Das Reflexkriechen und seine Bedeutung für die krankengymanastische Frühbehandlung

Zusammenfassung Das Reflexkriechen stellt einen koordinierten Bewegungskomplex dar, in welchem wir die Anfänge der niedrigsten ontogenetischen Stufen der Motorik festhalten können. Der ganze Koordinationskomplex wird durch verschiedene, jedoch ganz charakteristische Zonen ausgelöst. Durch die Anwendung dieser Auslösungszonen verwirklicht sich ein massives Bahnungssystem mittels einer spatial summation. Dieses massive Bahnungssystem können wir begreiflicherweise jedoch nur als phylogenetische Persistenz der alten Lokomotion begreifen, und sein Koordinationsgebiet ist wahrscheinlich tiefer gelegen als der obere Hirnstamm. Aus den eben beschriebenen Komponenten des Reflexkriechens geht, hervor, daß wir schon vom früh-postnatalen Alter an die Möglichkeit haben, die Motorik systematisch auszuweiten und die Entwicklung des frühesten ontogenetischen Zeitabschnittes zu fördern ohne Unterschied, ob wir ein Risikokind oder ein Kind mit einer peripheren Bewegungsstörung vor uns haben. Bei Kindern mit schon entwickelten pathologischen Bewegungssyndromen (spastischen, athetotischen und atonischen) ermöglichen wir das physiologische Nachholen der posturalen Unzulänglichkeiten und finden damit bessere Bedingungen für die spontane Entwicklung der motivierten Acralbewegungen. Somit sichern wir normale Bedingungen für eine physiologische Entwicklung der ersten ontogenetischen Fortbewegung.

---

Reflex creeping as an early rehabilitation programme

Summary Reflex creeping as a motor-complex may be understood as the lowest stage of motor ontogenesis. The whole coordination complex, set off from well characterized trigger zones, is integrated by a system of facilitation as a result of spatial summation. This massive system of facilitation can be understood only if a phylogenetic old locomotion can be used. The coordination of single responses of different trigger zones is probably situated below the upper brain stem.The nature of the components of reflex creeping offers a possibility of systematically enhancing motor development from the perinatal age, i.e. in pathological cases where the central pathological motor development may be expected to occur.The activation of the final common path—in cases of peripheral paresis—may be achieved from different parts of the whole coordination complex.In cases of C.P. (spastics, athetotics, atonics) — where the lowest stages of postural ontogenesis are notoriously affected — these stages are incorporated phylogenetically in a form of reflex creeping. Thus we ensure better conditions for the spontaneous development of acral motor movements. In these cases, without reflex creeping, development of the first physiological (ontogenetical) stage of locomotion—crawling — is impossible.

     

Tissue oxygenation index measured using spatially resolved spectroscopy correlates with changes in cerebral blood flow in newborn lambs

Background/Objective  Abnormal cerebral haemodynamics in very preterm infants undergoing neonatal intensive care have been associated with adverse outcome, but cerebral blood flow (CBF) is difficult to assess at the cotside. Spatially resolved spectroscopy (SRS) continuously measures cerebral tissue oxygen saturation expressed as tissue oxygenation index (TOI, %), and TOI would reflect changes in CBF with constant cerebral metabolic demand. We aimed to evaluate the relationship between simultaneous measurements of CBF (Transonic System) and TOI (Hamamatsu NIRO-200) in newborn lambs (n = 8). We hypothesised that alterations in CBF of different magnitudes and frequencies would be reflected as changes of TOI in both time domain and frequency domain analyses. Methods  A silicon cuff positioned around the common brachiocephalic artery was inflated to induce 10–30% reductions in cerebral perfusion pressure so as to produce mild-to-moderate variations of CBF. Relationships between changes in CBF and TOI were evaluated in the time domain (Pearson correlation) and frequency domain (Coherence). Results  In time domain analysis, there was significant correlation between ΔTOI (%) and ΔCBF (%) (R ² = 0.69, P < 0.001). In frequency domain analysis, CBF-TOI coherence was ≥0.5 at frequencies below 0.1 Hz, but <0.5 at higher frequencies. Conclusions  We conclude that overall TOI changes are concordant with CBF variations, when arterial oxygen saturation and cerebral oxygen consumption are constant. While TOI reflects CBF, it is more sensitive to variations of CBF of low frequency (<0.1 Hz) than to more rapid, higher frequency changes.     

