Paralysis

PARALYSIS, acting in approximately the same direction (m. brachialis internus, m. supinator longus), but the function of the biceps muscle is permanently lost. Finally, the third very important feature of peripheral paralysis is the profound disturbance of trophicity of the corresponding muscles: the elementary peripheral motor center is at the same time also the trophic center. The muscles atrophy and in them develop extremely characteristic changes in excitability (so-called reaction of degeneration), the detection of which has very great diagnostic significance in diseases of the nervous system. These three properties essentially constitute the entire semiology of peripheral paralysis, a semiology well studied and in general not presenting special difficulties in terms of pathophysiological interpretation. The question of central paralysis is much more complex. The number of central motor systems that manifest their action through the same peripheral system is large; only in comparatively recent times has the structure of the central motor apparatus begun to be clarified more or less fully in all its exceptional complexity. Anatomically and clinically, the so-called pyramidal system (the direct corticospinal tract, represented by only one central neuron and not a whole chain of them, as in other cerebrospinal motor systems) was studied earliest, which in primates and especially in humans apparently takes particularly large part in the construction of complex motor functions. In any case, in clinical medicine, the doctrine of pyramidal paralysis occupies a central position at present, and it receives exceptionally much attention. The symptomatology of pyramidal paralysis presents many typical features. First of all, the distribution of paralytic disorders itself presents many characteristic features. Of the cranial nerves, only the facial nerve's inferior branch and the hypoglossal nerve are affected to any significant depth, while the III, IV, and VI pairs, n. trigeminus, the superior branch of the facial nerve, and the IX and X pairs remain completely preserved or (the superior branch of VII, V pairs) weakened only to a very slight degree. The bilateral central innervation of the corresponding nuclei undoubtedly has great importance for such preservation, in other words, the possibility of wide compensation from the other hemisphere. While for example the nucleus of the XII pair receives innervational impulses from only the opposite hemisphere, the nucleus of the V pair is innervated from both hemispheres, so that the destruction of its connections with one contralateral hemisphere cannot in any way lead to such profound disturbances of function as in the case of the XII pair. The same must be said of the muscles of the trunk, where paretic phenomena, if observed in unilateral pyramidal lesion, are still completely insignificant—sometimes a slight asymmetry of movements of the chest wall during breathing is noted, as if pneumonia occurs more frequently after stroke on the affected side due to weakening of respiratory excursions precisely here. The same unevenness is also noted in the lesion of the limb muscles. First of all, it should be noted that under otherwise equal conditions, the upper limb is affected much more strongly than the lower, and the restoration of its functions proceeds much more slowly and weakly. In the execution of movements of the upper limb, as of highly differentiated movements, the pyramidal path must take particularly large part, in the movements of the lower limb the proportional weight of this participation must be much smaller. Furthermore, unevenness of involvement of individual muscles of the same limb is noted. On the upper limb, the shoulder and scapula elevators, forearm, hand, and finger extensors, and forearm supinators are particularly affected. On the lower limb, the abductor muscles and hip flexors, leg flexors, and foot flexors particularly suffer. Furthermore, the paralysis itself presents essential features. As with any central paralysis, here we are not dealing with a complete loss of motor functions, but with their dissociation, with the loss of one part of them and the preservation of another, which not only does not weaken but also undergoes a sharp intensification ('change due to isolation' of Munk, 'dynamosis' of Davidenkov). Indeed, in the very initial stages after a severe stroke, motor functions usually completely disappear. However, here essentially we are not dealing with phenomena of pyramidal paralysis in the strict sense of the word, but with phenomena of peripheral paralysis: due to diaschisis (see), the cells of the peripheral neuron undergo such a great dynamic disturbance that they temporarily lose the ability to function. After a certain period of time, diaschisis is overcome, the cells of the peripheral neuron again become capable of function, and the picture of true pyramidal paralysis with symptoms corresponding to the lesion of only the central neuron is established. Dissociation is expressed in the fact that while voluntary movements become impossible or more or less weakened, such elementary functions as reflexes or tone not only do not weaken but are intensified. Of reflexes, however, this cannot be said about all, since dissociation is also observed here. And precisely the skin and mucous reflexes, the arc of which apparently passes through the cerebral cortex and in its effector part coincides with the pyramidal path, disappear on the affected side (the disappearance of abdominal reflexes on the side of paralysis is called Rosenbach's symptom). On the contrary, the so-called deep reflexes, tendon and periosteal, the arc of which is closed in the spinal cord, are sharply increased. At the same time, the so-called pathological reflexes also appear, i.e., reflexes that do not occur in normal conditions. This includes above all Babinski's reflex (see Babinski's reflex). Oppenheim's reflex (see Oppenheim's reflex), Gordon's (see Gordon's sign, reflex, phenomenon), Schaeffer's, and Redlich's reflexes have the same form. All these reflexes are a component part of the protective flexion reflexes (see Protective reflexes) or reflexes of spinal automatism, which arise only under the condition of isolation of the spinal reflex arc from the influence of impulses from the brain, in other words, in the lesion of central motor neurons. In their fully expressed form, protective reflexes are revealed only in those cases where, along with the pyramidal neuron, other central neurons are also turned off. For the appearance of the most sensitive part of the protective reflexes, namely Babinski's reflex and its homologs, the destruction of only the pyramidal path is sufficient. Along with the extensor pathological reflexes mentioned, flexor reflexes also appear in pyramidal paralysis, characterized by flexion of the toes of the foot. These include Rossolimo's, Mendel-Bechterev's (see Mendel-Bechterev's reflex), and Zhukovsky's (see Zhukovsky's reflex) reflexes. The isolation from the inhibitory influence of the path on the lower motor centers also explains the appearance in pyramidal paralysis of the so-called associated movements, i.e., involuntary movements accompanying voluntary movement. This includes above all the so-called global synkinesia: during forced muscle contraction on the healthy side, on the affected side abduction of the shoulder, flexion and pronation of the forearm, flexion of the hand and fingers, extension of the thigh and leg are observed. This also includes a number of so-called coordinator synkineses (see), of which on the upper limb the pronator and radial phenomena of Strümpel have the greatest significance, and on the lower limb—the tibial phenomenon of Strümpel, abductor and adductor synkineses of Raimiste, and Grasse's symptom (see Grasse's signs). Along with the increase of deep reflexes in pyramidal paralysis, muscle tone also increases, which is also a reflex. The hypertonia has a special character in this case: resistance either immediately arises with great force, and then after overcoming it passive movement proceeds relatively freely, as is observed in the extensors of the leg, or initially movement proceeds freely, and resistance appears only jerkily in one or another of its phases, as happens in the flexors of the forearm. In all these cases, resistance has a springy character. If the hypertonia is strongly expressed, contractures develop, the distribution of which is just as typical as the distribution of paralyses: the upper limb is adducted to the trunk, flexed and pronated at the elbow, flexed at the hand and in the fingers, the lower limb is extended at the hip and knee, the foot is plantarly flexed. Due to the extensor contracture of the lower limb, the gait of patients takes a characteristic character, they describe a semicircle with the elongated paralyzed limb at each step. The distribution of pyramidal paralysis, characterized by all the mentioned signs, depends on the localization of the lesion. With a lesion of the motor cortical zone, if the process does not involve the entire precentral gyrus, which happens comparatively rarely, usually upper or lower monoplegia (cortical monoplegias or monopareses) is observed.

