Sweating disorders: pathogenesis

The study of sweating disorders in terms of their topical affiliation is of fundamental importance for clarifying the localization of the pathological process, which is important in the conduct of differential diagnosis. There are central and peripheral disorders of sweating. In cerebral sweating disorders, which are more often due to cerebral strokes accompanied by hemiplegia, first of all there is hyperhidrosis on the side of hemiplegia - hemihyperhidrosis. More rarely in such cases, there is hemygipohydrosis. With predominantly cortical lesions (in the region of pre- or postcentral convolutions) of a small extent, contralateral hyperhidroses of a monotype may occur, for example, involving one arm or leg, half the face. However, the area of the cortex that is capable of influencing the intensity of sweating is much greater (sweating is not affected only by the occipital lobe and the anterior poles of the frontal lobes). Unilateral sweating disorders were noted in brain stem lesions at the level of the bridge and especially the medulla oblongata, as well as subcortical formations.

Spinal disorders of sweating are of two types - conductive and segmental. Conductive disorders of sweating occur in diseases that affect the lateral columns of the spinal cord. A complete conduction block in the spinal cord leads to a bilateral disturbance of sweating, usually as a paranhidrosis. The localization of its upper limit depends on the level of damage to the spinal cord. The coincidence of the anhidrosis boundary and anesthesia is possible only with the location of the lesion within ThVII-IX. At a higher location, the anhidrosis margin is significantly higher than the sensitivity level of the disorders, and at low foci its border is below the upper limit of the sensitive disorders. With incomplete spinal cord injury, hypohydrosis usually occurs, sometimes with a full spinal cord break, compensatory sweating can occur.

Segmental disorders of sweating are observed with damage to the neurons of the lateral horns of the spinal cord. They are most frequent in syringomyelia, when the zone of an- or hypohydrosis has the appearance of a "half-jacket" or "jacket", and the upper limit of sweating is usually higher than the border of sensitive disorders. Infringement of a diaphoresis at a syringomyelia can be localized in the field of the face. Segmental innervation of the sweat glands of the face begins predominantly from the cells of the lateral horn of the Da segment of the spinal cord. The fibers from these cells come out of the spinal cord in the front roots, then in the form of white connective 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. Part of the postganglionic fibers through the gray connective branches connects to the spinal nerves, forming the cervical plexus, and innervates the dermatomes CII-CIV. The other part forms the periarterial plexus of the external and internal carotid arteries.

Violation of sweating in the 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 the segments of CVIII-LII, and the sweat-forming neurons - at the level of ThII-LII, the spinal nerve rootlets above the level of ThII and below LII do not contain preganglionic perspiration fibers. Consequently, spinal root injuries above the level of ThII and damage to the horse's tail are not accompanied by a violation of perspiration on the hands and feet. This is an important differential diagnostic feature that makes it possible to distinguish the damage to the spinal roots at these levels from damage to the cervical or lumbar plexus, which usually causes sweating disorders. Consequently, violations of sweating in the pathology of the spinal roots are possible only with multiple lesions.

Hypo or anhidosis of the peripheral type without concomitant sensitivity disorders indicates a sympathetic chain injury. However, with a severe lesion of sympathetic nodes, there may be a pronounced hyperhidrosis, for example, a hyperhidrosis of a half of the face - in the pathology of the cervical, sometimes the upper thoracic sympathetic nodes, after thoracoplasty, in Horner's syndrome. Facial hyperhidrosis in the defeat of the ear-temporal nerve is due to the fact that it consists of sympathetic postganglionic fibers to the blood vessels and sweat glands and parasympathetic fibers to the parotid gland, while the sweating reaction during meals may be due to cross-stimulation of sympathetic and parasympathetic fibers . Impulses that cause abnormal sweating occur more quickly through parasympathetic fibers.

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

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

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

The pathology of the plexus or peripheral nerves in the case of their complete break leads to anhidrosis, and at partial interruption to hypohydrosis. In addition, in the denervated zone, not only sweating, but also sensitivity is reduced or lost.

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

Generalized hyperhidrosis serves as a well-known manifestation of psychovegetative syndrome. Increasing the activity of the sympathetic nervous system can be the cause or consequence of symptoms that are observed in a state of anxiety or depression, fear or anger. Hyperhidrosis of the generalized type often accompanies intense pain, which can occur as a result of exogenous and endogenous stimuli. Temperature irritations are transmitted along the same vegetative nervous pathways as painful ones, so the sensation of pain can be accompanied by profuse sweating.

[1], [2], [3], [4], [5], [6], [7], [8]