Early cyclosporin A treatment retards axonal degeneration in an experimental peripheral nerve injection injury model

Injury to peripheral nerves during injections of therapeutic agents such as penicillin G potassium is common in developing countries. It has been shown that cyclosporin A, a powerful immunosuppressive agent, can retard Wallerian degeneration after peripheral nerve crush injury. However, few studies are reported on the effects of cyclosporin A on peripheral nerve drug injection injury. This study aimed to assess the time-dependent efficacy of cyclosporine-A as an immunosuppressant therapy in an experimental rat nerve injection injury model established by penicillin G potassium injection. The rats were randomly divided into three groups based on the length of time after nerve injury induced by penicillin G potassium administration (30 minutes, 8 or 24 hours). The compound muscle action potentials were recorded pre-injury, early post-injury (within 1 hour) and 4 weeks after injury and compared statistically. Tissue samples were taken from each animal for histological analysis. Compared to the control group, a significant improvement of the compound muscle action potential amplitude value was observed only when cyclosporine-A was administered within 30 minutes of the injection injury (P < 0.05); at 8 or 24 hours after cyclosporine-A administration, compound muscle action potential amplitude was not changed compared with the control group. Thus, early immunosuppressant drug therapy may be a good alternative neuroprotective therapy option in experimental nerve injection injury induced by penicillin G potassium injection

Creutzfeldt-Jakob disease presented with dizziness, weakness and neuropsychiatric symptoms: 2 Case Reports

Creutzfeldt-Jakob disease (CJD) is among very rare, progressive, untreatable, neurodegenerative prion diseases. While the incidence is reported as 1/1000000 years in European countries, sporadic cases are rarely presented in Turkey. Clinical findings are in the form of rapid progressive dementia, myoclonus, cerebellar, pyramidal and extra pyramidal symptoms. Definitive diagnosis is established by histopathological examination. Our case is a 64-year-old male and 70-year-old female patients admitted with dizziness emerged as sub-acute weakness, nausea, vomiting, insomnia, imbalance and additional neuropsychiatric complaints. Focal activity slowness and common periodic sharp wave activities were observed in EEG. CJD was considered because bilateral symmetrical diffusion limitation was observed at both sides in the basal ganglia level in cranial diffusion MRI's and 14-3-3 protein was resulted as positive in CSF examinations. CJD, which is a very rare disease in patients presenting with progressive neuropsychiatric symptoms and seizure, is one of the diagnosis to be considered and we wanted to emphasize that there is no treatment for it and preventive measures should be taken