Negative motor seizure arising from the negative motor area: is it ictal apraxia?

PURPOSE: Seizure manifesting motor arrest, that is, negative motor seizure (NMS), is a rare epileptic condition in which only inability to conduct voluntary movements or praxis is produced, although consciousness is preserved. The negative motor area (NMA) seems to be responsible, but its generator mechanism has not yet been clarified. PATIENTS AND METHODS: Three patients manifesting NMS were investigated. Two patients (ages 33 and 17) with intractable frontal lobe epilepsy had subdural grid implantation for epilepsy surgery, and one (age 77) had scalp electroencephalography (EEG) monitoring. RESULTS: Ictal semiologies commonly observed, at least in the two patients, were found as follows; (1) indescribable or ill-localized aura, (2) repetitive involuntary vocalization, (3) inability to speak, (4) inability to move the extremities, and (5) subsequent evolution to positive motor seizures. Awareness and comprehension were preserved throughout the episode before generalized seizures. In two patients with epicortical EEG recording, ictal activity arose from the lateral NMA in one, and from the rostral supplementary motor area in the other. Cortical stimulation at NMA in one patient elicited symptoms identical to NMS. Another patient had scalp EEG and magnetic resonance imaging (MRI) abnormality, both suggesting the epileptogenic focus in the mesial frontal area. CONCLUSION: We showed that (1) NMS was a rare condition in patients with seizure focus in the frontal lobe, and (2) that the NMA was responsible for the symptoms. The documented state in the present study may reflect ictal apraxia, but it requires further investigation.

Reversible restricted diffusion of entire corpus callosum.

MR imaging of a 31-year-old man with bacterial meningo-encephalitis associated with infectious endocarditis demonstrated T2 prolongation and restricted diffusion involving the entire corpus callosum and symmetrically involving the cerebral hemispheric white matter. His neurological signs and symptoms were mild, and recovery was complete within a week. Follow-up MR imaging with a 9-day interval revealed complete resolution of these lesions. The clinical and radiological courses were identical to those previously reported with a reversible lesion isolated to the splenium, or to the splenium and peripheral fronto-parietal white matter. This suggests that such reversible lesions are not necessarily restricted to the splenium, but may involve the entire corpus callosum.

Effects of scavengers for active oxygen species on cell death by cryptogein.

The hypersensitive reaction is a type of programmed cell death in plants. Cryptogein is a proteinaceous elicitor secreted from Phythophthora cryptogea. In one current model, active oxygen species (AOS) trigger programmed cell death in plants. In this study, we examined a variety of AOS scavengers to elucidate the function of AOS in the death program. Most of these AOS scavengers, including tiron, a scavenger for superoxide radical, catalase for hydrogen peroxide, and hydroquinone, sodium ascorbate and propyl gallate for free radicals, almost completely removed extracellular AOS. However, none of the reagents completely blocked the cell death process. Other reagents, such as histidine and dimethylfuran, scavengers for singlet oxygen, and diphenyleneiodonium chloride, an inhibitor of NADPH oxidase, showed significant toxicity in BY-2 cells. These results indicate that AOS produced in the extracellular space do not play a role in hypersensitive cell death.

Lipid-binding form is a key conformation to induce a programmed cell death initiated in tobacco BY-2 cells by a proteinaceous elicitor of cryptogein.

Cryptogein, a proteinaceous elicitor secreted by Phytophthora cryptogea, induces a remarkable hypersensitive cell death in tobacco cells. Two cryptogein mutants were analysed to characterize the induction mechanism of cell death; one was a newly synthesized mutant N93A whose 93rd Asn residue was changed to Ala, the other was K13V whose Lys at position 13 was replaced with Val. The effect of these mutations was evaluated in terms of extracellular alkalization, production of active oxygen species (AOS) and progression to death. The mutation N93A resulted in a reduction in activity to 71.0, 74.6 and 24.5% for original rates of extracellular alkalization, AOS production and cell death progression, respectively. In the case of the K13V mutation, these rates changed to 114, 3.38 and 7.40%, respectively. The lipid-binding activities of the mutants were analysed using fluorogenic lipid of dehydroergosterol. The results for N93A and K13V were 38.3 and 3.40% compared with the wild type, respectively. These findings indicate that the lipid-binding form was the only conformation to induce the production of AOS and programmed cell death in plants.

A versatile assay for the accurate, time-resolved determination of cellular viability.

A convenient and versatile method for the accurate, time-resolved determination of cellular viability has been developed. The conventional viability indicator fluorescein diacetate (FDA), which is converted to the fluorescent compound fluorescein in living cells, was employed as a viability probe. Fluorescence emission from cells was measured using a spectrofluorimeter equipped with a magnetic stirrer. Using this assay cell suspensions exhibiting densities in the range 0.5 x 10(5) to 2.0 x 10(5) cells displayed a linear response when FDA concentrations less than 12 micro M were employed. To calibrate the method, viability standards were elaborated using different proportions of living and dead cells, and a correlation coefficient for the viability of tobacco BY-2 suspensions was calculated as 0.998. This viability assay was also found to be applicable to Chlamydomonas reinhardtii and Arabidopsis thaliana cultured cells. Using this cell viability assay, kinetic analyses of cell death could be performed. Using the proteinaceous elicitor from Phytophthora cryptogea, cryptogein, to induce cell death in tobacco cell suspensions, values for the maximum velocity of death induction rate (V(max)) and the LD50 (half-maximal velocity or k(1/2)) were calculated as 17.2 (% death/h) and 65 nM, respectively.