BackgroundLatency of P300 subcomponent of event-related potentials (ERPs) increases in Alzheimer disease (AD) patients, which correlate well with cognitive impairment. Cholinesterase inhibitors (ChEIs) reduce P300 latency in AD patients with parallel improvement in cognition. It is not known whether N200 response to ChEIs is similar to that of P300.The aim of this study was to evaluate and compare characteristics of P300 and N200 in AD patients, treatment-naïve and on stable donepezil treatment, matched by age, education, sex, and cognitive function.Material/MethodsWe recruited 22 consecutive treatment-naïve AD patients (AD-N group), 22 AD patients treated with a stable donepezil dose of 10 mg/day for at least 3 months (AD-T group), and 50 healthy controls were recruited. Neuropsychological testing (MMSE, ADAS-Cog, and additional tests) and ERP recording was performed and analyzed.ResultsAll groups did not differ according to age, duration of education, or sex (p>0.05). AD-N and AD-T groups did not differ according to cognitive function. The AD-T group had longer duration of disease than the AD-N group (p<0.001). The AD-T and AD-N groups did not differ in P300 latencies (p=0.49). N200 latency was longer in the AD-T group (p<0.001). The general linear model showed that significant predictors of P300 latency were age (p=0.019) and AD treatment status (p<0.001). Duration of AD was a significant predictor of N200 latency (p=0.004).ConclusionsThe response of N200 latency to donepezil treatment differs from the response of P300. P300 is a better marker of ChEI treatment-dependent cognitive functions. N200 is more dependent on the duration of AD.

A 63-year-old woman residing in northern Lithuania was admitted to the Department of Neurosurgery at Republican Vilnius University Hospital with severe headache, progressive left-sided hemiparesis, and seizures. These symptoms, along with ataxia and left-sided facial nerve palsy, were present for several weeks and gradually worsened. The patient was diagnosed 6 years before with liver alveolar echinococcosis (AE) stage IV P4N4M1 with transdiaphragmatic bilateral pulmonary dissemination (►Figs. 1, 2).1 The case was considered nonsurgical, and treatment with albendazole 400 mg twice a day was initiated. This treatment resulted in elevation of hepatic enzymes, and the dose was reduced to 200 mg per day. The patient developed pruritus, headache, and cardiac Keywords► alveolar echinococcosis ► Echinococcus multilocularis ► cerebral alveolar echinococcosis AbstractThe fox tapeworm Echinococcus multilocularis causes human alveolar echinococcosis, commonly affecting the liver. However, in $1% of cases, systematic spread of the disease involves the brain as well. A patient had a 6-year history of liver and lung alveolar echinococcosis that was considered not suitable for surgery, and treatment with albendazole was introduced. After the appearance of neurologic disturbances, an intracranial mass lesion was demonstrated by radiologic imaging. The lesion was surgically removed, and histologic analysis revealed metacestode tissue of E. multilocularis. Despite the surgical resection of the lesion, the patient died of progression of systemic alveolar echinococcosis. The authors highly recommend implementing neurologic monitoring to the follow-up algorithm for patients with systemically disseminated alveolar echinococcosis. When neurologic symptoms occur, radiologic imaging of the brain should be obtained immediately. Surgery should be considered for all intracranial echinococcal lesions, unless the lesion is located in the eloquent brain area.