REFERENCES.
[1] Meillère, G.: Le Saturnisme. Paris, 1903.
[2] Blyth, Wynter: Proc. Chem. Soc, 1887-88.
[3] Peyrusson and Pillault: Meillère’s Le Saturnisme, chap. iv.
[4] Newton Pitt: Trans. Path. Soc, No. 42, 1891.
[5] Glibert: Le Saturnisme Expérimental: Extrait des Rapports Ann. de l’Inspect. du Travail, Brussels, 1906.
[6] Moritz: Mediz. Woch., St. Petersburg, 1901.
[7] Schmidt: Arch. für Hygiene, vol. lxiii., p. 1, 1907.
[8] Glibert: Ibid.
[9] Boycott: Journal of Hygiene, 1910.
CHAPTER IX
THE NERVOUS SYSTEM
Symptomatology and Diagnosis (Continued)—The Nervous System.
—The most definite objective symptoms of chronic poisoning by means of lead are those of the nervous system. From the time of Tanquerel[1] affections of the hands and fingers and the muscles of the back have all been well known. Associated with the paralysis are local vaso-motor effects, such as cyanosed condition of the skin over the paralyzed muscles, cold hands, etc.; whilst later, if the paralysis be severe and persists, atrophic changes take place in the skin, muscles, bone, whilst definite contracture occurs from unopposed contraction of the unaffected muscles. Paralysis will therefore be associated with two of the great systems into which the body is divided for the purposes of medical and physiological description—namely, the muscular and the nervous—and, on account of the similarity of the clinical symptoms of lead paralysis, attention has been drawn rather to the nerve changes preceding muscular paralysis and degeneration than to other influences affecting the nerve inflammation.
Lancereaux[2] considered that lead poisoning resulting in paralysis takes the form of a gradual impregnation of the nervous tissue with lead salts, until such a time as degenerative effects are set up, and with it muscular paralysis.
Meillère[3], who has given much attention to the ætiology of lead poisoning, as well as to the clinical study of the disease, considers that plumbism may be divided into three periods:
(a) Impregnation of the tissues of the body, the nervous tissue being the chief one affected by lead salts.
(b) Retardation of the general oxidation changes of the body, resulting in malnutrition and general loss of tone.
(c) Establishment of intoxication, with the generalized affections, paresis, etc.
If three such periods can be recognized, as no doubt they can, as divisions of the time during which lead gradually affects the tissues, the symptoms in the more severe cases would be expected to be those associated with the more prolonged exposure. This, no doubt, is true to a limited extent, more particularly in industrial poisoning, depending for its development on a long-continued dosage of lead in minute quantities, and for the most part of metallic lead. On the other hand, with some of the salts of lead, notably the hydrated carbonate, acute disease may take place during the first stage—namely, impregnation of lead—the determining factor then being either the retardation of the elimination of lead, or a suddenly increased quantity in lead dosage, or some intercurrent disease, or even alcoholic excess, whereby a sudden large excess of the poison is thrown into the general circulation.
The commonest type of paralysis occurring is the one affecting the muscles of the hands, which may for a considerable time show some diminution in their extensor power before the actual onset of the disease takes place. The onset of paralysis is practically always unaccompanied by pyrexia; the only occasions in which pyrexia may be associated with the onset of the attack are those cases in which some secondary cause determines the paralysis, and the pyrexia in these instances is due to the intercurrent disease, and not to the lead infection.
Although weakness of the extensor muscles of the hands may be present in persons subjected to lead absorption for a considerable time, the actual onset of the disease itself is frequently sudden; but in the majority of cases it is distinctly chronic, and is rarely, in the case of paresis, associated with any definite prodromal symptoms. Prodromal symptoms have been noted, such, for instance, as lassitude, general debility, and more especially loss of weight. Cramps of the muscles the nerve-supply of which is becoming affected, alteration of the skin over areas corresponding to definite cutaneous nerves, hyperæsthesia, anæsthesia, or analgesia, may occasionally be present. Neuralgic pains have also been described, but these are inconstant, and generally of the arthralgic type related to the periarticular tissues of joints rather than to pain in the course of the nerves. The pain is rather of the visceral referred type than a definite neuralgia. Tremor is, however, frequently associated with the preliminary condition of paresis, and in several cases variations in the amount of weakness of the extensor muscles of the wrist have been noticed, as far as can be estimated clinically without the use of a dynamometer. Associated with this weakness is tremor of a fine type, often increased by movement (intention tremor), and in every case more marked during the periods of increased weakness. Instances have occurred where definite wrist-drop followed after a prolonged period of weakness; in others the weakness has temporarily cleared up for six months, and no difference could be determined in the extensor power of the two wrists; while in others, again, the weakness is progressive, but slight, and insufficient to warrant the removal of the workman from his occupation. Again, progressive weakness may remain a symptom of the wrists of workmen for years.
The Forms of Lead Paresis.
—The paralysis may be partial or generalized, but the chief muscles affected are the extensors of the wrists and the forearm, and the interossei of the hand. As a rule, the first muscles to be affected are the extensor communis digitorum and the extensor indicis. The muscles of the shoulder—mainly the deltoid—come next in order, followed by the muscles of the leg, particularly the peroneus longus and brevis, with occasionally the interossei of the foot; the muscles of the back, neck, and abdominal walls, are occasionally affected, as are those of the larynx and diaphragm, and it is of interest to note that Trousseau pointed out that among horses employed in lead works paralysis of the superior laryngeal nerve often occurred.
