scholarly journals Recovery of function from septal damage and the growth of sympathohippocampal fibers

1982 ◽  
Vol 10 (4) ◽  
pp. 391-398 ◽  
Author(s):  
M. D. Chafetz ◽  
S. Evans ◽  
F. H. Gage
Keyword(s):  
Recovery Of Function ◽  
Septal Damage

Infarct Size, Myocardial Hemorrhage, and Recovery of Function After Mechanical Versus Pharmacological Reperfusion

Circulation ◽  
1997 ◽  
Vol 96 (2) ◽  
pp. 659-666 ◽  
Author(s):  
Sorin V. Pislaru ◽  
Laurentino Barrios ◽  
Tony Stassen ◽  
Lin Jun ◽  
Cristina Pislaru ◽  
...  
Keyword(s):  
Infarct Size ◽  
Recovery Of Function ◽  
Myocardial Hemorrhage

scholarly journals Neural correlates of memory recovery: Preliminary findings in children and adolescents with acquired brain injury

2021 ◽  
Vol 39 (1) ◽  
pp. 61-71
Author(s):  
Anne-Laure Mouthon ◽  
Andreas Meyer-Heim ◽  
Reto Huber ◽  
Hubertus J.A. Van Hedel
Keyword(s):  
Brain Injury ◽  
Spectral Power ◽  
Recovery Of Function ◽  
Acquired Brain Injury ◽  
Neural Correlates ◽  
Sleep Eeg ◽  
Brain Maturation ◽  
Brain Areas ◽  
Memory Recovery ◽  
Posterior Parietal

Background: After acquired brain injury (ABI), patients show various neurological impairments and outcome is difficult to predict. Identifying biomarkers of recovery could provide prognostic information about a patient’s neural potential for recovery and improve our understanding of neural reorganization. In healthy subjects, sleep slow wave activity (SWA, EEG spectral power 1–4.5 Hz) has been linked to neuroplastic processes such as learning and brain maturation. Therefore, we suggest that SWA might be a suitable measure to investigate neural reorganization underlying memory recovery. Objectives: In the present study, we used SWA to investigate neural correlates of recovery of function in ten paediatric patients with ABI (age range 7–15 years). Methods: We recorded high-density EEG (128 electrodes) during sleep at the beginning and end of rehabilitation. We used sleep EEG data of 52 typically developing children to calculate age-normalized values for individual patients. In patients, we also assessed every-day life memory impairment at the beginning and end of rehabilitation. Results: In the course of rehabilitation, memory recovery was paralleled by longitudinal changes in SWA over posterior parietal brain areas. SWA over left prefrontal and occipital brain areas at the beginning of rehabilitation predicted memory recovery. Conclusions: We show that longitudinal sleep-EEG measurements are feasible in the clinical setting. While posterior parietal and prefrontal brain areas are known to belong to the memory “core network”, occipital brain areas have never been related to memory. While we have to remain cautious in interpreting preliminary findings, we suggest that SWA is a promising measure to investigate neural reorganization.

Dobutamine responsiveness, PET mismatch, and lack of necrosis in low-flow ischemia: is this hibernation in the isolated rat heart?

2003 ◽  
Vol 285 (1) ◽  
pp. H316-H324 ◽  
Author(s):  
Richard Southworth ◽  
Pamela B. Garlick
Keyword(s):  
Rat Heart ◽  
Recovery Of Function ◽  
Electron Microscopic Examination ◽  
Left Ventricular ◽  
Isolated Rat Heart ◽  
Low Flow ◽  
Hibernating Myocardium ◽  
Heart Model ◽  
Electron Microscopic ◽  
Isolated Rat

