Body size perception in stroke patients with paresis.

Recent studies have suggested that people's intent and ability to act also can influence their perception of their bodies' peripersonal space. Vice versa one could assume that the inability to reach toward and grasp an object might have an impact on the subject's perception of reaching distance. Here we tested this prediction by investigating body size and action capability perception of neurological patients suffering from arm paresis after stroke, comparing 32 right-brain-damaged patients (13 with left-sided arm paresis without additional spatial neglect, 10 with left-sided arm paresis and additional spatial neglect, 9 patients had neither arm paresis nor neglect) and 27 healthy controls. Nineteen of the group of right hemisphere stroke patients could be re-examined about five months after initial injury. Arm length was estimated in three different methodological approaches: explicit visual, explicit tactile/proprioceptive, and implicit reaching. Results fulfilled the working hypothesis. Patients with an arm paresis indeed perceived their bodies differently. We found a transient overestimation of the length of the contralesional, paretic arm after stroke. Body size and action capability perception for the extremities thus indeed seem to be tightly linked in humans.

Trifluoperazine-Induced Suicidal Erythrocyte Death and S-Nitrosylation Inhibition, Reversed by the Nitric Oxide Donor Sodium Nitroprusside.

BACKGROUND AND PURPOSE: The high potency antipsychotic drug trifluoperazine (10-[3-(4-methyl-1-piperazinyl)-propyl]-2-(trifluoromethyl)-(10)H-phenothiazine dihydrochloride; TFP) may either counteract or promote suicidal cell death or apoptosis. Similar to apoptosis, erythrocytes may enter eryptosis, characterized by phosphatidylserine exposure at the cell surface and cell shrinkage. Eryptosis can be stimulated by an increase in cytoplasmic Ca2+ concentration ([Ca2+]i) and inhibited by nitric oxide (NO). We explored whether TFP treatment of erythrocytes induces phosphatidylserine exposure, cell shrinkage, and calcium influx, whether it impairs S-nitrosylation and whether these effects are inhibited by NO. METHODS: Phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, [Ca2+]i from Fluo3-fluorescence, and protein nitrosylation from fluorescence switch of the Bodipy-TMR/Sypro Ruby signal. RESULTS: Exposure of human erythrocytes to TFP significantly enhanced the percentage of annexin-V-binding cells, raised [Ca2+]i, and decreased S-nitrosylation. The effect of TFP on annexin-V-binding was not affected by removal of extracellular Ca2+ alone, but was significantly inhibited by pre-treatment with sodium nitroprusside (SNP), an effect significantly augmented by additional removal of extracellular Ca2+. A 3 hours treatment with 0.1 µM Ca2+ ionophore ionomycin triggered annexin-V-binding and cell shrinkage, effects fully reversed by removal of extracellular Ca2+. CONCLUSIONS: TFP induces eryptosis and decreases protein S-nitrosylation, effects blunted by nitroprusside. The effect of nitroprusside is attenuated in the presence of extracellular Ca2+.