Characteristics of the ventilatory response in subjects susceptible to high altitude pulmonary edema during acute and prolonged hypoxia

The present study compares the changes in ventilation in response to sustained hypobaric hypoxia and acute normobaric hypoxia between subjects susceptible to high altitude pulmonary edema (HAPE-S) and control subjects (C-S). Seven HAPE-S and five C-S were exposed to simulated high altitude of 4000 m for 23 h in a hypobaric chamber. Resting minute ventilation (V(E)), tidal volume (V(T)), and respiratory frequency (f(R)), as well as the end-tidal partial pressures of oxygen (P(ET(O2))) and carbon dioxide (P(ET(CO2))) were measured in all subjects sitting in a standardized position. Six measurement periods were recorded: ZH1 at 450 m at Zurich level, HA1 on attaining 3600 m altitude, HA2 after 20 min at 4000 m, HA3 after 21 h and HA4 after 23 h at 4000 m altitude, and ZH2 immediately after recompression to Zurich level. At ZH1 and HA3, the measurements were first done in lying, then in sitting, and afterwards in standing. Peripheral arterial oxygen saturation (Sa(O2)) was continuously recorded. All respiratory parameters were also measured during exercise lasting 30 min, the work load being 50% of maximal oxygen consumption (V(O2max)) at Zurich level and 26% of the Zurich V(O2max) at 4000 m. V(E), P(ET(O2)) and P(ET(CO2)) did not significantly differ between HAPE-S and C-S at rest and during exercise periods at Zurich level and at high altitude. However, Sa(O2) was significantly lower in HAPE-S than in C-S at rest and during exercise at 4000 m. Breathing through the mouthpiece during ventilation measurements increased significantly the Sa(O2) in HAPE-S in posture tests at HA3. This effect was most pronounced in the supine posture, in which HAPE-S had the lowest Sa(O2) values. These data provide evidence that (1) gas exchange might be impaired on the level of ventilation-perfusion mismatch or due to diffusion limitation in HAPE-S during the first 23 h of exposure to a simulated altitude of 4000 m, and (2) contrary to C-S, the Sa(O2) in HAPE-S is significantly affected by body position and by mouthpiece breathing.     

Evidence for two senescence loci on human chromosome I

Microcell-mediated introduction of a neo-tagged human chromosome I (HC-1-neo) into several immortal cell lines has previously been shown to induce growth arrest and phenotypic changes indicative of replicative senescence. Somatic cell hybridization studies have localized senescence activity for immortal hamster 10W-2 cells to a cytogenetically defined region between 1q23 and the q terminus. Previous microcell-mediated chromosome transfer experiments showed that a chromosome 1 with an interstitial q-arm deletion (del-1q) lacks senescence inducing activity for several immortal human cell lines that are sensitive to an intact HC-1-neo. In contrast, our studies reveal that the del-1q chromosome retains activity for 10W-2 cells, indicating that there are at least two senescence genes on human chromosome 1. Sequence-tagged site (STS) content analysis revealed that the q arm of the del-1q chromosome has an interstitial deletion of approximately 63 centimorgans (cM), between the proximal STS marker D1S534 and distal marker D1S412, approximately 1q12 to 1q31. This deletion analysis provides a candidate region for one of the senescence genes on 1q. In addition, because this deletion region extends distally beyond 1q23, it localizes the region containing a second senescence gene to approximately 1q31-qter, between D1S422 and the q terminus. STS content analysis of a panel of 11 10W-2 microcell hybrid clones that escaped senescence identified 2 common regions of loss of 1q material below the distal breakpoint of del-1q. One region is flanked by markers D1S459 and ACTN2, and the second lies between markers W1-4683 and D1S1609, indicating that the distal 1q senescence gene(s) localizes within 1q42-43. Genes Chromosom Cancer 16:55–63 (1996). © 1996 Wiley-Liss, Inc.