Neuritis

NEURITIS (neuritis), in the literal sense, means inflammation of nerves. However, in clinical practice, the term neuritis is applied not only to changes in nerves of an inflammatory nature, but also to those based purely on degenerative changes in nerve fibers without signs of inflammation. This conditional broad and essentially incorrect use of the term N. is partly due to the insufficiently clear distinction between degenerative and inflammatory processes occurring in the nervous system (see also Myelitis, Encephalitis), and partly because the symptomatology of degenerative and inflammatory changes in nerves is identical. General data regarding the etiology of N. Neuritis are caused by various etiological factors, which can be divided into several groups: 1) infections; 2) exogenous intoxications; 3) autointoxications, including metabolic disorders (gout, diabetes), 4) injuries and 5) functional factors. Almost every infection can give as a complication inflammation of a single nerve with the corresponding clinical picture. Sometimes, elements of a certain organotropism of a known infection to certain nerves can be noted. Thus, diphtheria can give an isolated neuritis of the nervus vagi, typhoid fever sometimes affects the n. ulnaris, etc. Often the nature of the infection is known; in a number of cases, it concerns some unstudied infection, which, due to its external connection with cold, cooling, is called 'rheumatic'. A classic example of cases of this kind is paralysis of the n. facialis. In particular, such an infection as syphilis also not infrequently gives neuritis, mainly of cranial nerves. Exogenous intoxications very often give isolated neuritis when using morphine, absinthe, and sometimes with traces of a certain organotropism (e.g., alcoholic and lead paralyses of the n. radialis). Autointoxications can give both multiple and isolated N. (e.g., neuritis of the n. medianus in diabetics). Here can also be included avitaminotic N. Injuries provide the richest material for isolated damage to all sorts of inaccessible nerve trunks. Finally, a number of N. are associated with increased nerve function. - N. from professional overwork, mainly from monotonous and prolonged work by a small group of muscles. Thus, for example, partial N. of the n. medianus (paralysis of the thumb) in drummers, milkers, etc. With the growth of industry, professional N. acquire special importance both in terms of their spread and the need to develop measures to combat them along preventive and therapeutic lines. Areas of labor where professional N. are particularly frequent include primarily all types of work involving contact with lead-containing compounds and compositions: printing, mainly work of typesetters, glazing work in the ceramic industry, work of solderers, tinsmiths, dyers, etc. More or less prolonged engagement in these types of work without observance of appropriate prevention gives manifestations of general saturnism, lead neuritis and lead polyneuritis. Without touching here on the first and third links of this chain (see Lead, Polyneuritis), it is necessary to dwell on professional neuritis of lead origin. Their classic representative is N. of the n. radialis (see Radialis nervus). The basic property of lead - to be slowly absorbed and slowly excreted from the body - in turn determines the main clinical feature of lead N. - their slow development and prolonged course. Lead N. constitute the main mass of professional N. of toxic origin, in comparison with which all others are only a small minority. Next come N. arising on the basis of the most diverse intoxications in workers of the chemical industry, alcoholic paralyses in workers of breweries and distilleries. Pathological anatomy. Changes in the nerve trunk can be of the nature of a small focus located somewhere along the nerve pathway, and sometimes even topological diagnosis is possible. An example of such a type of process can be N. of the facial nerve. In other cases, the process begins from the most distal parts of the nerve and spreads in the central direction (neuritis ascendens, s. migrans). This type of anatomical process is most often observed in multiple N., but apparently can also occur in mononeuritis. The third, theoretically conceivable type - the formation of a focus somewhere along the nerve pathway and spread in the direction from the center to the periphery - was previously