The clinical hallmarks of hibernating myocardium include hypocontractility while retaining an inotropic reserve (using dobutamine echocardiography), having normal or increased [18F]fluoro-2-deoxyglucose-6-phosphate (18FDG6P) accumulation associated with decreased coronary flow [flow-metabolism mismatch by positron emission tomography (PET)], and recovering completely postrevascularization. In this study, we investigated an isolated rat heart model of hibernation using experimental equivalents of these clinical techniques. Rat hearts ( n = 5 hearts/group) were perfused with Krebs-Henseleit buffer for 40 min at 100% flow and 3 h at 10% flow and reperfused at 100% flow for 30 min (paced at 300 beats/min throughout). Left ventricular developed pressure fell to 30 ± 8% during 10% flow and recovered to 90 ± 7% after reperfusion. In an additional group, this recovery of function was found to be preserved over 2 h of reperfusion. Electron microscopic examination of hearts fixed at the end of the hibernation period demonstrated a lack of ischemic injury and an accumulation of glycogen granules, a phenomenon observed clinically. In a further group, hearts were challenged with dobutamine during the low-flow period. Hearts demonstrated an inotropic reserve at the expense of increased lactate leakage, with no appreciable creatine kinase release. PET studies used the same basic protocol in both dual- and globally perfused hearts (with 250MBq18FDG in Krebs buffer ± 0.4 mmol/l oleate). PET data showed flow-metabolism “mismatch;” whether regional or global,18FDG6P accumulation in ischemic tissue was the same as (glucose only) or significantly higher than (glucose + oleate) control tissue (0.023 ± 0.002 vs. 0.011 ± 0.002 normalized counts · s-1· g-1· min-1, P < 0.05) despite receiving 10% of the flow. This isolated rat heart model of acute hibernation exhibits many of the same characteristics demonstrated clinically in hibernating myocardium.

Rate of Recovery of Taste Function after Preservation of Chorda Tympani Nerve in Middle Ear Surgery with Special Reference to Type of Disease

2003 ◽  
Vol 112 (1) ◽  
pp. 52-56 ◽  
Author(s):  
Masafumi Sakagami ◽  
Mieko Sone ◽  
Keijiro Fukazawa ◽  
Kojiro Tsuji ◽  
Yasuo Mishiro
Keyword(s):  
Recovery Of Function ◽  
Inflammatory Diseases ◽  
Chronic Otitis Media ◽  
Normal Function ◽  
Middle Ear Surgery ◽  
Chorda Tympani ◽  
Chorda Tympani Nerve ◽  
Taste Disturbance ◽  
Postoperative Symptoms ◽  
Rate Of Recovery

To study the recovery of function of the chorda tympani nerve, we examined by electrogustometry 79 patients (83 ears) with both preoperative normal function of the nerve and operative preservation of the nerve, every 2 days during hospitalization and at 6 months after surgery. For symptoms such as tongue numbness and taste disturbance, patients with noninflammmatory (NI) diseases (13/20 or 65.0%) showed a significantly higher rate of symptoms than did patients with chronic otitis media (COM; 13/35 or 37.1%) at 2 weeks after surgery (p = .032). The patients with NI diseases (5/20 or 25.0%) tended to show a higher rate of symptoms than did the COM patients (2/35 or 5.7%) or cholesteatoma patients (2/28 or 7.1%) at 6 months after surgery. The rate of recovery of the EGM threshold to normal at 2 weeks after surgery was significantly lower in NI disease patients (6/20 or 30.0%) than in COM patients (23/ 35 or 62.9%) or cholesteatoma patients (19/28 or 67.9%; p = .015 and .008, respectively). Thus, the patients with NI diseases had postoperative symptoms and elevation of EGM threshold more frequently than did the patients with inflammatory diseases.

Molecular and Cellular Mechanisms of Myocardial Stunning

1999 ◽  
Vol 79 (2) ◽  
pp. 609-634 ◽  
Author(s):  
Roberto Bolli ◽  
Eduardo Marbán
Keyword(s):  
Free Radical ◽  
Myocardial Stunning ◽  
Recovery Of Function ◽  
Myocardial Dysfunction ◽  
Calcium Overload ◽  
Global Ischemia ◽  
Stunned Myocardium ◽  
Common Mechanism ◽  
Regional Ischemia

