The development of epilepsy due to disruption of the blood-brain barrier

June 24, 2018 15:30 | Symptoms And Treatment
The metabolism between the central nervous system and other physiological systems is carried out primarily through the blood-brain barrier. This is the transfer of oxygen. The way of supplying the liquid and those substances that can not penetrate this barrier, lies through the hematopoietic barrier. The blood-brain barrier is localized in the endothelial membrane facing the lumen of the vessels.

Based on a series of experiments with intravenous and subcutaneous injection of trypan blue, experts believe that, in addition to blood-brain and hematopoietic barriers, there is a peripheral external system of cerebrospinal fluid barriers, which prevents the flow of colorant from borderline cerebral and spinal zones, whose vessels do not perform any barrier functions, insubarachnoid space. Both barriers are closely related, since the composition of the CSF is mainly determined between the cellular fluid of the brain tissue. An intact blood-brain barrier lets only a small part of the blood substances in the brain tissue, regulates the metabolism between the blood and the central nervous system, and thereby provides the brain with plastic and energy resources. The throughput capacity of this barrier in different parts of the brain is different: it passes for coarse-grained colloids, for example fats and proteins, and also for gases such as CO2, O2, for anions of bromine type, for alkaline dyes. The intact blood-brain barrier is impenetrable for H and OH ions, for such highly dispersed colloids as methylene blue, for cations. Sodium, potassium, magnesium and calcium become due to the connection with phosphates and other compounds soluble in lipoids and therefore can penetrate the blood-brain barrier.

The dysfunction of this barrier, which, apparently, is associated with various kinds of cerebral complications, is expressed primarily in increased permeability. This permeability is abnormally high in newborns, but it is still quite high in older children. The increased permeability of the blood-brain barrier is caused by such diseases of the central nervous system as, for example, meningitis, encephalitis, cerebral trauma and severe brain concussion, as well as lowering the pH in the brain tissues, brain tissue acidosis and blood alkalosis, ie any reduction in the differencepH between blood and CSF.An increase in the permeability of the blood-brain barrier also occurs under the influence of high doses of ACTH, epinephrine, hypophysin, histamine, thyroid hormones and ovaries. Weak concentrations of drugs cause a reversible increase in permeability, higher doses - a reversible decrease in it, and the largest dose - an irreversible increase. A distinct tendency to increase permeability was found in exogenous psychoses. After a rapid injection of cardiazole at a dose exceeding the convulsive threshold, a breakthrough of the blood-brain barrier occurs, lasting about 15 minutes. Since convulsions occur several seconds after intravenous injection, and before the breakthrough of this barrier takes more than 3 minutes, at this time tissue changes occur.

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The "seal" of the blood-brain barrier is due to acidosis of the blood, any increase in the pH difference between the blood and the brain, under the influence of calcium, morphine, arsenic, ascorbic acid, routine.

According to G. N. Kassil, the permeability of the barrier, increased due to craniocerebral trauma, decreases under the influence of atropine, sympathomimetic and ganglio-plegic drugs. The average doses of drugs, as well as anticonvulsants, also cause a reversible decrease in permeability. Megaphene can prevent the breakthrough of the blood-brain barrier in the case of cardiac spasm. In the old age, the permeability of this barrier is small. In contrast to inflammatory diseases of the central nervous system and symptomatic psychoses, degenerative nerve diseases and endogenous psychoses in approximately 80% of cases are accompanied by a decrease in the permeability of the blood-brain barrier.

In young patients with epilepsy, a tendency toward reduced barrier permeability is noted, whereas in persons suffering from seizures over two decades this permeability rises. With hereditary epileptiform cramps in rats during seizures, an increase in the permeability of the blood-brain barrier can be observed;after injection of experimental trypan blue animals, the sound stimulation of seizures no longer provoked. An anticonvulsant effect also has a lowering permeability barrier blood acidosis( caused by ammonium chloride).All these methods of "sealing" the barrier weaken the propensity for seizures in humans.

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