Inhibition deficit. Disinhibition.

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At rest and activity of neurons able to experience persistent inhibitory influences. Upon excitation of neurons occurs weakening of inhibitory processes. This disinhibition is metered, it is monitored and the required level of neuron activity, so it is a physiological nature.

If disinhibition having pathological neuron becomes hyperactive and out of control. Pathological disinhibition occurs when a significant deficiency and uncontrolled braking. This condition occurs in direct damage to the brake mechanisms with selective action on them some toxins (e.g., tetanus toxin strychnine).

Deficiency of braking and brake release are found in almost all forms of pathology of the nervous system, so they are typical pathological processes of the nervous system. inhibition deficit plays a significant role in the formation and activities of GPEE.

A typical experimental release syndrome is decerebrate rigidity. She called on Sherrington, transection of the brainstem between the front and rear quadrigemina. In these circumstances, there is loss of inhibitory influences from supraspinal structures and especially the red nuclei, and manifested tonic excitatory influence of the vestibular nuclei of Deiters on spinal cord motoneurons, especially γ-motor neurons that are normally under inhibitory control of the red nuclei. Break (for example, by sectioning the dorsal root) disinhibited, pathologically enhanced in-loop at the level of the spinal cord leads to the disappearance of the rigidity of the respective muscles. Therefore, this type of decerebrate rigidity is also called γ-rigidity (R. Granit).

At loss of inhibitory influences disinhibited hyperactivity and especially those neurons which normally are in a state of excitation of the tonic. In humans and many animals such neurons are neurons of the muscles that perform the function of anti-gravity. As a consequence, decerebrate cat throws up his head, front and hind legs are extended, the tail is raised, etc. In humans, a roll of motor cortical influences (eg after hemorrhagic stroke) occurs spastic flexor setting the upper and lower limb extensor installation (Wernicke-Mann pose).

A number of pathological reflexes occurs in a loss of influences from the cortex and subcortical structures; These reflexes are the result of release centers or spinal medulla. They are exaggerated uncontrolled reactions that are normal in the early postnatal period and then were suppressed during the development of regulatory influences from the higher parts of the CNS. These include the Babinski reflex (rastopyrivanie toes instead of bending at the foot of irritation), grasping, sucking, and other reflexes.

A full break of the spinal cord may occur and incorporated genetically suppressed with age spinal automatism in a relatively coordinated flexor-extensor movements. If giperaktiviruyutsya disinhibited and inhibitory neurons, there is a pathologically enhanced braking effect which can be manifested in the form of oppression and loss of function.