Polyneuritis

POLYNEURITIS (from the Greek polys—many, neuritis—inflammation of a nerve), multiple inflammation of nerves (syn.: symmetrical peripheral neuritis, multiple neuritis). Establishing the concept of inflammation of peripheral nerves is an achievement of relatively recent times; although the term "neuritis" has existed for a long time, it was used to denote mechanical (traumatic) injuries of nerves and the fact of their involvement in a purulent process. In connection with the previously existing idea of the absence of vessels in nerves, the possibility of an inflammatory process in them was also denied. The famous Dutch physician Boerhaave (1668–1738) formulated this view with the following aphorism: nemo forte unquam vidit inflammationem in nervo (no one has ever seen inflammation in a nerve). Cruveilhier (1791–1874) admitted the possibility of inflammation "in the neurilemma and adipose tissue located in the thickness of each nerve trunk," but "not in the nerve fiber itself." Despite, however, the lack of familiarity with the pathological-anatomical essence of polyneuritis, its clinical picture was beautifully described by English physicians Lettsom in 1789 and Jackson in 1822. For the first time, the connection of this symptom complex with nerve damage was suggested by Graves, who expressed the view about the possibility of "very remarkable cases of disease of the nervous system, starting from the extremities and not depending on damage to the brain or spinal cord." Soon after this, Dumesnil (1866) described two cases of multiple neuritis, in which he managed to establish the presence of nerve inflammation pathologically-anatomically. Starting from the last third of the 19th century, the concept of polyneuritis as an inflammation of nerves was precisely established. In 1862, the neuritic nature of diphtheritic paralysis was established. In 1871, changes in nerves were established in relation to lead paralysis. During the same period, alcoholic polyneuritis was studied in detail. In 1889–90, the clinical picture of polyneuritis was significantly supplemented thanks to the description by Korsakoff and his students of the psychotic symptom complex observed in polyneuritis (see Korsakoff's psychosis). Finally, in the very recent time, in connection with the doctrine of vitamins, the connection of some forms of polyneuritis with avitaminosis has been established. To the definition given above of polyneuritis as an inflammation of nerves, it is necessary to make a reservation: firstly, many of the diseases classified in the group of polyneuritis represent, by their pathological-anatomical nature, not inflammatory but degenerative processes; secondly, in very many cases, the changes are not limited to peripheral nerves but also extend to the central nervous system; such changes are found especially often in the spinal cord, namely in the cells of its anterior horns. Such a change in nerve trunks, combined with damage to the cells corresponding to them, was proposed to be designated by the term "cellulo-neuritis," "polyneuritis" (V. K. Roth), or "polyneuromyelitis." Besides these cases of more or less sharp damage to the cells of the anterior horns, which can be considered as the starting point of the disease of peripheral nerves, very often in polyneuritis, insignificant changes are observed in the cells of the anterior horns (partial chromatolysis), which represent an expression of retrograde degeneration and are not the cause, but the consequence of damage to the nerve trunks. Finally, in some cases, the changes in the cells of the anterior horns represent neither the cause nor the consequence of changes in the nerve trunks, but only a phenomenon accompanying them, which is dependent on cachexia, high temperature, etc. The fact of the involvement of the brain in the pathological process during polyneuritis is evident especially in those cases that are accompanied by mental disorders in the form of Korsakoff's syndrome; changes in the brain are detected in such cases also histologically in the form of minute plaques consisting of glial fibers that have overgrown in the places of decay of nerve cells. With strong overgrowth of these plaques, macroscopic changes in the cerebral cortex also arise in the form of more or less noticeable thinning of the convolutions. As for the essence of the changes observed in polyneuritis in the nerve trunks, it is customary to subdivide them into two main forms: parenchymatous (degenerative) and interstitial (inflammatory). Although there are gradual transitions between these two forms and although in many cases of polyneuritis there are combinations of parenchymatous and interstitial changes, for acquaintance with the details of the changes occurring in nerves during polyneuritis, it seems convenient to adhere to such a division. Parenchymatous polyneuritis, in