Considerable difficulty is experienced in estimating the reason of the predilection of lead for the musculo-spiral nerve, this being the nerve mainly affected in wrist-drop. Owing to the fact that the supinator longus receives an additional nerve-supply to the musculo-spiral, this muscle frequently escapes paralysis when the whole of the other extensors of the hand are involved. Moreover, the predilection for given nerves differs in different animals, and one of us (K. W. G.) has found experimentally that in cats the first nerve to be affected is the anterior crural supplying the quadriceps extensor, whilst the second group of muscles affected are the spinal muscles, particularly in the lumbar region.
Among the speculations which have been made with regard to this predilection for definite groups of muscles supplied by one nerve, Teleky[4] examined forty cases of paralysis with special reference to Edinger’s theory—namely, that the function of muscles (and of other organs) breaks down under certain circumstances before the strain set upon them. In this way Edinger explains paralysis following lead poisoning as being due to excessive strain on the particular group of muscles affected, based on a consideration of the relative volumes and weights of the muscles of the hand and forearm, and the demands made on the several groups, flexors, extensors, supinators, etc., by the coarse or fine work respectively demanded of them in industrial employment. He concludes that—
1. Of the forearm, the flexors (triceps, anconeus, extensors, biceps, brachialis anticus, and supinator longus) possess a high degree of capacity for work, but are not called into play mainly in the execution of fine work; while the supinators are characterized by great mass, and are brought into play mainly in work of coarse and heavy nature, and not during fine manipulations.
2. The muscles concerned in pronation are of small capacity for work, and are not called on for sustained work.
As for the muscles acting on the wrist and hand, he concludes that the extensors (carpi radialis longior and brevior, carpi ulnaris, and the extensors of the fingers) are powerful, and much exceed in capacity for work the flexors (flexor carpi radialis, flexor carpi ulnaris, the flexors of the fingers, etc.), but in all fine manual work, and specially where close grasping movements enter into association with the flexors, external strain is put upon them, whilst the flexors merely support their action.
The extensor communis digitorum is the weakest of all the long finger muscles; its volume is hardly one-fourth that of the corresponding flexors, and while it acts only on the first of the phalanges, the flexors act on all three. In all fine work they are called on for heavy strain, especially the interossei and the lumbricals, but in harmony with the long flexors when grasping movements are performed. The small muscles of the fingers have nearly the same mass as the extensor communis, and in all fine movements the grasping efforts are taxed severely; but their play is under considerably more favourable physical relations than that of the extensors, whilst in addition they are aided in their work at times by the long flexors. The chief adductor muscle of the thumb (extensor metacarpi pollicis) is particularly powerful; the other extensors of the thumb are very weak, and work under unfavourable physical conditions, but are supported in their action by the strong abductor muscle. The muscles of the abductor, opponens and flexor brevis, in the complicated work thrown on the thumb in manipulation, are much exerted, so that the effects of overexertion show themselves first in this region.
Thus, Edinger maintains that the muscle-supply of the arm is designed for coarse heavy work, the muscles of the fingers and the hand having to carry out more work than can be expected of them from a consideration of their volume and their physical action.
The commonest form of lead palsy, the antibrachial type of Déjerine-Klumpke[5], is explicable from consideration of overexertion of the particular group of muscles named. The supinator muscle, supplied also by the musculo-spiral nerve which serves the paralyzed muscles, escapes because of its size, and the fact that functionally it belongs to the flexor group, and the first-named reason also, explain the frequent escape of the long abductor of the thumb.
Teleky[6] investigated thirteen slight cases of the antibrachial type. In one both hands were affected, in one the left only, and in all the others the right only—facts which he thinks bring out the rule of causation by employment. Of fourteen painters, three had the right forearm affected only, the other eleven both right and left, but always more marked in the right. Amongst them he cites cases where the shoulder muscles were paralyzed, which he considered was due to the extra strain of unusual employment, involving a raising of the arms above the head, or lying on the back painting the under parts of carriages. In several of the painters the index-finger was the least affected, by reason of the less exertion thrown on it by the position assumed in holding the brush between the second and third fingers. The long abductor, probably because of its size and power, is in no case completely paralyzed.
In file-cutters he insists that the predominant share, falling on a single or on several small muscles of the hands, makes the early appearance of paralysis of the small muscles the characteristic sign. In this connection we have frequently observed decrease in the size of the thenar and hypothenar eminences amongst lead rollers; in fact, in the majority of lead rollers who have followed their occupation for a large number of years the flattening of both thenar and hypothenar eminences is well marked, but it is only fair to point out that in these cases very considerable stress is thrown on the muscle of this part of the hand by the pressure of the lead plate in pushing it inwards into the roller and grasping it on its appearance back again through the roller, and that, further, the use of large and clumsy gloves with all the fingers inserted into one part, and the thumb only into the other, tends to produce inaction of portions of the lumbricals and of the opponens pollicis, and may, therefore, from purely mechanical reasons cause damage to this part of the hand.
Teleky[7] cites cases of right-sided paralysis of the adductor brevis pollicis supplied by the median nerve, and partial paralysis of the long extensors and of the extensor ossis metacarpi pollicis supplied by the radial nerve, and in one or two cases complete paralysis of the thenar muscles and adductor, whilst the extensors of the fingers and wrists were only partially paralyzed. The cases all occurred in lead capsule polishers. This particular selection of muscles is clearly the result of the peculiar movement necessary in polishing the capsules of bottles on a revolving spindle, involving specially the use of the opponens muscle.