readily admitted (neuritis descendens), but at present is considered doubtful. - The microscopic picture of N. in general can be classified into one of two types of changes - parenchymatous, i.e., degenerative, or interstitial, i.e., inflammatory. Parenchymatous change, relating to nerve degeneration, is expressed in changes in all three components of the nerve fiber: the axis cylinder, the myelin sheath, and the neurilemma. The axis cylinder homogenizes so that individual fibrils become indistinguishable, it thickens and most often unevenly in the form of club-shaped swellings; sometimes, on the contrary, it thins out, twists like a corkscrew and finally breaks into fragments. The myelin sheath cracks into separate lumps, which then further and further disintegrate until they turn into fine dust. This cracked myelin acquires the property of being stained black by osmic acid. The neurilemma gives active proliferation of Schwann sheath nuclei. In not too intense a process, the matter may not go as far as disintegration of the axis cylinder and may be limited only to changes in the myelin and Schwann sheaths (neuritis periaxialis). The breakdown of myelin is absorbed by macrophages, and their presence is as it were a connecting link with another anatomical form - true inflammation of the nerve. In inflammation of the nerve, in addition to the indicated degenerative changes of the nerve fiber, there are also changes in the tissue that connects the fibers in the nerve. They have the character of a usual angio-exudative reaction in the acute stage: liquid exudate, i.e., edema of the interstitial tissue, cellular exudate - leukocytes and lymphocytes, hemorrhages in places. Later, the liquid exudate is absorbed, the hemorrhages are resorbed, the cellular exudate becomes more uniform, takes the character of small-cell infiltration, and even later it also decreases. Instead, in the vessels, signs of hyalinosis or sclerosis appear, and the connective tissue (endoneurium and perineurium) proliferates and also shows a tendency to sclerosis. If in true inflammatory N. degenerative changes predominate from the side of the nerve fibers, while changes in the stroma are weakly expressed, then one can speak of parenchymatous N.; the reverse ratio of changes gives the right to attribute the change to interstitial neuritis; with limitation of the inflammatory process only to the connective tissue surrounding the nerve (in the perineurium) one can speak of perineuritis. The process in the nerve may be limited to one area or may involve several areas separated by normal tissue; in such cases, club-shaped or nodular changes of the nerve will be observed (neuritis nodosa). General symptomatology of neuritis. N. of each individual trunk has its own clinical picture, sometimes even with its own peculiarities of course and outcome. However, among all this large number of symptoms, one can note a certain number of common signs, which in sum constitute the general symptomatology of neuritis. Peripheral nerves can be either purely sensory or purely motor, but in most cases are mixed, i.e., simultaneously motor and sensory. In addition, one must keep in mind the frequent, and perhaps constant, admixture of autonomic nerve fibers. Each of these three anatomical components of the nerve gives its own group of symptoms. Break of motor fibers gives paralyses with features characteristic of damage to the peripheral motor neuron: decrease in tone in the paralyzed muscles, their atrophy, decrease in tendon reflexes. Break of sensory fibers gives various disorders of sensitivity: anesthesias, hyperesthesias, paresthesias, pains. The character of these disorders is determined by the character and degree of damage: complete break, partial, not so much destruction as irritation, etc. Among the disorders of sensitivity, a very frequent symptom is pain on pressure on the diseased nerve and paralyzed muscles. Very often there is a simultaneous combination of various factors - destruction of some fibers and irritation of others, as a result of which anesthesias and hyperesthesias, anesthesias and pains, etc., enter the clinical picture. The area of all these disorders generally coincides with the area of sensory innervation of the given nerve. Damage to the autonomic nerve component gives vasomotor, secretory and trophic disorders. An important method for the investigation of neuritis is electrodiagnosis.

