Dysphagia in children with infantile cerebral palsy.

PURPOSE: Dysphagia is a significant health problem in children with infantile cerebral palsy (ICP), but not frequently discussed in the literature. The study objective was to analyse dysphagia symptoms in children with a pyramidal form of ICP, including the oral and pharyngeal phases of deglutition and dysarthria severity. We searched for a correlation between dysphagia severity and ICP type, mental development and occurrence of epilepsy. MATERIAL AND METHODS: A total of 67 children with a pyramidal form of infantile cerebral palsy were studied. Data were obtained based on case history elicited from the mothers, analysis of medical and psychological documentation, and logopaedic examination, including an examination of the action of swallowing. RESULTS: Dysphagia symptoms were found in 41 (61%) studied children, most frequently referring only to the oral phase (25 children), with concomitant mild and moderate dysarthria. Oral and pharyngeal dysfunctions were observed in 14 children and coexisted with more pronounced dysarthria symptoms. The most severe disorders were mainly found in the pharyngeal phase in 2 children. A statistically significant correlation was noted between the severity of dysphagia symptoms and the ICP type (p<0.044) and mental development (p<0.00002). CONCLUSIONS: Swallowing dysfunctions occur in the majority of children (>50%) with ICP. More serious disorders involving the oral and pharyngeal phases mainly affect children with tetraplegia and profound mental impairment. These disorders continue from early infancy through childhood and adolescence and improvement has been mainly observed when only the oral phase of swallowing is affected. These are always accompanied by dysarthria symptoms, which are especially severe when dysphagia involves the oral and pharyngeal phases. Early assessment and stimulation of the swallowing function should be a common element in the rehabilitation and care of children with ICP.

Topiramate as a neuroprotectant in the experimental model of febrile seizures.

PURPOSE: The aim of the study wad to estimate a potentially neuroprotective effect of topiramate (TPM) in the experimental model of FS. MATERIAL AND METHODS: 24 young male rats divided in 4 groups were involved in the study. Febrile seizures were induced by placing the animals in 45 degrees C warm water bath for four consecutive days. TPM at the dose 80 mg/kg b.m. was administered: before the FS and immediately after the FS. FS group and control rats received only normal saline. Thereafter hippocampal slices were prepared to performing histological and morphometric examination. RESULTS: Morphometric investigations revealed that FS caused death of 60% of the neurons in sector CA1 and a half of them in sector CA3. Histological examinations of hippocampal slices showed that TPM at a dose of 80 mg/kg b.m., administered before the seizures, considerably improved CA1 and CA3 pyramidal cell survival. Similar neuroprotective effect, but in a markedly lesser degree was observed when TPM was administrated after the FS. CONCLUSIONS: Our findings seem to confirm that FS exert a strong destructive effect on the sensitive hippocampal neurons and on the neuroprotective properties of TPM in this process, which may have practical implications. It can be assumed that in children with recurrent and prolonged FS, prophylactic drug administration could prevent hippocampal sclerosis and development of symptomatic epilepsy.

Neurophysiologic studies of brain plasticity in children with cerebral palsy.

The mechanisms of brain plasticity include: a change in the balance of excitation and inhibition; a long-term potentiation or long-term depression; a change in neuronal membrane excitability; the anatomical changes-formation of new axon terminals and new synapses. There are few tools for brain plasticity investigations. The utility of the neurophysiologic in the determination of brain reorganization and repair in patients with cerebral palsy (CP) are described. The authors discuss also their results of quantitative EEG, visual evoked potentials (VEPs) and somatosensory evoked potentials (SEPs) in children with CP. They showed the existence of brain reorganization and repair in children with CP.

Neuroprotection possibilities in epileptic children.

PURPOSE: The aim of this paper was to summarize of current knowledge about neuronal injuries during epileptogenesis process and possibilities of neuroprotection. RESULTS: Many of agents from a wide range of classes have been proposed to possess neuroprotective potential, but especially in experimental and preclinical conditions. Among the antiepileptic drugs topiramate (TPM) and levetiracetam (LEV) possess neuroprotective effects in experimental models of brain damage. Promising protection against cell loss display antioxidants and neurotrophins. CONCLUSIONS: Important and difficult problem of neuroprotective therapy in childhood epilepsy require further experimental and clinical investigations.

[Studies of damaged processes in the nervous system and possibilities of neuroprotection]. / Badania procesów uszkodzenia ukladu nerwowego i mozliwosci neuroprotekcji.

