Symptoms after sport-related concussions alter gestural functions.

OBJECTIVES: Symptoms after sport-related concussions (SRC) are common. Because post-concussion symptoms are often not clearly visible, speech-accompanying gestures may help clinicians to gain additional information about the patient's history and symptoms during medical consultation. We hypothesized that athletes with SRC and who suffered from persisting symptoms would display more gestures during concussion assessment protocols when compared to non-concussed athletes because of the athletes' previous motor-sensory experiences made during the concussive event. DESIGN: A retrospective cross-sectional study. METHODS: Three matched groups of 40 (active) athletes were investigated in the context of concussion assessment (/and baseline) protocols: 14 symptomatic and 14 asymptomatic athletes with a SRC, and 12 non-concussed athletes. Certified raters using a standard analysis system for nonverbal behaviour analysed videotaped hand movements and gestures during a standardized concussion assessment protocol. RESULTS: Symptomatic athletes spent significantly more time with in space hand movements, i.e., movements that act in the body-external free space without touching anything and specifically, motion quality presentation gestures than non-concussed athletes. CONCLUSIONS: Increased in space movements, which are functionally gestures, and specifically, motion quality presentation gestures in symptomatic athletes indicate that the more vivid sensory motor experience of the head trauma is reflected in more gestural expressions. Thus, hand movements and gestures differentiate athletes who suffer from post-concussion symptoms from non-concussed athletes indicating the athletes' motor-sensory experiences of the event and its aftereffects. The present study highlights the fact that gestures can be employed as behavioural markers of symptoms after sport-related concussions.

Preconditioning with diazoxide prevents reoxygenation-induced rigor-type hypercontracture.

Ischemic preconditioning has a powerful protective potential against a reperfusion-induced injury of the post-ischemic myocardium. Cardiomyocyte hypercontracture, i.e. excessive cell shortening, is an essential mechanism of the reperfusion-induced injury. Rigor contracture, i.e. Ca(2+)-independent contracture, has been shown to be an import component of the reperfusion-induced hypercontracture. Since rigor contracture is dependent on the rapidity of the metabolic recovery during reoxygenation, we hypothesized that preconditioning of the cardiomyocyte mitochondria may improve mitochondrial function to restore the energy balance during the initial phase of reoxygenation and may thus prevent rigor contracture. For this purpose adult rat cardiomyocytes were exposed to anoxia with subsequent reoxygenation. For preconditioning, cells were pre-treated with the mitochondrial ATP-sensitive K(+) channel opener diazoxide. Pre-treatment with 100 micromol/l diazoxide significantly reduced the reoxygenation-induced hypercontracture of cardiomyocytes due to an attenuation of the Ca(2+)-independent rigor-type contracture, which was accompanied by an acceleration of the phosphocreatine resynthesis during the initial phase of reoxygenation. Treatment with the mitochondrial ATP-sensitive K(+) channel antagonist 5-hydroxydecanoate (500 micromol/l) during preconditioning phase abolished these protective effects. Similarly, partial suppression of the mitochondrial function with 100 micromol/l NaCN during the reoxygenation phase abolished the diazoxide effects. Finally, in isolated rat hearts, preconditioning with diazoxide prior to global ischemia significantly improved left ventricular function and attenuated hypercontracture during reperfusion. This effect could be abolished by the treatment with 100 micromol/l NaCN during reperfusion. Taken together, pharmacological preconditioning of cardiomyocytes with diazoxide protects against the reoxygenation-induced rigor hypercontracture due to an improvement of the energy recovery at the onset of reoxygenation.

Tumor necrosis factor-alpha at acute myocardial infarction in rats and effects on cardiac fibroblasts.

Tumor necrosis factor-alpha (TNF-alpha) biosynthesis by the myocardium in response to several diseases has not been solely associated with activation of the immune system but may also serve as a stress response in the context of neurohumoral gene activation. In this regard, beneficial as well as adverse effects of the cytokine on injured myocardium have been reported. TNF-alpha has been suggested to modulate myocyte and fibroblast cell growth and function. Now, in a rat model of acute myocardial infarction TNF-alpha expression and effects on cardiac fibroblast were determined. TNF-alpha was detected in rat hearts with acute myocardial infarction, parallel to the presence of proliferating fibroblasts, at the border zone of the infarct region, to a lesser degree in the infarct zone and was still present in the surviving myocardium. Similarly, the TNF-alpha mRNA level was, compared to sham-operated heart, higher in the infarct area. In the remote myocardium, a trend to an elevated TNF-alpha mRNA level was observed. TNF-alpha stimulated proliferation and expression of fibronectin in fibroblasts isolated from the infarct, non-infarct-region and sham-operated hearts. Angiotensin II is mitogenic for fibroblasts post-myocardial infarction and effects might be mediated indirectly by TNF-alpha. Addition of a neutralising anti-TNF-alpha antibody inhibited angiotensin II stimulated proliferation of fibroblasts only from the infarcted myocardium. The regional differences in TNF-alpha protein and mRNA levels, parallel to proliferating fibroblasts and proliferative effects may foster the reparative, reactive and adverse post-infarct remodeling of the heart.

[Severe course of an infection with Leptospira grippotyphosa (author's transl)]. / Foudroyanter Verlauf einer Infektion mit Leptospira grippotyphosa

In a 22 years old female patient severe jaundice, renal failure and myocarditis developed 3 days after the onset of fever and other uncharacteristic symptoms. In dark-field microscopy leptospires were found. Inspite of high-dose penicillin therapy exitus letalis occurred in myocardial and circulatory failure, due to a severe interstitial myocarditis. Leptospira grippotyphosa could be proven serologically as the causative bacterium. It is pointed out, that leptospirosis inspite of their rare occurrence should be included in the differential diagnosis of infections of undetermined origin, especially if jaundice develops. The demonstration of leptospira in blood, cerebro-spinal fluid or urin by means of darkfield microscopy may quickly support the diagnosis. Since the course of severe leptospirosis can be influenced significantly only up to the 4th day after the onset, high-dose penicillin G or tetracycline therapy should be initiated already when the clinical suspicion is present.