The past two decades have witnessed an explosive growth of knowledge regarding postischemic myocardial dysfunction or myocardial “stunning.” The purpose of this review is to summarize current information regarding the pathophysiology and pathogenesis of this phenomenon. Myocardial stunning should not be regarded as a single entity but rather as a “syndrome” that has been observed in a wide variety of experimental settings, which include the following: 1) stunning after a single, completely reversible episode of regional ischemia in vivo; 2) stunning after multiple, completely reversible episodes of regional ischemia in vivo; 3) stunning after a partly reversible episode of regional ischemia in vivo (subendocardial infarction); 4) stunning after global ischemia in vitro; 5) stunning after global ischemia in vivo; and 6) stunning after exercise-induced ischemia (high-flow ischemia). Whether these settings share a common mechanism is unknown. Although the pathogenesis of myocardial stunning has not been definitively established, the two major hypotheses are that it is caused by the generation of oxygen-derived free radicals (oxyradical hypothesis) and by a transient calcium overload (calcium hypothesis) on reperfusion. The final lesion responsible for the contractile depression appears to be a decreased responsiveness of contractile filaments to calcium. Recent evidence suggests that calcium overload may activate calpains, resulting in selective proteolysis of myofibrils; the time required for resynthesis of damaged proteins would explain in part the delayed recovery of function in stunned myocardium. The oxyradical and calcium hypotheses are not mutually exclusive and are likely to represent different facets of the same pathophysiological cascade. For example, increased free radical formation could cause cellular calcium overload, which would damage the contractile apparatus of the myocytes. Free radical generation could also directly alter contractile filaments in a manner that renders them less responsive to calcium (e.g., oxidation of critical thiol groups). However, it remains unknown whether oxyradicals play a role in all forms of stunning and whether the calcium hypothesis is applicable to stunning in vivo. Nevertheless, it is clear that the lesion responsible for myocardial stunning occurs, at least in part, after reperfusion so that this contractile dysfunction can be viewed, in part, as a form of “reperfusion injury.” An important implication of the phenomenon of myocardial stunning is that so-called chronic hibernation may in fact be the result of repetitive episodes of stunning, which have a cumulative effect and cause protracted postischemic dysfunction. A better understanding of myocardial stunning will expand our knowledge of the pathophysiology of myocardial ischemia and provide a rationale for developing new therapeutic strategies designed to prevent postischemic dysfunction in patients.

Effects of septal damage and ovariectomy on feeding, drinking and body weight

1978 ◽  
Vol 3 (5) ◽  
pp. 457-466 ◽  
Author(s):  
Paula J. Geiselman ◽  
C.Robert Almli
Keyword(s):  
Body Weight ◽  
Septal Damage

Septal lesions and the recovery of function in the juvenile hamster

1976 ◽  
Vol 16 (4) ◽  
pp. 445-452 ◽  
Author(s):  
William B. Janzen ◽  
B.N. Bunnell
Keyword(s):  
Recovery Of Function ◽  
Septal Lesions

Interhemispheric Competition After Stroke: Brain Stimulation to Enhance Recovery of Function of the Affected Hand

2009 ◽  
Vol 23 (7) ◽  
pp. 641-656 ◽  
Author(s):  
Dennis A. Nowak ◽  
Christian Grefkes ◽  
Mitra Ameli ◽  
Gereon R. Fink
Keyword(s):  
Brain Stimulation ◽  
Motor Behavior ◽  
Cortical Excitability ◽  
Recovery Of Function ◽  
Repetitive Transcranial Magnetic Stimulation ◽  
Hand Function ◽  
Clinical Effects ◽  
Sensorimotor Network ◽  
Interhemispheric Competition ◽  
Plastic Changes

Background and purpose. Within the concept of interhemispheric competition, technical modulation of the excitability of motor areas in the contralesional and ipsilesional hemisphere has been applied in an attempt to enhance recovery of hand function following stroke. This review critically summarizes the data supporting the use of novel electrophysiological concepts in the rehabilitation of hand function after stroke. Summary of review. Repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are powerful tools to inhibit or facilitate cortical excitability. Modulation of cortical excitability may instantaneously induce plastic changes within the cortical network of sensorimotor areas, thereby improving motor function of the affected hand after stroke. No significant adverse effects have been noted when applying brain stimulation in stroke patients. To date, however, the clinical effects are small to moderate and short lived. Future work should elucidate whether repetitive administration of rTMS or tDCS over several days and the combination of these techniques with behavioral training (ie, physiotherapy) could result in an enhanced effectiveness. Conclusion. Brain stimulation is a safe and promising tool to induce plastic changes in the cortical sensorimotor network to improve motor behavior after stroke. However, several methodological issues remain to be answered to further improve the effectiveness of these new approaches.

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