turn, is subdivided into axial, in which the decay of the nerve fiber occurs according to the type of Wallerian degeneration (death of all elements of the nerve fiber downward from a known level), and periaxial, in which it is a matter of the decay of the myelin sheath intermittently, i.e., in limited areas, while the axial cylinders remain intact. In periaxial neuritis, due to the preservation of the axial cylinder, the conductivity of the nerve is not disturbed, and functional disorders may be absent. Between axial and periaxial processes, there are various combinations, and sometimes the periaxial process is only the initial stage of degenerative neuritis, passing then into the stage of axial neuritis. The periaxial process represents a mild, reversible form of parenchymatous polyneuritis. In interstitial polyneuritis, it is a matter of inflammatory infiltration with edema and hemorrhages, localized in the connective tissue sheaths of the nerve fibers with subsequent organization. One should not, however, think that the changes in nerve fibers during interstitial polyneuritis are caused exclusively by their compression by the thickening connective tissue; independent changes occur in the nerve fibers due to phenomena of axial and periaxial processes. Thus, parenchymatous and interstitial processes are often combined with each other. In general, it can be said that interstitial processes are characteristic of more acute infectious polyneuritis, and parenchymatous—of chronic intoxication polyneuritis. However, this position represents no more than a general scheme, and on the basis of the histological picture, it is far from always possible to correctly establish the nature of the harmful agent that caused the given polyneuritis. The predominance of parenchymatous or interstitial changes is determined more by the degree of the harmful effect of the given factor than by its nature. Regarding the localization of pathological changes in polyneuritis, the following can be noted: polyneuritic changes are usually symmetrical; they are expressed exclusively or at least significantly predominate in the nerves of the extremities compared to the nerves of the trunk and head; as a rule, these changes are expressed most sharply in the distal (peripheral) sections of the nerves. From an etiological point of view, polyneuritis can be subdivided into infectious, intoxication, and autointoxication, or "dyscrasic." Along with toxic-infectious factors, a certain role in the development of polyneuritis also belongs to predisposing moments. In childhood, polyneuritis is observed much less often than in adults, which is only partly explained by the lesser susceptibility of children to those harmful agents that are pathogenetic factors of polyneuritis (alcohol, lead, etc.), since childhood also shows insignificant susceptibility to those diseases of nerve trunks whose pathogenetic factors are also inherent in childhood. It is enough to recall that "colds" inflammation of the sciatic nerve ("sciatica"), so common in mature age, is not observed at all in children. Only diphtheritic paralysis constitutes a very frequent phenomenon in childhood, which is in connection with the frequency of diphtheria in childhood, and it is possible that the number of diphtheritic polyneuritis in relation to the number of cases of diphtheria in general is no greater than in adults. General exhaustion of the body and infectious diseases predispose to the development of polyneuritis; thus, alcoholic polyneuritis sometimes develops in old alcoholics under the influence of accidental infection; the same was noted in relation to lead polyneuritis. There are observations that force one to admit that in the presence of long-standing alcoholism, the immediate push for the development of polyneuritis can serve as emotive experiences. Polyneuritis can also be observed during pregnancy. More often it arises on the basis of intoxication and belongs in such cases to the group of toxicoses of pregnancy; less often, infectious polyneuritis is observed (joining postpartum infection). During pregnancy, polyneuritis can arise as an independent disease or it can develop as one of the subsequent symptoms of intractable vomiting (see Vomiting) and then takes the form of Korsakoff's syndrome. Not only the nerves of the extremities can be affected, but also the optic nerve, phrenic nerve, vagus nerve, etc. The prognosis is usually favorable; in severe cases and especially in polyneuritis accompanying intractable vomiting, artificial termination of pregnancy is indicated. From the point of view of occupational medicine, the fact of the connection of certain professions with susceptibility to certain harmful agents, which are pathogenetic factors of polyneuritis, is of particular importance. The main place among these harmful agents belongs to lead poisoning (see Neuritis).