This observation of Teleky’s is in direct accord with the observation quoted above of the hands of persons engaged in lead rolling.
In the lower extremity, paralysis of the muscles associated also with paralysis of the adductor and extensors of the thumb was found by Teleky in a shoemaker who had contracted plumbism by the use of white lead. He explains this lower extremity paralysis by the exertion thrown on the adductor muscles of the thigh whilst holding the shoes.
In children affected with lead palsy the lower extremities are more frequently paralyzed than the upper, due to the relatively greater strain in childhood on the legs than on the arms.
Edinger’s theory, supported as it is undoubtedly by Teleky’s observations, is a matter of the greatest importance in the production of paralysis; for if we accept the view that lead is a poison that has a selective power on certain nerves, we have still to consider which is the greatest force, the selection of certain groups of muscles or the effect of functional action. The theory of muscular overexertion certainly falls in with the type of paralysis, and Teleky has undoubtedly shown that under certain circumstances, by special exertion of other muscle groups not usually affected, these muscles alone, or to a greater extent than those usually affected, are involved in the paresis. If, therefore, lead has a selective action, which is exceedingly doubtful, it must be very slight.
Such selective action is, of course, exceeded by a functional activity which brings about the affection of those nerves which supply the muscles most used. If, therefore, we judge of paralysis as being due to the selective action of lead on certain nerves, we are met at once with the objection that the muscles affected do not always correspond to such a nerve distribution, and that muscles supplied by other than the musculo-spiral nerve are affected by paralysis.
Careful consideration of the chapter on [Pathology], and more particularly of the histological findings described, in which the preliminary action of lead is found to be typically and invariably on the blood, setting up degenerative changes microscopical in size and limited in area, affecting the vessel walls and producing a yielding of the vessel, determining minute microscopical hæmorrhages distributed, not necessarily in one position of the body, but all over the body, and peculiarly in the case of the cat affecting those muscles called upon to perform sudden and violent movement—namely, jumping—enables us to regard such microscopical hæmorrhages as an adequate explanation of the association of paralysis in muscle groups, functionally related to various trades and industrial processes.
It may be argued, and we think with considerable reason, both from pathological and clinical findings, that, as muscular exertion is apparently associated with the onset of paralysis, particularly in those muscles which may be regarded as physically somewhat inadequate to the work they have to perform, and that, as the paralysis is associated with definite functional groups of muscles, and to a curious extent varies according to the trade in which the sufferer is engaged, therefore greater stress thrown upon the muscular tissue at some period or another during occupation determines the microscopical hæmorrhage in the nerve supplying the muscles, or in the muscle itself, so that the paralysis affects just such muscles as have an increased strain thrown upon them. It does not necessarily follow that the preliminary initial hæmorrhage occurring should be a large one—in fact, from the whole of the histological history, hæmorrhages are exceedingly minute; neither does it follow that it is essential for such hæmorrhages to take place in the whole length of the nerve itself; but it is only necessary that the finer branches of the nerve should have their venioles or arterioles affected, and it is of course in the finer branches particularly, as has been pointed out in relation to the venioles, that degeneration of the intima of the vessels takes place.
Finally, the effect of early treatment on lead palsy tends to bear out this theory. If a case of lead palsy be treated in the early stages, the clinical course of the case is good; increased paralysis generally takes place in the first week, and, where, perhaps, only two or three fingers are involved when the case is first seen, spreads generally to other regions within a week, and the whole hand is affected; but from this moment onwards improvement takes place on the application of suitable treatment, and, if continued, almost invariably results in the entire recovery from the paresis.
There is little doubt that this is the true explanation of the ordinary paresis of lead poisoning, and a very great deal more evidence is required to combat it and to prove the selective action of lead upon individual nerves, since the theory of hæmorrhage does not owe its origin to conjecture, but is based on clinical and histological examination of early cases of poisoning.
In attempting to find a cause for the paralysis of the hands so commonly present in painters, it has been suggested that lead is absorbed through the skin, and affects the nerves at their junction with the muscles, setting up a peripheral neuritis [Gombault[8]]. The theory breaks down at once when such commonly-occurring affections as paralysis of the ocular muscles, paralysis of the peroneal type, paralysis of the muscles of the shoulder, etc., are considered.
For the convenience of description lead paralyses are generally divided into a series of groups, the grouping varying according to the function of the various muscles rather than to their anatomical grouping. The various types of paralysis have to be considered in detail:
1. Antibrachial Type (Déjerine-Klumpke—Remak).
—The first muscle affected is the extensor communis digitorum, with dropping of middle and ring fingers, while extension of the first and fourth is possible because of their separate muscles of extension (extensor minimi digiti and extensor indicis). Paralysis may be limited to these, and not advance farther, but it is common to see these two muscles primarily affected, and for other muscles to become involved after the patient is put on treatment, although exposure to lead has ceased. Usually, however, the paralysis advances, involving the extensors of the index and little fingers, so that the basal phalanges of the four fingers cannot be extended. The long extensor of the thumb is next involved, but this may be delayed. The two terminal phalanges are still able to be extended by the interossei (as shown by Duchenne) when the basal phalanx is passively extended on the metacarpal. Abduction and adduction of the fingers also remain unaffected. The wrist muscles are affected next. The hand remains in semi-pronation, and when hanging down forms a right angle with the forearm, the fingers slightly flexed with the thumb towards the palm, and the hand deflected to the ulnar side. In grasping an object the flexors remain unaffected, the wrist is much flexed owing to the shortening of the flexors in consequence of the extensor paralysis. The hand cannot pass the median line. The long abductor of the thumb—that is, the extensor ossis metacarpi pollicis, also known as the “extensor primi internodii pollicis”—is only very rarely involved, but has been described as being the muscle alone involved in the paralysis affecting persons engaged in polishing lead capsules.
