Lyme borreliosis (LB) is a clinically heterogeneous bacterial zoonosis caused by the spirochete
Borrelia burgdorferi (Bb)
, that is transmitted to humans by a tick bite [
1]. LB is endemic in North America, Asia, central and northern Europe and is continually rising in Western Europe [
1‐
3]. Incidence of infection peaks in 5–14 years old children and middle-aged adults (40–50 years old) [
3]. Clinically, the illness develops in different sequential stages. The primary stage exhibits a peculiar skin rash (erythema migrans), a painless round shaped rash with slow enlargement that tends to resolve from the center that typically appears seven to 14 days after the bite. Fatigue or headache is often seen at this stage [
1]. Blood or peripheral nerve dissemination of the bacterium lead to the subsequent stages, with various signs and symptoms. The secondary stage, that starts from three to 5 weeks after the bite, typically involves the neuronal or the cardiac tissue, usually causing atrioventricular blocks [
1,
3]. The third and chronic stage is only rarely reached and is mainly represented by arthritis or late neurological complications [
1,
4]. When the
Borrelia burgdorferi sensu lato-complex invade the nervous system, the resulting clinical entity is called Lyme neuroborreliosis (LNB) [
1,
3,
4]. Neurological symptoms usually occur between one and 12 weeks after the tick bite. Both the peripheral and central nervous systems can be affected by LNB. Cranial nerve neuritis, meningitis and radiculitis more often occur in the early period. Differently, late LNB usually presents with encephalitis, myelitis, encephalomyelitis and neuritis [
1,
3,
5]. Early LNB, defined as signs and symptoms lasting less than 6 months after the tick bite, represent the vast majority of the cases (95%) [
6]. While early LNB is typically self-limiting, late LNB is a chronic debilitating disease that probably reflects a persistent infection in nervous tissue [
6]. Signs and symptoms of LNB can differ between distinct endemic areas, probably reflecting the geographical distribution of various genospecies of
Borrelia, each of which has different neurotropic and neurovirulent properties [
6]. The species involved in european Lyme disease are mostly
B. afzelii and to a lesser extent
B. garinii and
B. burgdorferi. In the USA LNB is virtually due only to
B. burgdorferi sensu stricto. Clinically, painful meningoradiculitis (Bannwarth’s syndrome) is the most common presentation of LNB in Europe [
1,
3,
6,
7]. Patients with Bannwarth’s syndrome experience radicular pain, cranial nerve paresis and meningeal signs and symptoms [
1,
3,
6,
7]. The pain is usually described as different from other previously experienced types of pain and is usually resistant to analgesic treatment [
8,
9]. In the USA, erythema migrans and arthritis are more frequent compared to Europe and the main neurological manifestation is lymphocytic meningitis. Furthermore, LNB usually has different presentations according to age: in European children, the most common manifestation of LNB is acute facial nerve palsy, followed by other cranial nerve palsies and lymphocytic meningitis [
6,
7]. Preschool children may present with unspecific symptoms such as loss of appetite and asthenia. Although rare, central nervous system involvement such as myelitis or encephalitis has been reported in children with LNB. In this case, it can manifest with a very wide (and non-specific) range of symptoms including anorexia, ataxia and attention deficit [
6].