With lesions of the internal capsule, hemiplegia occurs. With lesions of the brain stem at various levels, a peripheral paralysis of one or another cranial nerve on the side of the focus is added to the hemiplegia (see Alternating syndromes). With a lesion of one half of the spinal cord, hemiplegia occurs on the side of the lesion, not accompanied by paralysis of the VII and XII pairs, which is characteristic of cerebral hemiplegia. Finally, with bilateral lesions of the spinal cord, spastic paraplegia occurs. Extrapyramidal paralysis, like pyramidal paralysis, is characterized not by a complete loss of motor functions, but by their dissociation. However, this dissociation goes in a completely different direction here, namely - here the synergistic and automatic movements that normally accompany any of our actions are lost. As a result, a typical poverty of movement occurs; the patient appears as if frozen, moves like an automaton, not swinging his arms, not making any accompanying movements of the trunk or head. And the movements themselves are impaired, with their tempo being particularly affected (see Bradykinesia). The greatest difficulty is especially in their beginning; the patient cannot quickly rise from a chair on command, quickly open his eyes, etc. Just as severely affected is the ability to quickly change the direction of movement: the patient cannot turn quickly, he also cannot stop quickly, his forward movement becomes increasingly accelerated due to inertia (propulsion), with which he is unable to cope, etc. The tone changes in a typical manner. Here too, as in pyramidal paralysis, hypertonia occurs, however it is sharply different from spastic hypertonia. While there the resistance to passive movement has a springy character, in the rigidity characteristic of extrapyramidal paralysis, the plastic, waxy character is typical: the resistance is more or less uniform in all phases of movement and more or less uniform in agonists and antagonists, inhibition appears already at the beginning of the movement and remains until its end at approximately the same height. Pathological reflexes of the Babinski and Rossolimo type, in contrast to pyramidal paralysis, are absent, just as any marked increase in tendon and periosteal reflexes is usually absent. Instead, an increase in the so-called postural reflexes (see) occurs, i.e., those reflexes by virtue of which the limb tends to remain in the position given to it during passive movement. Of particular clinical importance in this group is the paradoxical Westphal phenomenon: a passively dorsiflexed foot freezes in this position, its extensors appear tense. Synergistic movements not only do not increase in extrapyramidal paralysis, as in pyramidal paralysis, but are sharply weakened or even disappear completely. Hysterical paralyses are deeply different from organic ones both in their essence and in their symptomatology (see Hysteria). Indeed, these paralyses can simulate both peripheral paralysis and hemiplegia and paraplegia and monoplegia of organic origin, however the similarity remains purely external, and especially the characteristic signs of organic paralysis, the so-called organic symptoms, are absent in such cases. Thus, in cases resembling peripheral paralysis, atrophies, if they occur, never reach a large extent, and most importantly, are never accompanied by qualitative changes in excitability, the appearance of reaction of degeneration. In paralyses simulating organic central paralysis, such "typical symptoms as Babinski, Rossolimo reflexes and their homologues are absent, cranial nerves are spared. In hysterical paraplegias, there are no disorders of the sphincters, which often accompany organic paraplegias, etc. Valuable diagnostic indications can also be given by an analysis of the general condition and character of the patient, as well as an analysis of other symptoms from the nervous system (nature of sensory disturbances, etc.). The causes of organic paralyses are extremely diverse. Paralysis is always only a symptom of the disease, not the disease itself; any lesion of the motor apparatus, whatever its cause, determines its occurrence. The prognosis is determined primarily, of course, by the causal disease. If the paralysis depends, for example, on the presence of a tumor somewhere in the area of the motor pathway, then the paralytic disorders will increase along with its growth. If it is a completed process, for example, residual phenomena of hemiplegia after a stroke, then the paralytic phenomena will either remain in statu (residual paralysis) or will improve due to compensatory help from other central motor apparatuses, etc. But some prognostic indications are also given by an analysis of the paralysis as such. Thus, in peripheral paralysis, the study of excitability can give very valuable indications for prognosis. In hemiplegia, the analysis of its course during the first weeks or months after a stroke is of great importance in this regard. The absence of any significant improvements during this time excludes hope for the restoration of motor functions later on. A special place in terms of prognosis is occupied by repeatedly recurring paralyses of the oculomotor and facial nerves, as well as the periodic paralysis of the limbs of Westphal, in which rapidly occurring paralytic phenomena last only a few hours, disappear, but then periodically reappear at certain intervals. Therapy should be primarily causal, i.e., the underlying disease should be treated first: suturing of the peripheral nerve in its traumatic injury, specific therapy in hemiplegia caused by specific endarteritis or in paraplegia in syphilitic myelitis, etc. But symptomatic therapy of the paralysis as such should not be neglected. In peripheral paralyses, electrotherapy, faradization (if excitability to faradic current has not disappeared) or galvanization with the cathode, as well as other physiotherapy, especially massage, are of great importance. In pyramidal paralysis, electrotherapy is often useless, and in the very common tendency to develop contractures, even harmful. If there are no contraindications from the general condition, heat procedures, the use of warm baths that reduce tone, are appropriate. Massage and gymnastics have some importance. The latter should be used with caution and in no way tire the patients.