The paper presents the results of experimental studies and clinical trials associated with mechanism underlying nervous system damage and pharmacological interventions to be employed in such processes. Abnormal lipid peroxidation was demonstrated in experimental seizures, epilepsy and cerebral stroke. The authors presented the mechanism of calcium channel blockers activity in epilepsy and their experience in employing such agents in epileptic patients. Results of studies on S-100 protein determinations as a marker of the blood-brain barrier damage in epilepsy and hydrocephalus were discussed, along with the employment of evoked potentials in diagnostic management of headaches and the effects of complex treatment of epilepsy in children using Nootropil. Selected data on experimental valproate encephalopathy were also presented. The authors believe that these studies contribute to the understanding of mechanism that are responsible for nervous system dysfunction, as well as to the evaluation and treatment of their effects.

Role of NMDA receptor in the effects of arginine-vasopressin on memory processes.

The mechanism of facilitatory action of vasopressin on memory processes, dependent probably on different neurotransmitter systems, remains unclear. We decided to study the interactions between arginine-vasopressin and ionotropic NMDA receptor. We estimated the influence of various antagonists of NMDA receptor on beneficial effect of arginine-vasopressin on consolidation of conditioned avoidance responses and on retrieval of memory in passive avoidance situation. We have shown that effect of vasopressin on consolidation is significantly reduced by noncompetitive antagonist of ion channel in the NMDA receptor--dizocilpine (MK-801) and competitive antagonist of glycine recognization site--HA-966. Distinctly, effect of the peptide on retrieval is decreased by competitive antagonist of glutamate recognition site--AP-7, competitive antagonist of polyamines site-arcaine and noncompetitive antagonist--MK-801. This suggests that NMDA receptor may participate in the action of vasopressin on memory, but it plays different roles in consolidation and retrieval processes.

The estimation of interactions between arginine-vasopressin (AVP) and NMDA receptors in memory and learning processes.

Arginine-vasopressin (AVP) is a neuropeptide which facilitates learning and memory processes. We examinated the participation of NMDA receptors in beneficial effects of peptide. The results of our study show that noncompetitive antagonist of NMDA receptor-MK-801 impairs the effect of AVP on the consolidation of conditioned avoidance responses and antagonist of polyamines site-arcaine reduced advantageous effect of AVP on the retrieval of memory in passive avoidance situation.

The role of NMDA receptors in central action of angiotensin II.

The influence of noncompetitive (MK-801), competitive (AP-7) and the antagonist of polyamines site of NMDA receptor (arcaine) on the central activity of angiotensin II (A II) was studied. The open field test, conditioning of active avoidance responses (CARs) and passive avoidance situation was used to investigate learning and memory in rats. All used antagonists decreased beneficial action of A II on these processes.

Estimation of central activity of hydroxyproline--the amino acid characteristic for collagen degradation products.

The central activity of hydroxyproline - the amino acid characteristic for collagen degradation products was studied. The levels of urinary and serum hydroxyproline are elevated in many disturbances, among them is a mental deficiency connected with hydroxyprolinemia. Previous studies showed that the mixture of collagen degradation products is biologically active and exerts and effect on central nervous system. In our study hydroxyproline significantly decreased the psychomotor activity of rats in Lat's test, enhanced amphetamine stereotypy in lower doses, and enhanced catalepsy in one of used doses. It prolonged the time of thiopental sleeping. The pentylenetetrazole seizures latency was not significantly prolonged and duration of seizures was shorter after injection (icv) of hydroxyproline. Our investigations show, that hydroxyproline is the active amino acid in the mixture of collagen degradation products and may be responsible for central activity of this mixture.

Central activity of peptide Gly-Pro-Hyp--the main component of collagen degradation products mixture.

The effect of tripeptide Gly-Pro-Hyp on the central nervous system was studied. The peptide Gly-Pro-Hyp is a main component of the mixture of collagen type I degradation products obtained by 6-h digestion with bacterial collagenase. The investigated peptide in the doses 1 microgram, 2 micrograms, and 5 micrograms significantly reduces the psychomotor activity of animals, intensifies haloperidol-induced catalepsy and enhances stereotypy behaviour after apomorphine administration. The central activity of Gly-Pro-Hyp is similar to the action of collagen degradation products mixture. This suggests that this peptide may be the active substance responsible for the effects of degradation products of collagen type I.