Creutzfeldt-Jakob disease mimicking Lewy body dementia - a case report. / Choroba Creutzfeldta-Jakoba o poczatkowym przebiegu nasladujacym otepienie z cialami Lewy'ego ­ opis przypadku.

Lewy body dementia and Creutzfeldt-Jakob disease are recognized on the basis of certain diagnostic criteria. However, common symptoms such as: dementia, extrapyramidal syndrome, psychotic disorders may cause difficulty to make the correct diagnosis especially in the early stage of the disease. Each of these diseases may have atypical onset. The further course and the appearance of other symptoms indicate a proper diagnosis. Electroencephalogram and examination of 14-3-3 proteins in cerebrospinal fluid are helpful in the differential diagnosis. We present a case of a 66-year-old patient initially suspected of Lewy body dementia. On admission, psychomotor retardation, dysarthria, upper extremities dysmetria, extrapyramidal tension in the upper limbs, lower extremities ataxia, slow gait and unstable Romberg test were present. Mini-Mental State Examination (MMSE) score was 24/30. On neuropsychological assessment early stage of dementia was diagnosed. Anxiety-depressive symptoms were observed with periodic visual-auditory components. After less than 3 weeks there was a deterioration of neurological state. Dysarthria and lower limbs ataxia were increased, ataxia of the trunk appeared and psychomotor retardation got worse. There was significant progression of cognitive impairment, therefore complete neuropsychological examination was impossible to perform. MMSE score was 12/30 (12 points less than three months earlier). The course of the disease and additional tests results confirmed the diagnosis of sporadic Creutzfeldt-Jakob disease.

Interneuronal activity in reflex pathways from group II muscle afferents is monitored by dorsal spinocerebellar tract neurons in the cat.

The main aim of the study was to investigate whether group II muscle afferents contribute to the inhibition of dorsal spinocerebellar tract (DSCT) neurons and thereby modulate information provided by these neurons in the cat. In intracellular recordings, we found disynaptic IPSPs from group II afferents in the majority of DSCT neurons, most often in parallel with IPSPs evoked from group I afferents. In an attempt to identify interneurons that mediate these IPSPs, the second aim of the study, laminas IV-VII in midlumbar segments were searched for interneurons antidromically activated by stimuli applied within Clarke's column. Such interneurons were found in regions in which focal field potentials were evoked by group I and II afferents, or ventral to them, and most were coexcited by these afferents. The input to these interneurons and their location indicate that they belonged to the previously identified population of premotor interneurons in disynaptic pathways between group I and II afferents and hindlimb motoneurons. The study leads thus to the conclusion that inhibitory actions of group II afferents on DSCT neurons are collateral to actions on motoneurons and that DSCT neurons monitor inhibitory actions of group II afferents on motoneurons as closely as they monitor actions of group I afferents. The results also indicate that interneurons mediating disynaptic reflex actions from tendon organ (group Ib) afferents and those mediating disynaptic actions from secondary muscle spindle (group II) afferents to motoneurons may be parts and parcel of the same interneuronal population rather than constitute distinct interneuronal populations.