**5. Vegetative distress-syndrome and pathomorphological signs of insufficiency of ANS**

The ANS performs an organizing and trophic function along with endocrine and other anatomical and physiological functional systems [78, 79]. Numerous experimental studies on the plasticity of the nervous system in various injuries of the central nervous system demonstrate the lack of specificity of changes in neurons—in the structure of the neuron nucleus appears invagination of the nuclear membrane, chromatin condensation, swelling of mitochondria, and all cisternal structures [80, 81]. These structural changes appear at any impact on the body, they are a universal ultrastructural expression of the general adaptation syndrome [78]. It is known that the structural and functional plasticity of the nerve cells is unusually high, but the appearance of morphological alterations occurs earlier and persists much longer than functional changes. Pathomorphological studies of the ANS performed on autopsy material of deceased neurosurgical patients revealed severe dystrophic and destructive changes at all levels of the ANS [82].

### **5.1 Afferent department of visceral reflexes**

A pathomorphological study of the structures of the ANS afferent department (receptor apparatuses and sensitive nerve fibers (dendrites) that perceive and conduct afferent impulses), spinal (Th2–Th4; L1–L4; S2–S3), and similar cranial nerve ganglia (trigeminal, inferior vagus node) revealed that regardless of the nature of acute cerebral damage, there are widespread and irreversible violations of the structure and function of the components of the afferent department [28, 82].

Thus, we are talking about the partial or complete death of the sensitive nervous apparatus, the state of which largely determines the reactivity and plasticity in the implementation of an adaptive reaction. Similar changes are found not only in the intramural plexuses but also in the trunk of the vagus nerve, which carries afferent and preganglionic fibers to intramural neurons; in the posterior roots of the spinal cord, where the axons of the neurons of the sensitive spinal ganglia pass. These are nonspecific reactive changes (marginal chromatolysis with preservation of the nucleus, central chromatolysis with preservation of the nucleus, central chromatolysis with "sintering" of lumps of Nissl substance along the periphery of neurons, hyperchromatosis of the nuclei and cytoplasm of the cell in combination with edema and without it), as well as destructive irreversible phenomena (karyolysis with wrinkled hyperchromic nucleus, hydropic changes with the formation of vacuoles and karyolysis, karyorexis in combination with swelling of the neuron body). A motley kaleidoscope of changes reflects the stages of neuronal death depending on local conditions (for example, the acidity of the environment, the degree of hypoxia, hydration of the ganglion, etc.).

### **5.2 Central parts of the autonomic nervous system**

The central parts of the ANS are associative (insertion) links of visceral reflexes. The associative link of the sympathetic nervous system is represented by the nuclei of the lateral horns of the gray matter of the spinal cord in the thoracolumbar region. During

### *General Anesthesia and Autonomic Nervous System: Control and Management in Neurosurgery DOI: http://dx.doi.org/10.5772/intechopen.101829*

spinal cord examination at the level of Th2–Th4, Th12, and L1–L2; the insertion link of the parasympathetic nervous system at the mesencephalic (Yakubovich-Westphal-Edinger nucleus), bulbar (vegetative vagus nerve nucleus), and sacral (S2–S3) levels in the associative links, regardless of the etiological factor, widespread damage to structures and, presumably, disorders of the function of nerve cells, which are mostly irreversible, were noted [74]. Thus, we are talking about partial or significant damage to the associative link, from which the efferent vegetative pathway begins.

Neurites (axons of associative neurons) of the peripheral nerves reach the autonomic ganglia, where they end with synapses. Thanks to synapses, all the links of the visceral reflexes are interconnected and, if necessary, can act as a whole. Significant reactive changes were also revealed in the synaptic apparatus of the associative links (sympathetic and parasympathetic)—argyrophilia (affinity of synaptic rings to nitric acid silver) and hypertrophy of synapses. Destructive changes in the form of fragmentation, granular-lumpy decay of presynaptic nerve fibers, and synaptic structures formed by them on associative neurons are more pronounced in long-term critical conditions of the patient, clinical manifestations of sympathetic hyperactivity syndrome [28, 82, 83]. Nonspecific reactive changes (central and peripheral chromatolysis, acute cellular swelling, process staining, hyperchromatosis of nuclei and cytoplasm) were detected in the central parts of the sympathetic and parasympathetic nervous system. Irreversible destructive phenomena were standard (karyocytolysis, karyolysis). They reflect the different stages of neuronal death. There was also a lively glial reaction [83].

