Dr. Murai Éva szerk.: Parasitologia Hungarica 24. (Budapest, 1991)

Lyme meningitis cases than in controls. Elevation of protein levels was even more striking in Bannwarth's syndrome: only one of our cases had normal CSF protein. In Lyme meningitis, CSF glucose is generally either stated to be normal in a majority of previous studies or not mentioned at all (2, 39, 63, 112, 114, 125). Low CSF sugar has only been reported by a few investigators (12,31,149). Our data show that in Lyme meningitis, especially in Bannwarth's syndrome, significantly more patients have low CSF glucose levels than meningitis controls. The selection of controls may influence the statistical analysis, especially since patients with tick-borne encephalitis are known to have elevated CSF sugar levels. In our control material there was, however, no difference in CSF sugar content between the tick-borne encephalitis cases and the other members of the control group. The combination of chronic lymphocytic pleocytosis + elevated CSF protein + decreased glucose content is generally considered to be unique for tuberculous meningitis. Our results show that this rare CSF profile is also a regular finding in Lyme meningitis. Especially in a case of chronic lymphocytic meningitis accompanied by radiculoneuritis, the probability of borrelia infection is very high. In our material, four cases of typical Bannwarth's syndrome had been treated with antituberculotic drugs for weeks until the correct diagnosis of borrelia infection was established. Although antituberculotic treatment will have to be given if mycobacterial infection is suspected, the differential diagnosis of borrelia infection must be kept in mind in endemic areas. It is important to emphasize that pleocytosis in the CSF is one of the diagnostic criteria of BS, but CNS involvement caused by Bb may occur with a mild CSF abnormality or even without a pathological CSF finding. A case of peripheral neuritis need not be accompanied by CSF disturbances (43,103,165). Peripheral facial palsy is a frequent symptom of LB (106,115,149). We tried to find a dividing line between the idiopathic and borrelia induced Bell's palsy. In our facial palsy material which consisted of 654 cases, 25.4% proved to have borrelia infection. A lower positivity ratio was reported by Jonsson (62) and Olsson (111), 16 and 20%, respectively. We could prove statistically that the bilateral facial palsy is very probably caused by Bb. A high incidence of bilateral palsy among Lb cases has also been reported by others (24,106, 114). The relapsing cases of facial palsy - especially if the relapse was multiple or occurred more than 6 months apart - were usually seronegative. The most typical hallmark of borrelia infection is a facial palsy accompanied by meningitis. The probability of borrelia origin is about 60% in that case. Lyme meningitis differed from other lymphocytic meningitis cases by its longer course and by the lack of meningeal signs. Only a few cases showed sensory loss or convulsion. These "conventional" encephalitic symptoms seem to be infrequent in neuroborreliosis but a few similar case reports have been published by others (33, 36). Five per cent of our cases showed memory impairment that could be measured by neuropsychiatrie or neurophysiologies examinations (43,128). Peripheral neuritis is a typical manifestation of neuroborreliosis. Both mild paraesthesia and serious lancinating neuralgia can occur. One of our patients was