2. The Superior or Brachial Type (Remak).
—The muscles affected are those of the Duchenne-Erb group—namely, the deltoid, biceps, brachialis anticus, and supinator longus. The supra- and infrascapular muscles are also as a rule involved, but the pectoralis major rarely. This type of paralysis is usually found in old cases associated with other forms of paralysis, but may be found as a primary affection (as already noted amongst painters); sometimes the deltoid is the only muscle affected, with diminution in electrical contractility of the other muscles of the group.
The arm hangs loosely by the trunk, with the forearm semi-pronated. The arm cannot be raised, nor can the forearm be bent on the upper arm. Extension is unaffected, as the triceps is never involved. Supination is impossible because of paralysis of the supinator brevis. Movement effecting rotation of the shoulders is involved, due to the paralysis of the supra- and infra-spinatus. Electrical reactions are said to be less marked in the brachial than the antibrachial type, and complete loss of faradic contractility is rare; but in one of the three cases described below, in which electrical reactions were carefully tested, the right deltoid showed entire loss of contractility to faradism.
3. Aran-Duchenne Type.
—The muscles of the thenar and hypothenar eminences and interossei are affected. This type of lead paralysis may be distinguished from progressive muscular atrophy by the electrical reactions, and the fact that the atrophy is accompanied by more or less pronounced muscular paralysis. The atrophy is almost always most marked, and advances pari passu with the paralysis. This form may occur alone, or be complicated with the antibrachial type, which is the most common. It is seen in file-cutters as the result of overstrain of the muscles in question. Moebius[9], in his observations on file-cutters, noted in one case paralysis of the left thumb, with integrity of the other muscles of the left upper extremity. Opposition of the thumb was very defective; there was paralysis of the short flexor and of the adductor and atrophy of the internal half of the hypothenar eminence. Reaction of degeneration was noted in the muscles named, but not in the extensors of the fingers and wrist. In another case, in addition to feebleness of the deltoid, flexors of forearm on the upper arm, and small muscles of hand, there was paralysis and atrophy of the adductor of the thumb and first interosseous and paralysis of the opponens.
4. Peroneal Type.
—This is a rare type, and nearly always associated with the antibrachial or with generalized paralysis. In the former the paralysis is slight, especially when it affects the psoas; but there is predilection for certain groups of muscles, especially the peroneal and extensor of the toes, while the tibialis anticus escapes. Hyperæsthesia, or more rarely anæsthesia, precedes the onset.
The patient walks on the outside of the feet, has difficulty in climbing stairs, and cannot stand on the toes. The toes drag on the ground in walking, so that the foot has to be swung round at each step, and the inner side is lifted in excess by the action of the tibialis anticus, with uncertainty in gait. If walking is continued, the toes drag more, and “stepping” gait is assumed by bringing into action the muscles of the thigh. The foot cannot be flexed on the leg; abduction of the foot and extension of the basal phalanx of the toes is impossible. Later the peroneal muscles, extensor communis of toes, and extensor of great toe, are paralyzed, from which fact arises the difficulty of walking and of descending stairs, as the whole weight of the body is supported then by the tibialis anticus. This type corresponds with the antibrachial type of the upper extremity. If the tibialis anticus is paralyzed, it is in association with the gastrocnemius.
5. Paralysis of Special Sense Organs.
—Tanquerel[10] called attention to the aphonia of horses in lead works, necessitating tracheotomy, and Sajous[11] described adductor paralysis of the glottis in a house-painter. Morell Mackenzie[12] also described unilateral paralysis of the adductors in persons suffering from lead poisoning, whilst Seifert[13] particularly describes a curious case in which paralysis of the transverse and oblique arytenoid muscles prevented contraction of the cord in its posterior quarter, and in a second case of paralysis, affecting the posterior crico-arytenoid muscles on both sides, the adductors remained unaffected. What is still more interesting in Seifert’s case is the fact that at the post-mortem old hæmorrhages were found in the mucosa of the arytenoids and aryepiglottidean folds. Occasionally sensory paralysis may be found in the special sense organs—such, for instance, as loss of taste, loss of smell, and, in addition, diminished power of hearing—but these defects rarely if ever occur unless accompanied by distinct mental changes and generalized paralysis.
6. Eye.
—Poisoning affects the eye in two ways:
- (a) Defects of the visual mechanism.
- (b) Defects of the muscular mechanism of the eye.
Lockhart Gibson[14] describes a large number of cases of paralysis of the muscles of the eye met with amongst children in Queensland. The cause was traced to the painted railings near which the children had been playing. The white lead paint had somewhat disintegrated under the action of the sun’s rays, forming an efflorescence; the children admitted to have rubbed the paint and then sucked their fingers.
Between July, 1905, and 1908, sixty-two cases of plumbism in children were admitted to the children’s hospital, and of these sixty-two cases thirteen had well-marked ocular symptoms. The paralysis of the muscles of the eye was almost invariably one of the external rectus, but other muscles were at the same time affected; occasionally paralysis of the whole of the oculo-motor muscles was seen with the exception of the superior oblique. It is worthy of note that amongst these children a very large number suffered, in addition to their eye paralysis, with foot-drop and wrist-drop, and, on the whole, suffered from foot-drop to a much larger extent than from paralysis of the hands.