All these symptoms, in terms of their distribution, must coincide with the area of motor and sensory innervation: this position is the basic requirement in the diagnosis of N., as it provides reference points for distinguishing it from processes of another genesis, e.g., from root processes, plexitis. However, in practice, deviations from this rule are quite common, but they mostly have a typical character, for example, the area of anesthesia is always smaller than the boundaries indicated by anatomy due to the overlapping of adjacent sensory zones (see Nerves). Clinic. N. of the major nerve trunks, such as n. radialis, ulnaris, medianus, ischiadicus, etc.-see respective articles.-Neuritis n. phrenici. N. phrenicus is most often affected by a neuritic process in diphtheria, rarely in other infections. Mechanically, it can be compressed by tumors, aneurysms in carious processes of the cervical vertebrae, etc. The area of its motor innervation is the diaphragm, and therefore the result of its N. is paralysis of the diaphragm. The picture of the latter consists of the following symptoms: 1) subjectively - a feeling of lack of air, suffocation, especially during muscular exertions; 2) objectively-a) increased frequency of breathing; b) in respiratory movements, the work of the upper part of the chest predominates; c) an inverted, or paradoxical type of respiratory movements: during inspiration, the subumbilical area sinks in, and during expiration it bulges out (in normal conditions-the opposite); d) sometimes hiccups due to spasmodic contraction of the diaphragm in the initial stage of N.; e) high position of the liver; f) difficulties in emptying the intestines. Fluoroscopy makes visible the disturbance of diaphragm movements. The entire described picture refers to bilateral paralysis of n. phrenici; in unilateral cases it is expressed much weaker, but on the contrary, it is more distinct in fluoroscopy. The prognosis in unilateral paralysis is quite serious, in bilateral it is very severe. Therapy-apart from causal, if it is possible-comes down to quiet maintenance, the use of strychnine under the skin, electrization of n. phrenici. Neuritis n. axillaris. The area of motor innervation-m. deltoideus and teres minor. The first raises the arm to the horizontal, the second rotates it outward. The sensory branches supply the skin over m. deltoideus. In paralysis of n. axillaris, the motor disturbances consist in the inability to raise the arm to the horizontal; rotation of the shoulder outward is little disturbed, since the deficiency is compensated by m. infraspinatus. Sensory disturbances are expressed by slight hypesthesia over m. deltoideus. The etiology is mostly traumatic: dislocations and fractures of the arm, gunshot wounds in the area of the brachial plexus, etc., more rarely-accidental complications after various infections.-Neuritis n. thoracalis longus. The nerve supplies motor branches to m. serratus anticus major. In its paralysis the clinical picture is as follows: 1) with the arm hanging down, the scapula on the affected side stands a) slightly higher than on the healthy side-result of traction by m. rhomboidei, b) closer to the spine-for the same reason, and c) its lower angle is turned upward (same mechanism). 2) Raising the arm above the horizontal is impossible, since it is performed by rotation of the scapula, which is done by m. serratus. 3) When raising the arm forward to the horizontal, the scapua lags strongly behind the body- the so-called scapula alata is obtained. The mechanism of this lag is as follows: mm. serratus and rhomboideus together form something like a shoulder strap diagonally encircling the body, and the scapula is attached by its inner edge to this muscular shoulder strap, like a buckle. When m. serratus is paralyzed, the muscular ring does not fit tightly around the body, and the scapula lags in general, and especially strongly when the raised arm, as a lever, strongly pulls the scapula. The causes of N. are the same as for the previous nerve. Neuritis n. dorsalis scapulae. The area of motor innervation of this nerve is m. rhomboideus and m. levator anguli scapulae. The common function of the mentioned muscles: 1) the scapula is raised upward, 2) it approaches the midline, and 3) its lower angle is turned upward and inward. Accordingly, in paralysis of n. dorsalis scapulae, the lower angle of the scapula is turned outward, and when raising the arm forward, it turns outward even more. The functional disturbances in movements are insignificant, as they are compensated by the action of m. cucullaris. To distinguish from paralysis of m. serrati, the patient is asked to raise the arm forward to the horizontal: in this case, paralysis of m. serrati gives a strong lagging of the scapula