Effects of injuries to descending motor pathways on restoration of gait in patients with pontine hemorrhage.

BACKGROUND AND PURPOSE: Gait disturbance due to injuries of the descending motor pathway, including corticospinal tract (CST), corticoreticular pathway (CRP), and medial and lateral vestibulospinal tracts (VSTs), are commonly encountered disabling sequelae of pontine hemorrhage. We investigated relations between changes in the CST, CRP, and medial and lateral VST and corresponding changes in gait function in patients with pontine hemorrhage. METHOD: Nine consecutive stroke patients with pontine hemorrhage, and 6 age-matched normal subjects were recruited. Four patients were allocated to group A (can't walk independently) and 5 to group B (can walk independently). Diffusion tensor imaging (DTI) data were acquired twice at acute to subacute stage and chronic stage after stroke onset. Diffusion tensor tractography (DTT) was used to reconstruct CST, CRP, medial and lateral VST. RESULT: The CRP shows a significantly different between groups A and B in both initial and follow up DTT (p > 0.05). In contrast, CST, medial VST and lateral VST did not show a significant difference (p > 0.05). Regarding DTI parameters of CRPs in group A, percentages of patients with fractional anisotropy (FA) and mean diffusivity (MD) values more than two standard deviation from normal were higher by follow up DTI than by initial DTI, however, the CRPs in group B only showed increased abnormal range of MD. CONCLUSIONS: The CST does not play an essential role in recovery of independent walking and vestibulospinal tracts may not crucially affect recovery of independent walking in patients with pontine hemorrhage. In contrast, and intact CRP or changes of the CRP integrity appear to be related to the recovery of gait function.

The spatial distribution pattern of Connexin26 expression in supporting cells and its role in outer hair cell survival.

Mutations in the GJB2 gene (which encodes Connexin26 (Cx26)) account for about a quarter of all cases of non-syndromic deafness. Previous studies have indicated that knockout (KO) of Gjb2 gene during early postnatal days can cause outer hair cell (OHC) loss in mouse models. However, the postnatal spatial distribution pattern of Cx26 in different types of supporting cells (SCs) and the role of such distributions for the survival of OHCs is still obscure. In this study, the spatial distribution patterns of Cx26 in SCs were observed, and based on these observations different spatial Cx26-null mouse models were established in order to determine the effect of changes in the spatial distribution of Cx26 in SCs on the survival of OHCs. At postnatal day (P)3, unlike the synchronous expression of Cx26 along both longitudinal and radial boundaries of most types of SCs, Cx26 expression was primarily observed along the longitudinal boundaries of rows of Deiter's cells (DCs). From P5 to P7, radial expression of Cx26 was gradually observed between adjacent rows of DCs. When Gjb2 gene was knocked out at random in different types of SCs, about 40% of the total DCs lost Cx26 expression and these Cx26-null DCs were distributed randomly in all three rows of DCs. The mice in this randomly Cx26-null group showed normal hearing and no significant OHC loss. When using a longitudinal KO pattern to induce knockout of Gjb2 gene specifically in the third row of DCs, about 33% of the total DCs lost Cx26 expression in this specific longitudinally Cx26-null group. The mice in this group showed late-onset hearing loss and significant OHC loss, however, the morphology of corresponding DCs was slightly altered. In both experimental groups, no substantial DC loss was observed. These results indicate that longitudinal Cx26-based channels are predominant in DCs during P3-P5. The Cx26 expression along rows of DCs might play a key role in the survival of OHCs, but this longitudinal KO pattern in DCs has a limited effect on DC survival or on its postnatal development.

Cranial irradiation in childhood mimicking neurofibromatosis type II.

