Symptoms of peripheral nervous system damage

The peripheral nervous system is a topographically conditionally distinguished extracerebral part of the nervous system, including the posterior and anterior roots of the spinal nerves, spinal ganglia, cranial and spinal nerves, nerve plexuses and nerves. The function of the peripheral nervous system is to conduct nerve impulses from all extero-, proprio- and interoreceptors to the segmental apparatus of the spinal cord and brain and to conduct regulatory nerve impulses from the central nervous system to organs and tissues. Some structures of the peripheral nervous system contain only efferent fibers, others - afferent. However, most peripheral nerves are mixed and contain motor, sensory and vegetative fibers.

The symptom complexes of damage to the peripheral nervous system are composed of a number of specific signs. The shutdown of motor fibers (axons) leads to peripheral paralysis of the innervated muscles. When such fibers are irritated, convulsive contractions of these muscles occur (clonic, tonic convulsions, myokymia) and the mechanical excitability of the muscles increases (which is determined when a hammer strikes the muscles).

To establish a topical diagnosis, it is necessary to remember the muscles innervated by a certain nerve and the levels of origin of the motor branches of the nerves. At the same time, many muscles are innervated by two nerves, so even with a complete rupture of a large nerve trunk, the motor function of individual muscles may suffer only partially. In addition, there is a rich network of anastomoses between the nerves and their individual structure in different parts of the peripheral nervous system is extremely variable - the main and scattered types according to V. N. Shevkunenko (1936). When assessing movement disorders, it is also necessary to keep in mind the presence of compensatory mechanisms that compensate for and mask true loss of function. However, these compensatory movements are never fully performed in the physiological volume. As a rule, compensation is more achievable in the upper limbs.

Sometimes the source of incorrect assessment of the volume of active movement can be false movements. After contraction of antagonist muscles and their subsequent relaxation, the limb usually passively returns to the initial position. This simulates contractions of the paralyzed muscle. The force of contraction of the antagonists of the paralyzed muscles can be significant, which underlies muscle contractures. The latter can also have a different origin. For example, when nerve trunks are compressed by scars or bone fragments, intense pain is observed, the limb takes a "protective" position, in which the intensity of pain decreases. Long-term fixation of the limb in this position can lead to the development of antalgic contracture. Contracture can also occur with long-term immobilization of the limb (with trauma to bones, muscles, tendons), as well as reflexively - with mechanical irritation of the nerve (with an extensive cicatricial inflammatory process). This is a reflex neurogenic contracture (physiopathic contracture). Sometimes psychogenic contractures are also observed. It is also necessary to keep in mind the existence of primary muscle contractures in myopathies, chronic myositis and polyneuromyositis (by the mechanism of autoallergic immunological damage).

Contractures and joint stiffness are a major obstacle to the study of limb motor disorders that depend on peripheral nerve damage. In the case of paralysis, due to the loss of function of the motor nerve fibers, the muscles become hypotonic, and soon their atrophy joins in (2-3 weeks after the onset of paralysis). Deep and superficial reflexes carried out by the affected nerve are reduced or disappear.

A valuable sign of damage to nerve trunks is a disturbance of sensitivity in certain zones. Usually this zone is smaller than the anatomical territory of branching of cutaneous nerves. This is explained by the fact that individual areas of the skin receive additional innervation from neighboring nerves ("overlap zones"). Therefore, three zones of sensitivity disturbance are distinguished. The central, autonomous zone corresponds to the area of innervation of the nerve under study. In case of complete disturbance of nerve conduction in this zone, loss of all types of sensitivity is observed. The mixed zone is supplied both by the affected and partially by neighboring nerves. In this zone, sensitivity is usually only reduced or distorted. Pain sensitivity is best preserved, tactile and complex types of sensitivity (localization of irritations, etc.) are affected less, the ability to roughly differentiate temperatures is impaired. The additional zone is supplied mainly by the neighboring nerve and least of all by the affected nerve. Sensory disturbances in this zone are usually not detected.

The boundaries of sensitivity disorders vary widely and depend on variations in “overlaps” by adjacent nerves.

When sensitive fibers are irritated, pain and paresthesia occur. Often, with partial damage to the sensitive branches of the nerves, perception has inadequate intensity and is accompanied by an extremely unpleasant sensation (hyperpathy). Characteristic of hyperpathy is an increase in the threshold of excitability: fine differentiation of weak stimuli is lost, there is no sensation of warm or cool, light tactile stimuli are not perceived, there is a long latent period of perception of stimuli. Painful sensations acquire an explosive, sharp character with an intense feeling of unpleasantness and a tendency to irradiation. An aftereffect is observed: painful sensations continue for a long time after the irritation has ceased.

The phenomenon of nerve irritation may also include the pain phenomenon of the causalgia type (Pirogov-Mitchell syndrome) - burning intense pain against the background of hyperpathy and vasomotor-trophic disorders (hyperemia, marbling of the skin, dilation of the capillary network of vessels, edema, hyperhidrosis, etc.). With causalgic syndrome, pain may be combined with anesthesia. This indicates a complete rupture of the nerve and irritation of its central segment by a scar, hematoma, inflammatory infiltrate, or the development of a neuroma - phantom pains appear. In this case, the tapping symptom (like the Tinel phenomenon when tapping along the median nerve) has diagnostic value.

When nerve trunks are damaged, vegetative-trophic and vasomotor disorders appear in the form of changes in skin color (paleness, cyanosis, hyperemia, marbling), pastosity, decrease or increase in skin temperature (this is confirmed by the thermal imaging method of examination), sweating disorders, etc.

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