Galezowski[15] describes paralysis of accommodation of the eye, and in cases described by Folker[16] some amount of orbital paralysis was also present.
7. Generalized Paralysis.
—These types do not differ in form from the previously described types, except, perhaps, as regards their rapidity of onset. Where the onset is slow (chronic) the subject is usually one who has been previously affected with paralysis of the extensors of the hand, followed by development of the paralysis in the shoulders, hand, leg, thorax. In the acute form, paralysis may affect all the muscles in a given limb or group, and reduce them in a few days to a complete condition of paralysis. In extreme cases the patient lies on the back and is incapable of rising, and sometimes even unable to eat. The intercostals, diaphragm, and larynx, are also affected, while there is generally dyspnœa and aphonia. The muscles of the head and neck appear to escape. In these acute cases, pyrexia may be a common symptom.
Electrical Reactions.
—The diagnosis of the affected muscle is greatly assisted by careful examination of all the muscles in the affected physiological group by means of the galvanic and faradic currents. The battery for the purpose of testing the electrical reactions must have an available electromotive force of over 40 volts. A battery of thirty-two Leclanché dry cells is ample. For the faradic current, a small induction coil operated by two Leclanché cells is sufficient. One large, flat electrode should be used, and several smaller ones.
The faradic current should be used first, as it stimulates the nerves directly, and the muscles only indirectly, through their nerve-supply. Each nerve trunk should be examined systematically. The motor points correspond for the most part with the points of entry of the motor nerves into the muscles which they supply. A small electrode, either a button or a small disc about the size of a sixpence, should be used for the examining electrode, while the larger electrode should be placed either on the abdomen or between the shoulders. The electrodes should be well soaked in normal saline.
The intensity of the minimum current required to produce a contraction for each point should be noted, and compared with the effect of a similar current on the opposite side of the body.
The reaction of degeneration of the faradic current consists in no contraction at all being elicited, even when a very strong current is employed. If there be unilateral wrist-drop in the left hand, consisting of loss of power of the extensor communis digitorum on that side, no movement of the muscle is produced at all when the electrode is placed across the motor points of the muscle. These are situated to the outer side of the arm when the dorsum of the hand is uppermost, about 1¹⁄₂ to 2 inches below the olecranon. The same quantity of current, when applied to the unaffected muscle on the opposite side, produces a brisk reaction.
Having observed the effect with the faradic current, and the results having been recorded, the continuous current is used, and the electrodes made use of in an exactly similar fashion. When a small electrode is used, the superficial nerves and muscles are more stimulated than those lying deeply. It is necessary, therefore, to begin with a small current and gradually increase it until the individual muscle responds.
The strength of the current employed is registered by means of a milliampèremeter.
With the continuous current quantitative as well as qualitative alterations may be determined, and with the quantitative change of the galvanic current the muscular excitability is increased, contraction following the application of a weaker current than is necessary to produce it in health or in the sound muscle on the other side of the body.
With the qualitative change, the contraction is no longer sharp, but sluggish. The anodal closing contraction is elicited with a weaker current than kathodal closing contraction, so that ACC>KCC.
The quantitative change depends partly on the nutrition of the muscle; the qualitative change depends on the fact that the nerve no longer regulates the character of the contraction, and also to a small extent is the result of changes in the muscle itself.
In a complete reaction of degeneration in an affected muscle, reaction to the faradic current is absent, contraction to the galvanic current is sluggish, and is produced with a smaller current in the anode than the kathode.[A]
[A] The kathode, or negative electrode, is attached to the zinc rod; the anode, or positive electrode, to the copper or carbon.
As the nerve lesion passes away, the voluntary contraction generally begins to return before the nerves show any reaction to electrical stimulus.
The following three cases in which the electrical reactions of the muscles were determined, give examples of typical cases of lead paresis. In No. 3, owing to the fact that the case was treated immediately the paralysis occurred, complete recovery had taken place, and, as will be seen, the electrical reactions have again become normal.
Case 1.—Litharge and blast-furnace worker. Employed in lead works, where a large number of different metallurgical processes associated with the recovery of lead from the ore were carried on. Double wrist-drop, existing for eight years, untreated until some four years after paralysis took place, when slight improvement occurred. The electrical reactions show that the extensor communis digitorum on the right side is completely degenerated, whilst the first interosseous of the right side show reactions of degeneration. On the left side the extensor communis digitorum showed normal but very feeble reaction. This latter point is one of considerable importance if early hæmorrhage accounts for lead paralysis, for if the nerve itself was completely destroyed, or if, as was the case, the muscle appeared completely paralyzed on inspection, obviously the nerve-supply must be completely cut off if the lesion was due to destruction of the nerve of the spinal cord or to the destruction of the lower motor neuron. On the other hand, the presence of small localized fibrillar contraction, found by the galvanic current, together with the presence of a slight reaction to faradism, suggests that some small portion of the nerve has remained unaffected, and that for this reason certain portions of the muscle have not undergone degeneration—a circumstance which can hardly be expected if the cause of the paralysis is in the destruction of the whole of the nerve-supply.
