Pathological hyperactivation of the nervous system

Causes and mechanisms of hyperactivation

Pathological enhancement of neural influences occurs when the normal balance between stimuli in the central nervous system is disrupted. The main factor is an excessive increase in the level of neuronal excitation, as well as a pathological increase in the duration of this excitatory process.

According to their origin, hyperactivation is divided into two categories:

• Primary genesis — initial pathological excitation of the neural structures themselves.
• Secondary genesis — occurs indirectly, including due to disinhibition (when the restraining influence of other centers is lost).

As a result of these processes, persistent foci of excitation are formed in the brain tissue. It is their stable and continuous functioning that becomes the foundation for the development of a number of neuropathological syndromes that exhaust the body's reserves.

Clinical syndromes in hyperactivation

The presence of persistent foci of excitation manifests with a vivid clinical picture. Depending on the localization of hyperactive neurons, three main groups of pathological syndromes are distinguished:

1. Pain syndromes. Occur when sensory pathways and centers are damaged. Classic examples include thalamic pain syndrome and phantom limb pain occurring after limb amputation.
2. Convulsive syndromes. Characteristic of pathology in the motor centers of the cortex and subcortical structures. The best-known example is epilepsy.
3. Autonomic disorders. Manifest as systemic failures in the functioning of internal organs. These include arterial hypertension, cardiac arrhythmias, and polyphagia (pathologically increased appetite).

The role of inhibition in sensory damage

In organic damage to neural structures (e.g., in the development of paralysis), the severity of the clinical deficit is determined not only by the tissue destruction itself. Two factors play a huge role:

• The direct size of the organic damage focus.
• Protective inhibition — temporary suppression of the activity of nearby undamaged neurons.

The clinical significance of protective inhibition is that it is reversible. As this inhibitory influence is removed, the patient's motor function can partially recover. This occurs even if the initial structural damage to the brain tissue remains unchanged.

Hyperactivation of inhibitory systems and decreased excitation

Pathological changes can affect not only excitatory but also inhibitory neurons, and can also be characterized by a global decrease in activity.

Decreased intensity of the excitatory process in the CNS Often caused by external chemical exposure (e.g., the effect of narcotic drugs). The pathogenesis of this condition reduces to a global decrease in driving influences on the effector structures of various organs and tissues.

Hyperactivation of CNS nuclei exerting an inhibitory influence Even the activation of neural centers can lead to the suppression of functions if these centers are inhibitory.

• Example: excessive activation of neurons in the reticular formation of the medulla oblongata.
• Mechanism: these nuclei emit a powerful descending inhibitory influence on the structures of the spinal cord. Under the influence of these stimuli, suppression of polysynaptic reflexes occurs.
• Clinical picture: the patient develops severe movement disorders (up to marked muscle paresis) and a noticeable decrease in tissue sensitivity.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Mechanisms of formation of primary and secondary neuronal hyperactivation
• Pathogenesis of the development of protective inhibition around the lesion focus
• The effect of the reticular formation on polysynaptic reflexes of the spinal cord
• Features of thalamic pain syndrome and phantom pain

Other topics in "Chapter 28. Standard forms of pathology of the nervous system"

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