Demand for neurological services in Central Eastern Europe: a 10-year national survey in Hungary.

BACKGROUND AND PURPOSE: In order to plan neurological capacities at a national level for the next decade, the current use of neurological services should be evaluated. We analyzed the utilization of neurological services in Hungary, a country with a single-payer health insurance system covering the whole population. METHODS: We created a database from medical reports submitted to the National Health Insurance Fund from all hospitals and outpatient services between 2004 and 2013. The number of subjects presenting to the neurological healthcare system and their major diagnoses by 10th International Classification of Diseases categories were analyzed. The overall healthcare service utilization of these patients was also estimated. RESULTS: Of the 10 million inhabitants, 2.9 million people used an inpatient or outpatient neurological service at least once over the 10-year period. Annually, 1% of the population was admitted to neurological inpatient wards and 6% of the population used some neurological outpatient service. Major reasons for using neurological services were: cerebrovascular diseases (I60-I69; 1.2 million patients), episodic and paroxysmal disorders (G40-G47; 1.3 million patients) and general symptoms and signs (R50-R56; 1.3 million patients). The 2.9 million people had 12.7 million hospital admissions to any ward and 365.7 million outpatient visits to any specialist during the 10 years. CONCLUSIONS: The demand for neurological services is high in Hungary; close to 30% of the population used an inpatient or outpatient neurological service at least once during this 10-year period. Results from this project provide data for international comparisons and help to ensure better informed and more focused resource allocation.

Characterization of somatodendritic neuronal nicotinic receptors located on the myenteric plexus.

The effects of nicotine and dimethylphenylpiperazinium (DMPP) on resting and stimulation-evoked release of [3H]-acetylcholine ([3H]ACh) from cholinergic interneurons and neuro-effector neurons of the ileal longitudinal muscle and the responses of the smooth muscle to nicotinic agonists were studied. (-)-Nicotine was 15 times more effective than (+)-nicotine in releasing ACh. Since tetrodotoxin (1 microM) completely antagonized the effect of nicotinic agonists, the site of action of the nicotinic agonists studied was on the somatodendritic nicotinic receptors. The electrical field stimulation-evoked release was not affected by nicotinic agonists and antagonists, indicating that the axon terminals of cholinergic interneurons are not equipped with nicotinic receptors. This preparation proved to be useful to study the effect of nicotinic agonists on somatodendritic receptors, to determine the affinity constants of nicotinic antagonists, and to characterize these receptors. The rank order of antagonists was d-tubocurarine = mecamylamine greater than pipecuronium greater than pancuronium greater than vecuronium greater than hexamethonium; the apparent affinity constants (KD) were 1.15, 1.55, 3.06, 3.98, 13.59 and 32.88 microM, respectively. alpha-Bungarotoxin had no antagonistic activity at all. This finding indicates that nicotine and the endogenous ligand ACh act via a postsynaptic, somatodendritic nicotinic receptor that is pharmacologically similar to those located on the axon terminals of sympathetic neurons or in ganglions, but is dissimilar to those located at the postsynaptic site of the neuromuscular junction.

Comparison of the effects of a bufodienolide and ouabain on neuronal and smooth muscle preparations.

The effect of a bufodienolide (monohydroxy-14,15-epoxy-20,22-dienolide glycoside) purified from toad skin was compared with that of ouabain on 3H-noradrenaline release and on the tension of rabbit pulmonary arterial strips. This compound exerted an ouabain-like activity. The neuronal effects of this bufodienolide derivative on squid axon were also studied and compared with those of ouabain. Both compounds enhanced the resting and stimulation-evoked (2 Hz, 360 shocks) release of 3H-noradrenaline. Moreover, in the presence of either this bufodienolide or ouabain, the tension of the rabbit artery increased gradually, and the contraction evoked by electrical stimulation was potentiated. Both compounds enhanced, in a prazosin-sensitive way, smooth muscle responses to noradrenaline and to electrical stimulation. In higher concentrations, they contracted smooth muscle cells of pulmonary artery, an action which was insensitive to prazosin. The bufodienolide was about 8 times more active in inhibition of 22Na efflux than was ouabain, but did not affect Ca efflux, which is not sensitive to ouabain. It is therefore concluded that compounds with an inhibitory effect on Na+,K(+)-ATPase are able to affect chemical neurotransmission of blood vessels in such a way that in lower concentrations they potentiate the release of noradrenaline, and in higher concentrations they contract directly the smooth muscle. These findings indicate that such compounds if they are present in the circulation might be involved in the physiological regulation of blood pressure or in the genesis of hypertension.

Presynaptic modulation by endogenous ouabain-like substances of noradrenaline release from blood vessels.

The effect of an endogenous ouabain-like compound (OCL) and of ouabain was studied on [3H]noradrenaline release and on the tension of rabbit pulmonary arterial strip. Similarly to ouabain, the OLC enhanced release of [3H] NA in resting and in stimulated condition. Moreover, in the presence of OLC and ouabain, the tension of the rabbit artery increased gradually and the contraction evoked by electrical stimulation was potentiated. It is suggested that this mechanism might be involved in the physiological regulation of blood pressure or in the genesis of hypertension.

Noradrenaline releasing effect of an ouabain-like compound on pulmonary artery.

The effect of ouabain and an endogenous ouabain-like compound (OLC) was studied on (3H)noradrenaline [3H)NA) release from rabbit pulmonary artery. Similarly to ouabain, OLC enhanced the release of (3H)NA in response to electrical stimulation. These findings are the first evidence that OLC is able to act presynaptically and enhance the amount of (3H)NA release per impulse. It is suggested that this mechanism might be involved in the physiological regulation of blood pressure or in the genesis of hypertension.