| ELECTRICAL REACTIONS IN LEAD PARALYSIS. (CASE 1.) | |||||||
|---|---|---|---|---|---|---|---|
| Muscle. | Galvanism. | Faradism. | Remarks. | ||||
| M.A. | M.A. | ||||||
| R. Deltoid (anterior portion) | K.C.C. | 8 | A.C.C. | 8 | Good | Evidently extensor communis digitorum on right side is completely degenerated.First interosseous on right side show reactions of degeneration. On left side extensor communis digitorum showsnormal but feeble contractions | |
| L. Deltoid (anterior portion) | K.C.C. | 6 | A.C.C. | 9 | Good | ||
| R. Deltoid (posterior portion) | K.C.C. | 6 | A.C.C. | 9 | Good | ||
| L. Deltoid (posterior portion) | Good | ||||||
| R. Supinator longus | K.C.C. | 6 | A.C.C. | 10 | Reaction brisk | Good | |
| L. Supinator longus | K.C.C. | 5 | A.C.C. | 6 | Reaction brisk | Good | |
| R. Extensor communis digitorum | No reactions either A.C.C. orK.C.C.[15] | No reaction | |||||
| L. Extensor communis digitorum | K.C.C. | 8 | A.C.C. | 12 | Brisk, but feeble | Feeble reaction | |
| R. Extensor primi internodii pollicis | K.C.C. | none at 13 | A.C.C. | 13 | Brisk | Good | |
| L. Extensor primi internodii pollicis | K.C.C. | 6 | A.C.C. | 12 | Reaction brisk | Good (but less than right) | |
| R. Extensor carpi ulnaris | K.C.C. | 8 | A.C.C. | 8 | Brisk Contraction | Good | |
| L. Extensor carpi ulnaris | K.C.C. | 8 | A.C.C. | 12 | Brisk Contraction | Good | |
| R. First interosseous | K.C.C. | 8 | A.C.C. | 6 | Contraction slow | No reaction | |
| L. First interosseous | K.C.C. | 6 | A.C.C. | 6 | Brisk contraction | Good | |
| R. Second interosseous | K.C.C. | 8 | A.C.C. | 10 | Brisk Contraction | Slight reaction | |
| L. Second interosseous | K.C.C. | 6 | A.C.C. | 8 | Brisk Contraction | Good | |
| R. Third interosseous | K.C.C. | 9 | A.C.C. | 6 | Brisk Contraction | Slight reaction | |
| L. Third interosseous | K.C.C. | 6 | A.C.C. | 8 | Brisk Contraction | Slight reaction | |
| R. Fourth interosseous | K.C.C. | 8 | A.C.C. | 6 | Brisk Contraction | Slight reaction | |
| L. Fourth interosseous | K.C.C. | 10 | A.C.C. | 9 | Brisk Contraction | Good | |
| ELECTRICAL REACTIONS IN LEAD PARALYSIS.(CASE 2.) | |||||||
| Muscle. | M.A. | Galvanism. | Faradism. | Remarks. | |||
| R. Deltoid | 9 | Slow reaction A.C.C. > K.C.C. | No reaction | Reaction of degeneration | |||
| L. Deltoid | 9 | Slow reaction A.C.C. > K.C.C. | Slow reaction | ||||
| R. Extensor communis digitorum | 9 | Slow reaction A.C.C. > K.C.C. | No reaction | ||||
| L. Ditto | 9 | Slow reaction | No reaction | ||||
| Ante brachial and brachial groups give normal reaction | |||||||
| ELECTRICAL REACTIONS IN CASE OF RECOVERED WRIST-DROP. (CASE 3.) | |||||||
| Muscle. | M.A. | Galvanism. | Faradism. | Remarks. | |||
| R. Extensor communis digitorum | 9 | Good reaction K.C.C. > A.C.C. | Good reaction | All muscles react well to both currents; no sign of any reaction of degeneration | |||
| L. Ditto | 9 | Good reaction K.C.C. > A.C.C. | Good reaction | ||||
| R. Extensor ossis metacarpi pollicis | 9 | Good reaction K.C.C. > A.C.C. | Good reaction | ||||
| L. Ditto | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| R. Deltoid | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| L. Deltoid | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| R. Extensor carpi ulnaris | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| L. Extensor carpi ulnaris | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| R. Interossei | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
| L. Interossei | Good reaction K.C.C. > A.C.C. | Good reaction | |||||
This case is a typical one of the anterior brachial type, showing partial recovery of function. The man is able to grasp, although the wrist becomes strongly flexed in so doing.
Case 2.—We are indebted to Dr. Gossage for this case, which was presented at the Out-patients of the Westminster Hospital; and to Dr. Worrell, who made the electrical investigations. We are further indebted to Dr. Worrell for the reports which are given in tabular form of the electrical reactions of these three cases.
This is a case of brachial type, with weakness of both deltoids, and the patient was unable to raise his right arm at the shoulder. It will be seen that there is here also evidence that the electrical contractility diminishes before the entire loss. It will be also noticed that the supinators are unaffected.
Case 3.—These are the electrical reactions of a case which had recovered. This man showed the ordinary anterior brachial type, which came on suddenly, although he had shown distinct weakness of wrists when forcible flexion was performed for nine months previously, but there had been no obvious increase in the weakness. He was immediately removed from his work, and within seven days paralysis, which at first only affected the extensor communis digitorum, had spread to the minimi digiti and the extensor indicis, the opponens pollicis being also involved on the right side. He was treated from the start with faradic current, and was instructed to use the battery himself, which he did twice a day for a year. At the end of two months he was sufficiently recovered to be given light work, and at the time of taking the reactions his wrists have so far recovered their power that we were unable to flex them forcibly.