The significance of occupation for the pathogenesis of polyneuritis, apart from toxic hazards associated with a specific job (lead, mercury, arsenic), is also determined by the exhaustion of the neuromuscular apparatus associated with that work. As is known, Edinger formulated the 'exhaustion theory' (Aufbrauchstheorie), according to which one of the main factors determining the localization of lesions under various toxic influences is the exhaustion of the neuromuscular apparatus: those elements that, being distinguished by low strength, must perform increased work under unfavorable conditions are damaged earliest and most severely. Although Edinger's theory cannot be considered at the present time to have been justified in its entirety, the basic idea regarding the significance of exhaustion as a factor contributing to the localization of the pathological process can be considered correct and should not be ignored in the matter of polyneuritis prevention. From the point of view of social medicine, the significance of polyneuritis is not exhausted by the possibility of their development under the influence of occupational hazards. The important role of alcohol in the etiology of polyneuritis and the frequency of alcoholic polyneuritis, leading to disability or at least to prolonged incapacity for work, are one of the grounds for the fight against alcoholism. The public health significance of familiarity with polyneuritis is also determined by the possibility of timely preventive measures against mass outbreaks of polyneuritis under the influence of poisoning by substandard food products. The best illustration of what has been said can serve the epidemic of polyneuritis in Manchester and its surroundings in 1900. Only thanks to the establishment by Reynolds of the arsenical nature of these polyneuritis cases and the detection in beer of arsenic, which had penetrated from insufficiently pure sulfurous copper used in the production of beer, was it possible to halt the further development of the 'epidemic.' The symptomatology of polyneuritis consists (see also Neuritis) of a combination of atrophic paralyses with sensory disorders. These two main groups of disorders combine in various ways in etiologically different forms of polyneuritis. As a general property of polyneuritis, one can note the features of motor and sensory disorders observed in polyneuritis, which were already indicated above: their symmetry and predominance in the distal parts of the limbs compared to the proximal ones. The etiological factor is placed at the basis of the classification. But since certain clinical symptom complexes are characteristic for etiologically different polyneuritis cases, and on the basis of the latter it is often possible to establish the etiological nature of polyneuritis, a classification based on the features of the clinical manifestations of polyneuritis also appears appropriate. From this point of view, polyneuritis is subdivided into the following varieties or types. - General, or mixed type, in which there is a more or less uniform disturbance of motor and sensory functions and trophic disorders; alcoholic and arsenical neuritis belong to this type. - Motor type, characterized by the exclusive presence or significant predominance of paralytic phenomena; lead polyneuritis and the polyneuritic form of Landry's syndrome [see Landry's ascending paralysis (disease)] belong to this group. Atactic type (syn.: polyneuritis atactica, neurotabes peripherica, pseudotabes, false tabes dorsalis). This form is characterized by three symptoms resembling tabes dorsalis: pain, loss of tendon reflexes, and severe ataxia due to a disorder of muscle-joint sensitivity; polyneuritis of various etiologies can take a pseudotabetic form, but it is observed especially often in diphtheritic and alcoholic polyneuritis. Vasomotor type - with a predominance of vasomotor disorders. Attempts to consider Raynaud's disease as a consequence of a neuritic process appear poorly substantiated; but one cannot deny the fact that sometimes in polyneuritis, vasomotor disorders reach a degree close to Raynaud's syndrome. This is observed, for example, in polyneuritis developing after typhus. In these same forms of polyneuritis, changes resembling erythromelalgia are sometimes observed. Recently, a form of polyneuritis has been described, observed mainly in Australia and North America. Its most characteristic symptoms are edema and sharp redness of the skin in the area of the face and distal parts of the limbs; hence the name of the disease 'erythro-edematous polyneuritis.' Paralyses are very indistinctly expressed, but there is significant hypotonia. The disease is observed in early childhood (about 2 years old). Pathoanatomically - phenomena of polyneuritis. The prognosis is favorable; as a rule - complete recovery. Atrophic type (polyneuritis acuta amyotrophica) is characterized by an extremely sharp and rapid development of atrophic phenomena; one gets the impression that atrophy precedes paralysis and that the degree of paralytic