from the chest, while in paralysis of m. rhomboidei and levat. anguli scapulae this does not happen. Regarding a special congenital deformation, the so-called 'high position of the scapula', there is an opinion that it owes its origin to paralysis of n. dorsalis scapulae due to damage during childbirth with subsequent retraction. A very rare form of neuritis. Neuritis n. suprascapularis. The nerve supplies 2 muscles: mm. supraspinatus and infraspinatus. Their function: m. supraspinatus slightly raises the shoulder and according to some slightly rotates it outward; m. infraspinatus rotates the shoulder outward. From this follows the theoretical construction of the picture of paralysis of n. suprascapularis: 1) raising of the shoulder upward should be somewhat weakened, although this deficiency can be compensated by mm. deltoideus and serratus; 2) supination of the shoulder should be somewhat weakened, although this can be neutralized by m. teres minor; 3) there may be a depression of fossae supra- and infraspinatae. Actually observed: 1) first of all, a very insignificant degree of any disturbances in general; 2) sometimes the patient raises the arm to the horizontal freely, and then slightly has to jerk it upward in order to then continue raising it higher; 3) sometimes in right-sided paralysis it is difficult during sewing to pull the needle through; 4) sometimes (under the same condition) writing is difficult: the left hand has to push the paper to the left (both of these last symptoms are the result of difficult supination of the shoulder); 5) in women, difficulty is revealed in such a movement as combing hair, i.e., raising the bent arm; 6) depression of fossae supra- and infraspinatae; 7) subjectively-pain in the arm, a feeling of weakness, rapid fatigue. Neuritis n. obturatorii. The area of motor innervation of nervi obturatorii: mm. adductor magnus, longus, brevis, gracilis, obturator externus, pectineus. M. adductor magnus receives additional branches from n. ischiadicus, and m. pectineus-from n. cruralis. Sensory innervation: the medial surface of the thigh, specifically-its lower two thirds. Corresponding to such an area of innervation, the picture of paralysis of n. obturatorii theoretically should consist of the following elements: 1) rotation of the thigh outward should be weakened, since almost all adductors (except the internal bundle of the great adductor), obturator externus and pectineus rotate the thigh outward; but this deficiency can be neutralized by the action of other outward rotators-obturator internus, gemelli, quadratus femoris, etc.; 2) adduction of the thigh should be weakened; 3) extension in the knee should somewhat suffer, but it is possible that the extraordinarily strong quadriceps compensates for the deficiency; 4) there should be anesthesia on the inner surface of the thigh. Actually, from among these possible symptoms, only 2 main ones are observed: 1) a small area of sensory disturbances on the inner surface of the thigh and 2) weakness of thigh adduction and everything that follows from this. This is first of all a slight disturbance of gait-a certain throwing out of the leg to the side, from which walking becomes tiring for the affected leg. Movements such as e.g. placing the affected leg on the healthy one (as for testing the knee reflex) become difficult. Horseback riding becomes difficult, in which one has to grip the horse. Of course, when examined in bed, squeezing of the thighs is also somewhat weakened. However, it must be borne in mind that complete paralysis of adduction does not occur, since m. adductor magnus receives additional innervation from n. ischiadicus, and pectineus-from n. cruralis. A very rare form of N., observed in diabetes, after anesthesia, suppurations in the pelvis, under the influence of childbirth in women. Neuritis n. cutanei femoris lateralis. A purely cutaneous nerve supplying the upper-outer part of the buttock and the outer surface of the thigh. Its N. is expressed by decreased sensitivity in the indicated area. It is more often associated with phenomena of irritation, giving in such cases a picture of so-called meralgia paraesthetica (see).-Neuritis n. sapheni, A purely sensory nerve supplying the inner surface of the calf. Its neuritis gives disturbances of sensitivity in this area.-Neuritis n. genitocruralis. A purely sensory nerve supplying a small oval spot on the middle of the anterior surface of the thigh below the inguinal fold and one half of the scrotum (or the large lip in women).-Neuritis n. glutaei. There are two nerves with this name: superior and inferior. N. glutaeus superior supplies the following muscles: m. glutaeus medius, minimus, m. tensor fasciae latae and piriformis. N. glutaeus inferior supplies m. glutaeus maximus.

