BackgroundThis article reports a rare case of active neurosyphilis in a man with mild to moderate dementia and marked hippocampal atrophy, mimicking early onset Alzheimer’s disease. Few cases have so far described bilateral hippocampal atrophy mimicking Alzheimer’s disease in neurosyphilis.Case presentationThe patient presented here is a 33 year old Bulgarian male, whose clinical features include progressive cognitive decline and behavioral changes over the last 18 months. Neuropsychological examination revealed mild to moderate dementia (Mini Mental State Examination score was 16/30) with impaired memory and attention, and executive dysfunction. Pyramidal, and extrapyramidal signs, as well as dysarthria and impairment in coordination, were documented. Brain magnetic resonance imaging showed cortical atrophy with noticeable bilateral hippocampal atrophy. The diagnosis of active neurosyphilis was based on positive results of the Venereal Disease Research Laboratory test/Treponema pallidum hemagglutination reactions in blood and cerebrospinal fluid samples. In addition, cerebrospinal fluid analysis showed pleocytosis and elevated protein levels. High-dose intravenous penicillin therapy was administered. At 6 month follow up, improvements were noted clinically, on neuropsychological examinations, and in cerebrospinal fluid samples.ConclusionThis case underlines the importance of early diagnosis of neurosyphilis. The results suggest that neurosyphilis should be considered when magnetic resonance imaging results indicate mesiotemporal abnormalities and hippocampal atrophy. Neurosyphilis is a treatable condition which requires early aggressive antibiotic therapy.

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Studying of placebo response in patients with Generalized Anxiety Disorder (GAD) was the aim of research. 90 patients (68 female, 22 male, mean age of 33 years) were studied. All patients accepted inactive placebo (P) within 7 days and then - Alprazolam (A) in a dose of 1-3 mg per day within 4 weeks. Efficacy of treatment was estimated weekly by the HAM-A scale. After week of placebo reception, patients with HAM-A score < 9 made group of remission (R), with ≥50% HAM-A reduction - placebo responders group (PR), with HAM-A reduction 25-49% - partial placebo responders group (PPR), ≤ 25% HAM-A reduction - placebo nonresponders group (PNR).After week of reception placebo 16.6% of patients HAM-A made group R, 26.7% - PR; 30% - PPR, 26.7% - PNR. After active therapy (A) Therapeutic Remission group (RT - HAM-A score < 9) consisted of 100% of group R, 75% of PR, 81.5% of PPR and 8,33% of PNR. 25% of PR, 18% of PPR and 8.33% of PNR became Therapeutic Responders (TR - HAM-A reduction >50%). Partial Therapeutic Responders (PTR - HAM-A reduction 25-49%) and Therapeutic Nonresponders (TNR ≤ 25% HAM-A reduction) consisted only of PNR (62.5% and 20.83%).Absent response on (P) frequently correlated with low efficacy of therapy of (A). High positive placebo effect (PE) was defined in patients in whom improvement after transferring on active therapy became even more expressed. The received data allow to consider presumably PE like predictor of efficacy of benzodiazepines therapy for GAD.

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