Thus, from a morphological point of view, the most dramatic situation develops in the associative link of the sympathetic nervous system.

The death of neurons nuclei in all parts of the hypothalamus (large-cell nucleus of the anterior hypothalamus, small-cell nuclei of the middle hypothalamus, nuclei, and pathways of the posterior) was also noted [83].

### **5.3 Efferent section of the visceral reflexes**

The efferent autonomic pathway is represented by neurites of associative neurons (preganglionic fibers) and effector neurons and their neurites (postganglionic fibers). The latter reach the innervated tissues, where they realize their impact. The studied sympathetic ganglia (cervical-thoracic or stellate, 2nd–6th thoracic paravertebral, abdominal plexus) are connected by preganglionic fibers with sympathetic centers of the spinal cord; parasympathetic ciliary node—with the Yakubovich-Westphal-Edinger nucleus; Auerbach and Meissner plexuses—with the autonomic nucleus of the vagus nerve.

In acute cerebral injury, extensive structural and functional disorders of the main components of the autonomic ganglion—neurocytes are revealed; at the same time, the "management" of special functions of some organs (glands, smooth muscles of internal organs and vessels, heart muscle, ciliary and pupillary muscles, etc.) and the general adaptive and trophic function suffer [83]. A motley pattern of reactive changes is observed in the sympathetic ganglia—central and peripheral chromatolysis, total chromatolysis with preservation of the nucleus and nucleolus and "sintering" of chromatophilic substance along the edge of the neuron body, hyperchromatosis of the nucleus and perinuclear edema, wrinkling of nuclear material into a homogeneous structureless mass with total chromatolysis (**Figure 9**).

Reactive changes in the parasympathetic ganglia were nonspecific—destructive changes were standard (karyolysis, karyocytolysis), a pronounced reaction from the

### **Figure 9.**

*Sympathetic ganglion 3 days after severe traumatic brain injury (column intermediolateral medullae spinalis). (A) Argyrophilia, hypertrophy, deformation of synapses on neurons. Impregnation by Kahal. Magnification X 100. (B) Destructive changes in the synaptic vesicle. Electronogram. Magnification X 1800.*

glia was noted in the ganglia (the number of glial cells (satellites) closely adjacent to the perikaryon of the neurocyte and penetrating it increased around the neurocytes).

The last link of the visceral reflexes is postganglionic fibers, which, as part of nerve trunks and bundles, penetrate all organs and tissues of the body, where they form effector nerve endings. The efferent section of the visceral reflex arches also detects gross dystrophic changes.

The duration of the patient's stay in critical condition correlates with the number of damaged and dead neurons—the longer the period, the more widespread the damage to the ANS was. The death of neurons and their processes can also be caused by their functional overload, excessive functional stress, malfunctions in the rhythm of work, etc.

Some patients who have suffered severe critical conditions recover and return to life with a deeply disabled ANS with a sharply narrowed range of adaptive reactions [28].

Death can occur from the disintegration of the organism as a system with the relative safety of the components of the system (organs) with far from exhausted reserves [83].

Thus, the totality of dystrophic and necrobiotic changes detected in the ANS is the morphological equivalent of vegetative distress syndrome and ANS insufficiency.

### **6. Conclusion**

To summarize, it is obvious that the autonomic nervous system is one of the main systems of life support. Control and monitoring of its functional activity is especially important when the patient is under the condition of general anesthesia. Neurosurgery causes specific central hemodynamic reactions related to reflexes from the brainstem. Management of autonomic reactions and vegetative tone are possible with neurovegetative stabilization and control of the depth of anesthesia.

### **Conflict of interest**

The authors declare no conflict of interest.

*General Anesthesia and Autonomic Nervous System: Control and Management in Neurosurgery DOI: http://dx.doi.org/10.5772/intechopen.101829*
