The Application of Biological Feedback in the Rehabilitation of Patients after Ischemic Stroke.

Balance disorders are the main concern for patients after an ischemic stroke. They are caused by an abnormal force on the affected side or paresis, which causes uneven loading and visuospatial disorders. Minimizing the effects of stroke is possible through properly conducted rehabilitation. One of the known ways to achieve this objective is biological feedback. The lack of proper muscle tone on one side of the body is manifested by the uneven pressure of the lower extremities on the ground. The study and control groups were composed of two equal groups of 92 people each, in which the same set of kinesiotherapeutic exercises were applied. Patients in the study group, in addition to standard medical procedures, exercised five days a week on a Balance Trainer for four weeks. The examination and training with the device were recorded on the first day of rehabilitation, as well as after two and four weeks of training. The assessment was performed using the following functional tests and scales: Brunnström, Rankin, Barthel, Ashworth, and VAS. Patients in the control group started exercising on the Balance Trainer two weeks after the first day of rehabilitation using traditional methods. The study results reveal statistically significant reductions in the time the body's center of gravity (COG) spent in the tacks, outside the tracks and in the COG distance, lower COG excursions in all directions. Post-stroke patients that received biofeedback training presented significantly better results than patients that did not receive such training.

[Caffeinol: a neuroprotective action in ischemic brain damage]. / Kafeinol: dzialanie neuroprotekcyjne w udarze niedokrwiennym mózgu.

Caffeinol--a combination of ethanol and caffeine in appropriate concentrations--exerts neuroprotective and anticonvulsive action. Research conducted on rats in models of ischemic brain damage have shown that caffeinol decreases the size of cortical damage by about 80%, improves motional coordination and memory. The sooner caffeinol was administered, the better were beneficial therapeutic effects. What is more, the medicine may be safely combined with other methods used in stroke treatment, such as hypothermia and thrombolysis, what additionally increases its neuroprotective influence. Research on people have shown that caffeinol is less effective as neuroprotective agent in patients abusing alcohol, while chronic intake of caffeine does not influence its activity. Mechanism of its activity is not known yet, however, it is assumed that it bases on an antagonism of NMDA receptors. Regarding the fact that the most of strokes in humans concern subcortical areas, it is justified to conduct further research on caffeinol, which would involve other brain structures, thus allowing to define its use in clinical practice.

Kynurenic acid as the neglected ingredient of commercial baby formulas.

The global increase in resorting to artificial nutritional formulas replacing breastfeeding has been identified among the complex causes of the obesity epidemic in infants and children. One of the factors recently recognized to influence metabolism and weight gain is kynurenic acid (KYNA), an agonist of G protein-coupled receptor (GPR35). Therefore the aim of the study was to determine the concentration of KYNA in artificial nutritional formulas in comparison with its level in human breast milk and to evaluate developmental changes in rats exposed to KYNA enriched diet during the time of breastfeeding. KYNA levels were measured in milk samples from 25 heathy breast-feeding women during the first six months after labor and were compared with 21 time-adjusted nutritional formulas. Animal experiments were performed on male Wistar rats. KYNA was administered in drinking water. The content of KYNA in human milk increases more than 13 times during the time of breastfeeding while its level is significantly lower in artificial formulas. KYNA was detected in breast milk of rats and it was found that the supplementation of rat maternal diet with KYNA in drinking water results in its increase in maternal milk. By means of the immunoblotting technique, GPR35 was evidenced in the mucosa of the jejunum of 1-day-old rats and distinct morphological changes in the jejunum of 21-day-old rats fed by mothers exposed to water supplemented with KYNA were found. A significant reduction of body weight gain of rats postnatally exposed to KYNA supplementation without changes in total body surface and bone mineral density was observed. The rat offspring fed with breast milk with artificially enhanced KYNA content demonstrated a lower mass gain during the first 21 days of life, which indicates that KYNA may act as an anti-obesogen. Further studies are, therefore, warranted to investigate the mechanisms regulating KYNA secretion via breast milk, as well as the influence of breast milk KYNA on mass gain. In the context of lifelong obesity observed worldwide in children fed artificially, our results imply that insufficient amount of KYNA in baby formulas could be considered as one of the factors associated with increased mass gain.

On the toxicity of kynurenic acid in vivo and in vitro.

BACKGROUND: Kynurenic acid (KYNA), a tryptophan metabolite is an antagonist of ionotropic glutamate receptors and alpha-7 nicotinic receptor. Moreover, it is an agonist of G-protein receptor GPR35. Its neuroprotective, anticonvulsant, anti-inflammatory and antioxidant activity was documented. KYNA is present in food and herbal medicines. However, the data on effects induced by a long-lasting treatment with KYNA is lacking. The aim of the study was the assessment of toxicity of a prolonged administration of KYNA in rodents. The cytotoxicity of KYNA in vitro was also examined. METHODS: Adult mice and rats were used. KYNA was administered in the drinking water in concentrations of 25 or 250mg/L for 3-21 days. The following cells were cultured in an in vitro study: mouse fibroblast (NIH/3T3), green monkey kidney cells and primary chick embryo cells (CECC). Cell viability was determined with methyl thiazol tetrazolium reduction assay, neutral red uptake assay and lactate dehydrogenase leakage assay. RESULTS: KYNA affected neither body gain nor body composition. Blood counts were also unaffected. The viability of cells in the culture was lowered at high millimolar concentrations of KYNA. An elevated viability of GMK and CECC cells was detected in the presence of KYNA in micromolar concentrations. CONCLUSIONS: The obtained results showed that a long-term application of KYNA in the drinking water is well-tolerated by rodents. No evidence of a toxic response was recorded. Achieved results indicate that diets containing a high amount of KYNA or enriched with KYNA should not cause any risk to the human health.

Cytisine inhibits the anticonvulsant activity of phenytoin and lamotrigine in mice.

BACKGROUND: Cytisine (CYT), the most commonly used drug for smoking cessation in Poland, was experimentally found to induce convulsions. There is a lack of studies on the influence of CYT on the anticonvulsant activity of antiepileptic drugs (AEDs). METHODS: The effects of CYT on the anticonvulsant activity of six AEDs were examined in maximal electroshock (MES)-induced seizures in mice. RESULTS: Single intraperitoneal (ip) administration of CYT in a subthreshold dose of 2 mg/kg antagonized the protective activity of ip phenytoin and lamotrigine against MES-induced seizures in mice. A dose of 1 mg/kg did not reverse the protective activity of phenytoin and lamotrigine. CYT in a dose of 2 mg/kg had no effect on the anticonvulsive activity of carbamazepine, oxcarbazepine, phenobarbital, and valproate magnesium. CONCLUSION: CYT ability to antagonize the anticonvulsive activity of phenytoin and lamotrigine can be of serious concern for epileptic smokers, who might demonstrate therapeutic failure to these drugs resulting in possible breakthrough seizure attacks.