Neurofibromatosis type II (NF2) is a genetic disease characterized by bilateral vestibular schwannomas (VS) and other nerve system tumors. However, such tumors may be associated with environmental, rather than a genetic, etiology. Individuals fulfilling the clinical criteria of NF2 who had been treated by head ionized irradiation at a young age were compared for disease characteristics and molecular analysis with non-irradiated sporadic NF2 cases. In the study cohort, three of 33 sporadic adult cases fulfilling NF2 diagnostic criteria had a history of early age cranial irradiation exposure. None of the irradiated patients had bilateral VS compared with 73.3% of the non-irradiated individuals. One of the irradiated patients had no VS, while none of the non-irradiated NF2 cases had absence of VS. All of the irradiated individuals had brain meningiomas and thyroid tumors compared with 47% and 0%, respectively, of the non-irradiated individuals. Molecular analyses for NF2 mutations in blood of the irradiated individuals failed to detect disease-causing mutations. This study suggest that environmental factors may mimic NF2. Identifying such non-genetic cases fulfilling clinical criteria of the genetic disease may be crucial for the purposes of genetic counseling and patient management.

[Functional effects of transcranial electromagnetic stimulation (60 and 70 Hz) of the brain of intact rats and rats with acute brainstem damage].

Behavior and brain electrical activity of 79 male Wistar rats (intact and with acute experimental brainstem injury) were studied during the course of therapeutic transcranial electromagnetic stimulation (TEMS) with frequencies 60 and 70 Hz. In intact animals this effect was accompanied by a decrease in voluntary motor activity and increase in synchronization of the brain electrical activity, in particular, in the delta and beta1 frequency ranges. This inhibitory effect was similar to that of sleep. In the early period of acute experimental stem pathology, the TEMS course was accompanied by suppression of EEG signs of adaptive post-operative stress response and could lead to increased severity of the condition of an animal, along with the slowing of postoperative recovery. Cytomorphological evidence was obtained to the importance of vascular factor in the formation of cerebral reactions to TEMS.

[Purkinje's cells in the vestibular and proprioceptive segments of rat's cerebellum following 14-day space flight].

Quantitative cytochemical and morphometric methods were used to investigate cytochrome oxidase activity and sizes of bodies and nuclei of Purkinje's cells in the medical nodulus and upper central lobule of the vermis obtained from rats sacrificed in 5-6 hours of landing after the 14-day SLS-2 mission of NASA space "shuttle" Columbia (STS-58). The reduced cytochrome oxidase activity was explained by suppression of the functional activity of Purkinje's cells in microgravity. Results of the investigations suggest weakening of the regulatory effect of the vermis Purkinje's cells on giant neurons of the dorsocaudal segment of Deiters nucleus. They also strengthen the earlier hypothesis that space flight decays the inhibitory effect of nodulus Purkinje's cells on the medial vestibular nucleus for the reason of change in the "velocity storage" in mammals during and after flight.

[Quantitative criteria for the evaluation of congenital chromatic vision disorders]. / Kolichestvennyi kriterii otsenki vrozhdennykh rasstroistv tsvetovogo zreniia.

The minimum angular size of a color stimulus required for its discrimination has been ascertained to be a quantitative criterion for evaluating the form and degree of congenital chromatic visual diseases. Unlike individuals with normal color perception who distinguish all basic and intermediate colors despite their saturation, anomalous trichromats discriminate more saturated colors with larger angular sizes of stimuli than those with normal color perception. Mild and moderate anomalous trichromats do not discriminate lowly saturated colors or for this they require the angular sizes tens of times greater those for normal trichromats. Persons with severe chromatic visual diseases (Type A) do not distinguish moderately saturated colors either. On recognizing the color of test objects, anomalous trichomats make the most mistakes in perceiving the green and yellow colors, the fewest mistakes in perceiving the red color. The minimum angular sizes required to distinguish colors, the percent of errors in their discrimination, and the range of vision of safety signs depend on the form and degree of congenital chromatic diseases. This makes it necessary to apply a differential approach to providing jobs that require rapid and accurate color discrimination in persons with the protanomalous forms of chromatic pathology.

Vestibular nuclei of hemilabyrinthectomized guinea pigs during decompensation.

1. The effects of the post-brachial section of the spinal cord on the field potentials recorded from the vestibular nuclei during stimulation of the right vestibular receptors have been studied in left hemilabyrinthectomized and then compensated guinea pigs. 2. Facilitation of the field potentials in the right vestibular nuclear complex and inhibition in the left nuclei have been observed. 3. These results confirm that the spinal cord is involved in the compensation of the release syndrome brought about by the lesion of one labyrinth. 4. The possible mechanisms underlying such a compensation are discussed.