Causes and Mechanisms of Efferent Control Disorders
Pathology of efferent innervation occurs due to failures along the pathway from the neuron to the target cell. Several basic mechanisms underlie these disorders. First, there is an impairment of specific neural activity affecting movement control, sensation, tissue trophic support, or higher nervous activity (HNA). Second, partial or complete post-traumatic interruption of impulse transmission leads to dysfunction. Failures of axonal transport also play an important role.
The problem may also lie within the target tissues themselves, when their perception of neural signals is impaired. This occurs against the background of hypoxia, transmembrane ionic imbalance, or changes in the number and affinity of neurotransmitter receptors.
In clinical practice, the main causes are divided into two broad groups:
- Acquired: ischemia, encephalitis, intracranial tumor growth, various intoxications.
- Genetically determined: often characterized by polygenic inheritance (interaction of genes and environmental factors). A clear example is multiple sclerosis: concordance in monozygotic twins reaches 50%, and the risk for close relatives is eight times higher than in the general population.
Denervation Syndrome and Locomotive Impairments
With partial or complete cessation of neural control, denervation syndrome develops. At this point, postsynaptic neurons and deinnervated target organs undergo a series of transformations. Profound metabolic shifts occur within them, neurotransmitter metabolism is reorganized, and cell structure and function are severely disrupted.
If efferent disorders affect the motor sphere, neurogenic locomotive disorders arise. These are characterized by alterations in basic motor activity parameters: the total number of movements performed, their rate, and spatial coordination are impaired.
Pathological Phase States
A special manifestation of higher nervous activity dysfunction and autonomic reactions is the development of parabiotic phase states. Normally, the nervous system responds adequately to external influences: the stronger the stimulus, the stronger the conditioned or unconditioned reflex response. With the development of pathological phase states, this correspondence is lost: the reaction no longer matches either the stimulus parameters or the biological needs of the body. This is accompanied by the appearance of pathological reflexes and a drop in adaptation.
These states are based on three fundamental mechanisms:
- Functional "disintegration" — the loss of normal interneuronal connections established during ontogenesis.
- Pathological integration — neurons form new, atypical connections, building a stable "pathological system."
- Decreased plasticity — a global loss of adaptability in neural tissue structures.
Classification of Phase Reactions
Pathological reactions are classified according to how neural tissue responds to stimuli of varying strengths:
- Equalizing phase: the response is identical regardless of whether a weak or strong stimulus (light, pain, verbal) is applied.
- Medium stimulus phase: the maximum response is recorded exclusively for stimuli of moderate intensity.
- Paradoxical phase: strong stimuli cause an extremely weak response (or none at all), whereas weak signals provoke a preserved or enhanced reaction.
Terminal phases of reactivity are distinguished separately:
- Narcotic state: stepwise extinction of responses (reactions to weak stimuli disappear first, followed by strong ones).
- Inhibitory state: absolute areactivity to any stimulus.
- Ultraparadoxical state: qualitative perversion of reactions. Positive stimuli provoke a negative response, and negative stimuli provoke a positive one (e.g., a patient bursting into anger in response to news of a favorable prognosis).
The development of phase states obeys the laws of "temporal mosaicism" (phases sequentially replace each other as the disease progresses) and "spatial mosaicism" (different phase states can be observed simultaneously in different areas of the nervous system).