phenomena is determined by the degree of atrophy. Some forms of acute infectious ('rheumatic') polyneuritis proceed according to this type. As a chronic form of 'atrophic polyneuritis,' neurotic muscular atrophy (Charcot-Marie type) can be considered. With less right, one can include here, as some do, 'progressive hypertrophic polyneuritis' (Dejerine-Sottas), since in this form, both clinically and anatomically, the matter is not limited to the involvement of peripheral nerves; the latter remark also applies to Charcot-Marie muscular atrophy. Psychotic type (synonyms: Korsakoff's syndrome, polyneuritic psychosis, cerebropathia psychica toxaemica) - see Korsakoff's psychosis. Psychic phenomena are usually discovered at the height of the development of neuritic symptoms. Only in exceptional cases do psychic phenomena precede paralytic ones. The described clinical manifestations of polyneuritis combine in various ways in individual cases, and very often, from a single clinical picture, it is impossible to make an accurate conclusion about the etiological nature of a given case of polyneuritis. Very often, the etiological diagnosis can be established only on the basis of anamnestic information. Besides the anamnesis and neurological symptoms, data from a general medical examination are, of course, also of important significance: detection of diabetes, pregnancy, tuberculosis, cancer, scurvy, etc.; laboratory and clinical establishment of signs of poisoning with lead, mercury, etc. Infectious polyneuritis is determined in regard to its nature by the underlying infection on the basis of which it develops. There exist, however, not a few cases when polyneuritis, having all the features of an infectious disease (acute onset, fever), develops 'primarily,' i.e., without the subject having any infectious disease. Such cases are designated by the terms 'rheumatic,' 'catarrhal,' 'idiopathic' polyneuritis. Those polyneuritis cases assigned to this group are apparently different in their nature: a part of them represents sporadic cases of the neuritic form of Heine-Medin disease (see) (Wickmann); the second group consists of cases in which it is a matter of toxic (alcoholic) polyneuritis, with the infection (influenza) serving only as a trigger for the development of neuritic phenomena; finally, in some cases, the underlying infection, perhaps, simply remains unrecognized. Diagnosis of polyneuritis does not present difficulties: it is based on a combination of flaccid paralysis, absence or reduction of reflexes, sensory disorders, and trophic disorders with their predominance in the distal parts and symmetry of distribution. The prognosis in polyneuritis can generally be considered favorable. It is determined by various factors: the vital importance of the nerves involved in the process (nn. vagus, phrenicus), age, general condition of the organism, etiological nature; infectious polyneuritis generally proceeds more favorably than toxic; among toxic ones, the most severe are alcoholic and arsenical polyneuritis. Treatment of polyneuritis. In toxic neuritis, first of all, it is necessary to protect the patient from the new intake of the harmful factor. In all polyneuritis cases, the elimination of toxins by means of enhancing metabolism, diuretics, and baths is indicated; light baths are especially useful. Treatment of motor disorders is according to the general rules of therapy for flaccid paralyses (massage, electrification, gymnastics); of very important significance is the prevention of the development of fibrous degeneration of joint capsules and tendons and their stretching under the influence of the hanging of the distal parts of the limbs, the pressure of the blanket on the feet, etc. Against pain - usual painkillers (not morphine), wet wrappings of the distal parts of the limbs. Prophylaxis is of important significance in toxic polyneuritis. It appears very important to detect early forms of chronic poisoning that have not yet given a picture of polyneuritis. Prophylaxis of occupational polyneuritis is divided into the following measures: 1. General hygienic - rational ventilation, a sufficient number of devices for washing hands; prohibition of eating and smoking without prior washing of hands; provision of milk to workers dealing with lead, etc. 2. Social prophylaxis: in especially harmful industries, temporary transfers of workers to other work are necessary; supervision over the precise execution of regulations limiting the danger of poisoning is necessary, and ensuring the possibility of implementing these regulations. 3.

Technical prophylaxis: changes and improvements in technology that eliminate or reduce the possibility of poisoning, such as: the introduction of machine processing instead of manual, the replacement of materials hazardous to health with harmless ones. 4. Personal prophylaxis, the basis of which should be popular but thorough familiarization of workers with methods of protecting themselves from the harmful influence of substances used in production through hygienic measures.