The progressive weakness noted in the three cases has already been referred to, and may be a prodrome of paralysis, but there may be recovery without paralysis supervening.
Tremor.
—Tremor may be observed in a large number of cases of lead poisoning, and is invariably associated with paralysis, although the symptom of tremor by no means always progresses to definite palsy. Two types of tremor are described—fine and coarse—and Gübler further describes a type of tremor which is both rhythmic and intermittent. The tremor is usually distinctly increased on attempting to grasp or point the hand (intention tremor), but it is difficult to separate tremor from alcoholic tremor, and, further, it must not be forgotten that persons engaged in arduous work may show a certain amount of tremor due to muscular fatigue. Persistent tremor, however, is a symptom that is always to be noted and carefully watched.
Of the types of paralysis, the antibrachial is the most common, and, secondly, probably the brachial. The least common is the peroneal. The table on [p. 54] shows the distribution of cases of paralysis, so far as they can be made out from reports received since 1904.
Closely associated with paralysis are affections involving the brain. Tanquerel, in his classical description of affections of the brain associated with lead poisoning, gives the following classification:
- 1. Delirium.
- 2. Lead mania.
- 3. Psychic depression.
- 4. Coma.
- 5. Convulsions, saturnine eclampsia, or epilepsy.
There is probably a very considerable relationship between insanity and lead poisoning, as pointed out by Robert Jones[17], the resident physician and Superintendent of Claybury Asylum.
Rayner[18] remarked that the compulsorily careful habits of life of painters and lead-workers ought to protect them against vicious habits, and should protect them against a too free indulgence in the use of alcohol! Our own experience is that paralysis, and particularly affections of the brain, occur in the majority of cases in persons who are addicted to alcohol, and the experiments quoted in the chapter on Pathology on the influence of alcohol in the production of encephalitis in animals is strong presumptive evidence that alcohol is one of the chief predisposing causes in the determination of saturnine encephalopathy.
Encephalitis is given as a cause of death in the report already referred to in 14·3 per cent. of 264 fatal cases. Amongst this number encephalopathy accounted for 14·3 per cent., cerebral hæmorrhage 9·8 per cent., and paralysis 9·2 per cent. Now, all these are cases in which cerebral lesions may be confidently stated to have existed, which brings the total to 34·4 per cent. of deaths at least due to brain involvement. We have already referred to the high incidence of paralysis amongst file-cutters—40 per cent. as against 21·1 per cent. for all industrial forms of poisoning.
When encephalitis occurs, it is usually an acute symptom, and often develops before paralysis is set up, but as a rule is preceded by a period of persistent headache, such headache being invariably temporal or occipital.
Robert Jones, in his paper, states that of the 133 cases who, from the nature of their work (painters, plumbers, etc.), were liable to lead impregnation, 19 had signs of poisoning upon admission, whilst 22 had a distinct history of lead poisoning at some time or other. He gives the following analysis of the mental condition:
| Mania | 37 |
| Melancholia | 33 |
| Dementia | 19 |
| Dementia with epilepsy | 10 |
| Dementia with general paralysis | 24 |
| ? General paralysis | 7 |
| Alcoholic mania | 3 |
| 133 |
Savage[19] is of opinion that lead will produce any of the symptoms of general paralysis of the insane, and may even be a contributory cause of the disease, but no statistics are available of the Wassermann reaction in these cases. Goodall[20] refers to the fact that nerve poisons, such as syphilis, alcohol, and fevers, injury or sunstroke, which are intermediate in fixity between alcohol and lead, seem to have an intermediate influence in the production of general paralysis.
Jones states that the mental symptoms found in the cases are to be grouped amongst one or other of the following varieties:
1. Of a toxæmic nature, with sensory disturbances, which tend to get well rapidly.
2. Hallucinations of sight and hearing, more chronic in nature, which may be permanent. The delusions in this class are almost invariably those of being poisoned or followed about, and are in the main persecutory.
3. Those resembling general paralysis with tremors, increased knee-jerk, inco-ordination, accompanied with listlessness amounting to profound dementia, but which tend to get well.
Eye Changes.
—Two main forms of eye change are to be found amongst lead-workers. In the first place, temporary and sudden amaurosis makes its appearance, due no doubt to vascular change, either vaso-motor or hæmorrhagic. The trouble may occur in one or both eyes, may come on gradually, the patient merely being unable to distinguish letters or faces at a distance, or he may become suddenly totally blind. In the majority of cases the affection disappears under treatment, but in a small number of cases total blindness persists.
Occasionally nystagmus may be seen, but is not a common symptom; but dilatation of the pupils, quite apart from retinal changes, is not unusual. Inequality of the pupils may be observed, but partial dilatation of both pupils is more common, and is often associated with early anæmia. Conjunctival hæmorrhages are to be noted from time to time, without obvious cause, such as injury, etc., but in the majority of cases these have been associated with other symptoms.
The first feature noticed in the eye is loss of brightness, and a curious lack-lustre of the eyes of persons intoxicated by lead is one of the general features making up the saturnine cachexia. Loss of brightness of the eye is associated in many other diseases with anæmia, but is particularly prominent in lead poisoning, much more so than is to be accounted for alone by the degree of blood-destruction, and is a point of which the examining surgeon should always take notice.