The function of these muscles: glutaeus medius and minimus 1) abduct the thigh, 2) rotate it with some fibers outward and others inward, 3) mutually fix the pelvis and thigh. Glutaeus maximus produces extension of the thigh. Tensor fasciae latae rotates the thigh inward. M. piriformis rotates it outward. Accordingly, the theoretically constructed picture of paralysis of the gluteal nerves should be as follows: for neuritis of the n. glutaei infer. 1) atrophy of the buttock (m. glutaeus maximus); 2) paralysis of extension of the thigh; 3) when standing and walking, there should be flexion of the thigh in the hip joint. In fact, isolated pictures are very rare, almost exclusively of traumatic etiology, and they consist of weakness of extension of the thigh in bed and atrophy of the buttock. Additionally, when standing, a certain lordosis in the lumbar region is observed as compensation for the weakened extension of the thigh. For N. p. glutaei super, the theoretical picture should be as follows: 1) weakness of abduction of the thigh; 2) weakness of its outward rotation; 3) some thinning of the lateral parts of the pelvis due to the m. glutaei medii. In fact: 1) weakness of abduction of the thigh, 2) the walk becomes waddling, 3) in bed, outward rotation of the thigh is not weakened, since the loss of m. piriformis is compensated for by many other rotators, 4) weakness of the m. tensoris fasciae latae, an energetic inward rotator of the thigh, as well as the anterior portions of glutaei medii, is manifested by the pulling of antagonists outward: in bed when the patient is lying on his back, the leg is turned outward; it also turns outward when walking. Prevention and therapy of N. Prevention of toxic N. first of all comes down to general hygienic measures necessary in any industrial institution. Premises must be sufficiently spacious and equipped with well-arranged ventilation, powerful enough to remove all poisonous products in the form of gases or the finest dust particles from the workroom. Workers must have the opportunity to wash their hands at any time. Eating in the workroom must be prohibited, for which special dining rooms must be available. During work, milk should be provided (to bind lead entering the stomach into albuminates). Periodic examinations of workers must be carried out in order to promptly detect intoxication in the very early stages. In the alcohol industry, the distribution of various alcoholic beverages to workers during production must be prohibited, which often occurs, for example, in breweries. Similar measures must be taken in other types of industry where poisoning is possible. In those places where dairy farming is well developed and where milking cows is a long and heavy work, mechanization of milking with special suction devices must be applied—and in many places has already been introduced—eliminating the possibility of professional N. among milkmaids. The same can be said about mechanization of cutting in tailoring, where manual cutting of heavy fabrics in several layers can give professional N. The widespread development of protective devices on various machines reduces the chances of traumatic neuritis. Prevention of infectious N. coincides with early diagnosis and proper therapy of the primary infection (early and quantitatively abundant use of serum in diphtheria, sufficiently long bed rest for the patient, etc.). Therapy of developed N. First of all, it is necessary, if possible, to eliminate the cause that caused the neuritis: leaving a harmful profession, treatment of the primary disease, etc. Then comes the application of physical therapy procedures—massage, electricity, etc. Massage gives better results in the case of manual massage; the so-called vibrational massage is already noticeably less effective. Massage can be applied already from the end of the 1st week after the onset of the disease. The duration of sessions can vary from 5 to 15 minutes daily. Simultaneously with massage or alternately, electrification of paralyzed muscles can be applied. Each muscle is irritated using a breaker electrode (it is best to use rhythmic electrotherapy with one or another current according to electrodiagnostic data). If there is no reaction of degeneration and the muscle is excitable to the faradic current, this latter can also be used. In recent years, stable electrification with electrodes moistened in solutions of calcium chloride, potassium iodide, etc. (ionogalvanization with calcium, iodine) is beginning to come into common use. The currently very widespread treatment of N. by diathermy is not entirely certain: along with the usual results, as with galvanization, sometimes a sharp exacerbation of pains has to be observed. Treatment with heat and light—dry air baths—is especially useful if it directly precedes a massage session: for example, the heated limb is wiped dry and then massaged. Of medicinal agents, the most useful is the subcutaneous administration of strychnine (Strychninum nitricum) in doses from 1 to 3 mg per dose, preparations of iron and phytin in usual doses (not arsenic!); specifically for lead N., preparations of iodine are recommended. For old-standing neuritis not amenable to conservative therapy, surgical treatment is indicated—anastomosis with one of the neighboring nerves, freeing the nerve from a scar in traumatic neuritis (neurolysis), resection of the changed area with subsequent suturing, muscle transplants, fixation of bones, e.g., of the scapula in paralysis of the n. thoracici longi, of the head of the humerus at a favorable angle for the patient to the scapula, etc. Here orthopedic-surgical assistance to the patient comes into play in the form of various active interventions and provision of appropriate prostheses.

