Sweating disorders - Pathogenesis

The study of sweating disorders in terms of their topical affiliation is of fundamental importance for specifying the localization of the pathological process, which is important for differential diagnostics. Central and peripheral sweating disorders are distinguished. In cerebral sweating disorders, which often occur as a result of cerebral strokes accompanied by hemiplegia, hyperhidrosis on the hemiplegic side is primarily noted - hemihyperhidrosis. Less often in such cases there is hemihypohidrosis. In predominantly cortical lesions (in the area of the pre- or postcentral gyri) of small extent, contralateral hyperhidrosis of a monotype may occur, for example, with the involvement of one arm or leg, half of the face. However, the area of the cortex capable of influencing the intensity of sweating is much larger (only the occipital lobe and the anterior poles of the frontal lobes do not affect sweating). Unilateral sweating disorders are noted with damage to the brainstem at the level of the pons and especially the medulla oblongata, as well as subcortical formations.

There are two types of spinal sweating disorders - conductive and segmental. Conductive sweating disorders occur in diseases affecting the lateral columns of the spinal cord. A complete block of conduction along the spinal cord leads to bilateral sweating disorder, usually of the paraanhidrosis type. The localization of its upper border depends on the level of the spinal cord lesion. The coincidence of the border of anhidrosis and anesthesia is possible only if the lesion is located within ThVII-IX. With a higher location, the border of anhidrosis is significantly higher than the sensitivity level of disorders, and with low foci, its border is below the upper border of sensory disorders. With incomplete spinal cord lesion, hypohidrosis usually occurs, sometimes with a complete rupture of the spinal cord, compensatory sweating can be observed.

Segmental sweating disorders are observed with damage to the neurons of the lateral horns of the spinal cord. They are most common in syringomyelia, when the zone of an- or hypohidrosis has the form of a "half jacket" or "jacket", and the upper border of sweating disorder, as a rule, lies above the border of sensory disorders. Sweating disorder in syringomyelia can be localized in the face. Segmental innervation of the sweat glands of the face begins mainly from the cells of the lateral horn of the Da segment of the spinal cord. Fibers from these cells exit the spinal cord as part of the anterior roots, then in the form of white connecting branches approach the sympathetic chain, rise without interruption through the lower and middle sympathetic ganglion and form a synapse with the cells of the superior cervical ganglion. Some of the postganglionic fibers connect with the spinal nerves via gray connecting branches, forming the cervical plexus, and innervate dermatomes CII - CIV. Another part forms the periarterial plexuses of the external and internal carotid arteries.

Impaired sweating in pathology of the peripheral nervous system has its own characteristics. Due to the fact that the lateral horns of the spinal cord are located between segments CVIII - LII, and sweating neurons - at the level of ThII - LII, the roots of the spinal nerves above the level of ThII and below LII do not contain preganglionic sweating fibers. Consequently, damage to the spinal roots above the level of ThII and damage to the equine tail are not accompanied by impaired sweating on the arms and legs. This is an important differential diagnostic sign that allows us to distinguish damage to the spinal roots at these levels from damage to the cervical or lumbar plexuses, damage to which usually causes sweating disorders. Consequently, sweating disorders in pathology of the spinal roots are possible only with their multiple lesions.

Hypo- or anhidrosis of the peripheral type without accompanying sensitivity disorders indicates damage to the sympathetic chain. However, with mild damage to the sympathetic nodes, severe hyperhidrosis may also occur, for example, hyperhidrosis of half the face - with pathology of the cervical, sometimes upper thoracic sympathetic nodes, after thoracoplasty, with Horner's syndrome. Facial hyperhidrosis with damage to the auriculotemporal nerve is associated with the fact that it contains sympathetic postganglionic fibers to the blood vessels and sweat glands and parasympathetic fibers to the parotid gland, while the sweating reaction during meals is possibly due to cross-excitation of sympathetic and parasympathetic fibers. The impulses that cause pathological sweating come rather through the parasympathetic fibers.

Sympathetic innervation of sweating in the head and neck is carried out by neurons located in segments ThIII-IV, and the shoulder and hand - in segments ThV-VII. The axons of these neurons end in the upper sections of the sympathetic chain, and sweating fibers from peripheral neurons pass further through the stellate ganglion.

There are a number of diagnostic rules that allow you to clarify the location of damage in this area:

1. anhidrosis on the face and neck with the simultaneous presence of Horner's syndrome indicates damage to the sympathetic chain above the stellate ganglion;
2. the spread of the anhidrosis zone below - to the arm, as a rule, indicates damage to the stellate ganglion;
3. in the presence of an anhidrosis zone in the head, neck, scapula and upper quadrant of the chest (but without Horner's symptom), the lesion is located directly below the stellate ganglion at the level of ThIII-IV.

Pathology of plexuses or peripheral nerves in case of their complete interruption leads to anhidrosis, and in case of partial interruption - to hypohidrosis. In addition, in the denervated zone, not only sweating is reduced or lost, but also sensitivity.

The phenomenon of anhidrosis is one of the manifestations of peripheral autonomic disorder. The main pathological changes are associated with segmental demyelination of peripheral nerve fibers.

Generalized hyperhidrosis is a well-known manifestation of psychovegetative syndrome. Increased activity of the sympathetic nervous system may be the cause or consequence of symptoms observed in a state of anxiety or depression, fear or anger. Generalized hyperhidrosis is often accompanied by intense pain, which may arise as a result of exogenous and endogenous irritants. Temperature irritants are transmitted along the same autonomic nervous pathways as pain irritants, so the sensation of pain may be accompanied by profuse sweating.

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