I. Filimonov. Paralysis in pregnant women develops as a result of organic lesions of the nervous system during pregnancy, childbirth, or in the postpartum period in women who were previously completely healthy. Paralysis in pregnant women occurs on the basis of disturbed metabolism, dysfunction of the endocrine and autonomic systems during pregnancy. As with other pathological processes caused by pregnancy itself (toxemias), and with paralysis in pregnant women, other organs are usually involved, and the function of the entire organism is disrupted. In paralysis in pregnant women, not only the nervous system but also other organs suffer. The predominant lesion of the nervous system in such cases can be explained partly by the variety of toxins produced, partly by the dysfunction of the hemato-encephalic barrier, whose permeability always suffers in toxemias of pregnancy, and partly by the fact that the nervous system may represent a locus minoris resistentiae. In addition to the influence of pregnancy itself, the occurrence of paralysis can be caused by infection and trauma. In infection, the process develops acutely, proceeds with elevated temperature; paralysis can occur as a result of pressure from the child's head on the nerve plexuses and nerve trunks of the pelvis or after the application of forceps (traumatic neuritis of the n. ischiadici, obturatorii, femoralis). Paralysis can also occur on the basis of kidney lesions or impaired cerebral circulation during pregnancy, and strokes during childbirth are often the most extensive and destructive. Paralysis in pregnant women develops at any age, sparing neither elderly nor young women. The history and laboratory studies give no indications of syphilitic infection. Paralyses are more common in the second half of pregnancy or during childbirth, less often in the postpartum period; starting with mild paresis, they reach their climax by the end of pregnancy or at the time of childbirth, progressing to complete paralysis of the limbs; after childbirth or artificial abortion, the paralysis phenomena gradually disappear. Paralysis occurs in both first-time and multiparous women. With a new pregnancy, repeated paralysis are often observed. In the absence of infection, paralysis mostly proceed with normal temperature. The blood in most cases shows no deviations from normal. In the urine, some authors found acetone, acetoacetic acid, sugar, and protein; but it should be noted that these findings are very rare, and in most cases the urine in these toxic paralyses remains normal. Paralysis in pregnant women occur with lesions of either the central or peripheral nervous system, or both simultaneously. In the first case, the brain or spinal cord or both at the same time suffer. Cerebral paralyses sometimes develop like a stroke without any precursors, but still prodromal symptoms are more often noted-headaches, nausea, vomiting, dizziness, then weakness in one or more limbs; by the end of pregnancy or even in the first days of the postpartum period, paresis often progresses to complete paralysis. After a short time, the paralysis phenomena begin to diminish and decrease; with appropriate treatment, recovery proceeds quite quickly, and the paralysis phenomena can completely disappear. A new pregnancy may lead to a repeated paralysis of the same or another limb. In central paralysis, hemiplegias are most often observed, less often mono-, tri-, and tetraplegias.-In spinal puerperal paralyses at the beginning of the disease, weakness of one or more limbs is also noted, which in case of continuation of pregnancy sometimes progresses to complete paralysis. Here, both lower limbs (paraplegia) are most often affected, although cases of paralysis of all four limbs have been observed. Windscheid observed paraplegia that recurred with a new pregnancy ('recurrent myelitis'). After childbirth or abortion, spinal paralyses improve significantly, and in mild cases, they disappear completely.