M. Zakharchenko. Experimental neuritis is caused by applying various harmful effects to the animal organism: 1) in the form of poisonings (lead, arsenic, alcohol), 2) through unilateral feeding to cause B-avitaminosis (rice polyneuritis of birds), 3) by introducing certain infectious agents either in the form of a live virus or 4) in the form of a toxin, 5) finally some mechanical effects in the form of pressure on the nerve trunk can cause anatomical changes of a neuritic nature. Experimental N. make it possible to more deeply understand the essence of the patho-anatomical processes underlying N., since only in the experiment is it possible to step by step trace both the development and spread of these processes, and the changes in the highly diverse histological picture depending on the nature and intensity of the harmful effect and the species of animal. The general histopathology of experimental N. has been studied in greatest detail in the toxic and avitaminotic forms. - To induce toxic neuritis, methods of subacute and chronic poisoning are usually used. The most convenient method has long been considered the introduction of lead salts (Gombault). The introduction is done either per os by mixing insoluble lead salt (white lead) with the feed, or by a single introduction of a suspension of white lead in oil into the subcutaneous tissue of the animal (0.2 - to a cat), or finally by daily subcutaneous injection of soluble lead salt (Villaverde). Depending on the method of introduction and the species of animal, clinical symptoms develop with varying degrees of intensity. Paralysis of the extremities (initially of their distal parts), dullness and loss of hair are common phenomena, sometimes ulcers develop on the extremities. In guinea pigs, epileptoid seizures appear very early, often taking the character of status epilepticus and frequently causing the death of the animal. Rice polyneuritis, or beriberi in chickens (Eijkman) and pigeons as a result of B-avitaminosis is an extremely demonstrative object for studying both the most acute forms of polyneuritis, which proceed under the clinical picture of acute ascending paralysis of Landry, as well as the chronic form. The development of the nervous disease can be accelerated by forced feeding, and in this case the first signs of the disease often appear as early as the third week from the start of the experiment. Clinically, the disease manifests as a progressive disturbance of gait in the form of paralysis and ataxia of the lower extremities; after a few days the paralysis spreads to the wings, neck muscles, and respiratory musculature; the comb becomes cyanotic, drowsiness, stupor set in, and after a more or less prolonged agony - death. Cerebellar symptoms are common, especially in pigeons, from the very first days of the disease. - Among bacterial toxins, diphtheria toxin causes polyneuritis when introduced intravenously and subcutaneously. When the toxin is injected into the nerve trunk of a dog (Babonneix), following the onset of paralysis of the corresponding extremity, paralysis of the other extremities gradually developed. In all forms of neuritis, the medullated nerve fibers are characterized by a segmental periaxial nature of changes in the medullary sheath (nevrite segmentaire periaxile - Gombault). The histopathology of non-medullated fibers is still very little studied; in any case, they prove to be more resistant to various harmful effects. The classical picture of the periaxial process is given by lead polyneuritis in guinea pigs with subacute or chronic poisoning. The first noticeable changes consist in an increase in the number of so-called Eltzholz bodies (Stransky), i.e., the detachment from the medullary sheath of small droplets of altered myelin, which acquire the property of being stained black by osmic acid according to the Marchi method due to the release of free fatty acids. Initially, the most distal parts of the nerves are affected. As the number of Eltzholz bodies increases, the medullary sheath of the affected segments locally thins, the reactively proliferating Schwann cells together with immigrating mobile elements from the endoneurium - polyblasts - phagocytize the products of myelin degeneration. In the area of individual segments, the axis cylinder begins to show local changes. Finally, at some level of the nerve fiber, a break in the altered axis cylinder may