The formation and operation of generators of pathologically enhanced excitation
The generator can be formed under the influence of various substances of endogenous or exogenous nature that cause any violation braking controls (which entails disinhibition and hyperactivation neurons) or direct neuronal hyperactivation. In the latter case, the brakes are saved, but they are functionally inefficient and not able to normalize the activity of neurons. In all cases, the prerequisite education and generator business is lack of inhibition of its constituent neurons.
An example of the formation of the generator at a primary violation of braking can be generators, arising under the action of tetanus toxin, strychnine, penicillin and other convulsant. An example for primary formation generator neurons may be hyperactive generators arising from prolonged and enhanced synaptic stimulation, effects of excitatory amino acids (such as glutamate), shallow and postischemic reperfusion ischemic CNS. The generator can also occur when neurons deafferentation after transection of the spinal cord and nerves, with associated deafferentatsionnye pain syndromes.
In the early stages of the generator when the brakes are still preserved, and neuronal excitability is low, the generator is activated sufficiently strong stimuli coming through a specific component of the entrance to his group of neurons. In the later stages, when there is a profound failure of brake mechanisms and significantly increased neuronal excitability, the generator can be activated by various stimuli from different sources, as well as spontaneous.
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