied in consideration of a clear or possible diagnosis of the disease, because evolution and complications depend on early diagnosis and initiation of therapy. The isolation of the bacterium is difficult, microscopic examination and the bacterial dezoxiribonucleic acid amplification shows low sensitivity. However, the diagnosis of Lyme neuroborreliosis is mainly based on serological methods that have a satisfactory sensitivity and specificity. A correct diagnosis can be performed by strictly respecting clinical guidelines and protocols and carefully interpreting the serological tests. The presence of anti-borrelia burgdorferi antibodies in the cerebrospinal fluid with evidence of intrathecal antibody production is the gold standard diagnosis of Lyme neuroborreliosis. Early administration of antibiotic treatment (third generation cephalosporins, cyclins, aminopenicillins) can produce the remission of neurological symptoms, the eradication of spirochetes in acute phase of the disease, thus avoiding the development of the chronic disease. Introduction Lyme neuroborreliosis (LNB) is a clinical manifestation of Lyme borreliosis (LB), which affects the central nervous system (CNS) and peripheral nervous system (PNS) caused by spirochetes of the genus Borrelia burgdorferi (Bb) sensulato complex and spread by the bite of ticks of the genus Ixodes. Nerve structures are affected by spirochetes both in acute and late phase of the disease. A distinction between early (acute) and late (chronic) phase of LNB can be made. The acute phase occurs in less than 6 months after contacting an infected arthropod and chronic LNB sets in more than 6 months or even years later after the initial infection [1,2].The clinical manifestations of LNB are various and different in patients from Europe compared to those from America, probably due to different vector agents and bacterial species of the two continents. According to Steere the frequency of neurological manifestations in case of LB is about 15-25% [3].