occur, and the entire distal segment of the nerve fiber undergoes Wallerian degeneration. At any stage of the segmental changes, the process may stop, and even in the case of Wallerian degeneration, regeneration of the nerve fiber may occur. Moreover, with continuing intoxication, provided the dose of the poison is not high, destructive and regenerative processes develop in parallel and simultaneously. The newly formed fibers growing from the central stump of the interrupted axis cylinders remain non-medullated under continued poisoning. In a more acutely developing lead neuritis in rabbits, the periaxial changes are much less pronounced, the altered myelin detaches in larger masses, and usually a break in the axon and Wallerian degeneration soon occurs at some level. With very intense poisoning by daily subcutaneous injection of lead acetate (Villaverde), Schwann cells undergo such severe regressive changes that they lose the ability to active proliferation. After cutting the nerve of a heavily poisoned animal, the tissue reactions in the peripheral segment of the nerve are markedly slowed and limited - fragmentation of nerve fibers is extremely slowed, there is almost no karyokinetic division of Schwann cells, regenerative phenomena from the side of the central stump of axons are almost entirely absent. - In acute rice polyneuritis of chickens, segmental changes in the medullary sheath are only barely outlined, only a marked reaction from Schwann cells is noticeable, and soon massive Wallerian degeneration of nerve fibers occurs. Wallerian degeneration is thus also in these most acute forms only the outcome of the degenerative segmental process. But even with such a rapid course of the disease, axis cylinders show regenerative phenomena. The more acute the process, the more intense the inflammatory reaction from the vascular-connective tissue apparatus. These parallelly developing and mutually influencing processes - degenerative phenomena - in the nervous parenchyma and the inflammatory reaction in the connective tissue sheaths, in which one or the other predominates, - determine the so polymorphous patho-anatomical picture of neuritis. In recent years, the question of the spread along the peripheral and central nervous system of certain neurotropic ultravisible viruses (rabies, herpetic encephalitis of rabbits, Born disease, poliomyelitis, neurovaccine) and the localization of anatomical changes in various parts of the nervous system has been of particular interest. Numerous experiments have proven the passage of these disease viruses along the peripheral nerves. Along with widespread changes in the central nervous system in the form of encephalomyelitis, patho-anatomical changes of varying degrees of intensity are observed in different parts of the peripheral, cerebrospinal, and autonomic nervous systems, with either degenerative or inflammatory phenomena predominating. Often, the intervertebral and cranial sensory ganglia (Gasser's node, gangl. nodosum n. vagi), as well as sympathetic nodes and intramural plexuses, are particularly affected, in which ganglioneuritis may be observed. Thus the concept of 'septineuritis' (Nicolau) has been created as a generalization through the peripheral nerves of an invisible virus throughout the entire nervous system, central, peripheral, and autonomic, in the presence of obvious histopathological changes in various parts of the peripheral nervous system - somatic and autonomic. The 'septineuritis' caused by ultravisible virus can be compared with septicemia caused by visible microbes in the blood. By inoculating the herpes virus either into the cornea or into the thickness of the sciatic nerve of rabbits, Pette found initial pathological changes in the corresponding segments of the brain on the side of inoculation. In the trigeminal nerve, neuritic phenomena were weakly expressed, but Gasser's node showed a picture of severe ganglioneuritis. Ganglioneuritis of the ciliary ganglion was established in such experiments by Marinescu and Draganescu (Marinescu, Draganescu). In rabies, the data on the dependence of the localization of initial anatomical changes in the central nervous system on the site of inoculation are contradictory, but experiments from the laboratory of A. D. Speransky (A. M. Cheshkov) speak in favor of the segmental initial localization of changes in the central nervous system (local rabies).