-Peripheral paralyses during pregnancy, childbirth, and in the postpartum period develop as a result of lesions of individual nerves or the entire peripheral nervous system ('neuritis of pregnancy', 'puerperal neuritis'). Of the cranial nerves, any nerve (facial, oculomotor, etc.) can be affected. On the upper limbs, the ulnar nerve is more often paralyzed, on the lower limbs-the sciatic nerve (n. peronaeus). The most severe disease is polyneuritis, accompanied by paralysis of 4 limbs and often combined with Korsakoff's psychosis. Severe cases always arise as a subsequent stage of intractable vomiting, whereas in local neuritis, vomiting (even simple) is almost absent. The disease mostly develops in the second half of pregnancy (in the presence of intractable vomiting and in the first months) and reaches its full development sometimes only after childbirth or abortion. While the disease sometimes develops quite rapidly, recovery can be prolonged for 1-2 years or more. Simultaneous lesion of the vagus or thoraco-abdominal nerves is life-threatening for the mother. Often the disease initially proceeds with elevated temperature.-Polyneuritis during pregnancy sometimes develops simultaneously with myelitis. The mortality rate in polyneuritis of pregnant women is 24-26%. Pathological anatomy. In cerebral paralyses of pregnant women, hemorrhage, thrombosis of vessels, embolism are found in the brain; then kidney lesions leading to brain disease (albuminuric paralysis of pregnancy-Hosslin) are encountered. In the latter case, foci of hemorrhage (apoplexia sanguinea) or limited brain edema (apoplexia serosa) are found. Cases are observed where in the picture of cerebral paralysis there are absolutely no indications of kidney lesions, embolism, hemorrhage, or thrombosis. In paralysis of spinal origin, there are myelitides (intoxicative, infectious, albuminuric, hematomyelitides), diffuse degenerative changes of the conducting pathways, atrophy of the cells of the anterior, posterior horns and Clark's column. In peripheral paralyses of pregnant women, parenchymatous neuritis with pronounced vascular phenomena, parenchymatous changes of the vagus and thoraco-abdominal nerves are found. In addition to changes in the central and peripheral nervous systems, at autopsy, various toxic changes in the kidneys, liver, and heart are always observed. Treatment. Paralyses developing during pregnancy are not an indication for interruption of pregnancy and do not exclude the possibility of normal childbirth. Therefore, one should not hurry and immediately resort to abortion if the symptoms are not increasing and nothing threatens the life of the mother and child. With progressive phenomena, before deciding on artificial delivery, it is necessary, along with complete rest, to try normal horse serum (15-20 cm^g intravenously or into the subcutaneous tissue several times, with intervals of 2 days), or Ringer's solution, or 5% glucose solution, which in a fairly large percentage of cases give very good results. If all these means do not improve the condition of the patient or if a decrease in vision is noted, it is necessary to interrupt the pregnancy regardless of its term. In polyneuritis, in most cases, it is necessary to interrupt the pregnancy. Since the blood in the second half of pregnancy and in the postpartum period often gives a nonspecific Wassermann reaction, one should be very cautious in applying antisyphilitic therapy, which often worsens the condition of the patient. The developed paralyses of pregnancy, as well as paralyses of other origins, must be treated by all usual physical methods. Paralysis during one pregnancy gives grounds to warn a woman against a second pregnancy (or at least to postpone its onset). If the latter occurs, it is necessary to strictly monitor the condition of the nervous system and at the slightest hint of deterioration to interrupt the pregnancy.