One other form of eye change requires attention—namely, retinal changes due to circulatory disturbances. In an advanced case the whole picture is one of severe albuminuric retinitis, but in the earlier stages some engorgement of the vessels without alteration of the surrounding tissue is seen. Elschnig[21] associated this alteration in the vessels of the eye with vaso-motor changes caused by direct action of the poison, producing a vascular constriction or dilatation, and is inclined to regard the kidney disease frequently associated with this condition of the eye as something quite apart. He would regard the two affections as independent, and merely correlated through their common origin—lead intoxication. It has even been suggested by some observers that the change in the eye is secondary to cerebral œdema. Thus Mannaberg[22] regards the encephalitis of saturnine origin as associated with chronic œdema of the brain and spinal cord, which thus produces reflex irritation of the nervous system of the eye. Bikler[23] and Weber[24] consider the symptoms as circulatory. From whatever cause the disease is set up, sooner or later changes in the form of obliterative arteritis take place, with gradual but ultimately complete loss of vision.
There are said to be no characteristic eye symptoms in acute cases of lead poisoning, whereas with chronic lead poisoning in many cases there is central and peripheral affection. The affections may be further divided into subjective and objective. Many of the subjective symptoms, such as loss of sight and blindness, are associated with definite eye lesions, which may be seen with the ophthalmoscope, but other definitely objective lesions may be present without any influence on sight to commence with. Folker[25] describes five cases of lead amblyopia in lead-workers from a pottery district, in all of which there was a peculiar symptom—the gradual failing of sight associated with colour flashes. When examined, the discs were described as white, and the vessels small.
Lockhart Gibson[26], in describing the cases of eye disease amongst the children in Queensland, found one symptom apparently in all the eyes examined—namely, great swelling of the discs. This swelling of the discs might be accompanied with no loss of sight whatever, and at other times had been accompanied with defective sight for many months previously. Some of the discs were excessively swollen. There were also to be seen patches of pigment and irregular swelling of the vessels, but no definite hæmorrhages. In the more acute cases, and particularly those associated with complete paralysis of the ocular muscles, total blindness usually followed.
As a rule, when complete amaurosis occurs in lead poisoning, blindness follows through double optic neuritis or neuro-retinitis, but amblyopia may be present without fundus changes. Occasionally the loss of sight may be regarded as of central origin. The renal disease so often associated with lead poisoning may cause the retinal changes accompanying it. An albuminuric neuro-retinitis may occur without albumin in the urine. As a rule, the eye of a lead-worker reacts to light and accommodation. Ophthalmoscopic examination may show very pink discs, patches of pigment scattered about irregularly outside the discs, with occasional definite hæmorrhage. The edge of the discs may show blurring, with further sclerosis and peri-arteritis of the vessels, a white sheath around the arteries being often visible. The neuritis on one or both sides may be associated with disturbances of sight, and diffusely red and cloudy papilla, with swelling or hæmorrhages. In choroidal atrophy pigmentation may also be seen.
Muscular System.
—One further point may be referred to in relation to the muscular system—namely, the occurrence of pain of a rheumatic type. Quite a number of cases of mild degrees of lead poisoning complain of arthralgic symptoms—that is to say, “rheumatism.” Careful examination of such cases shows no evidence that the pain is a true arthralgia, neither does it seem to have a true relation to gout. The pain as a rule is referable to the muscles themselves, and in such instances digital examination of the muscle in the region of the pain generally exhibits deep-seated tenderness. There does not appear to be any special marked tenderness along the trunks of the nerves supplying the muscle, nor is there evidence of hyperæsthesia of the skin. Such hyperæsthesia does occur in lead poisoning, but is generally associated with cerebral lesions. The pain, therefore, must be regarded rather as myalgic, and intercostal distribution of the pain is not infrequent; but although the symptom is one that is often complained of, it is an exceedingly difficult one to differentiate from other myalgias as a definite symptom of lead poisoning. The chief point in favour of the inclusion of this so-called lead rheumatism as a symptom of lead poisoning is the frequency with which it is noted in the reports by certifying surgeons. While, therefore, having no evidence to regard it as necessarily a definite symptom of poisoning, it is one which has been recorded in a considerable number of cases. As has been already suggested, there is some reason to think these myalgic pains may be due to minute hæmorrhages taking place in the muscles, thereby producing localized irritation to some extent comparable with the “bends” of divers.
Post-Mortem Signs of Plumbism.
—Very real difficulty exists in determining from naked-eye appearances at a post-mortem examination whether the cause of death be due to chronic plumbism or not. The changes produced by several other forms of intoxication, notably chronic alcoholism, produce many of the same changes in the tissues as lead. Inspection of the organs in the case of plumbism can only give rise to a surmise that the cause of death is due to lead poisoning.
There are, however, certain macroscopical appearances at an autopsy in the case of saturnism which should be carefully noted, and although alone they do not constitute sufficient evidence upon which to pass a definite opinion, they are still important as diagnostic signs in the light of histological and chemical examination.
Particular note should be paid at an autopsy of a case of suspected lead poisoning to the following points:
1. Mouth, for the presence or absence of blue line, which, if present, must be examined with a lens.
2. General condition of the abdominal viscera, and particularly of the mesenteric and perinephritic fat. In plumbism this is invariably reduced in quantity.
3. The condition of the mesenteric vessels, as to whether or not they are engorged with blood, or whether or not leakage appears to have taken place.
4. General condition of the arteries, for the presence of atheroma, etc.
5. The heart muscle, which in plumbism is generally pale, flabby, and with a tendency to general dilatation of the cavities.
6. Intestines.
(a) The presence of injection of the muscular coat, particularly the lower portion of the intestine, and about the ileo-cæcal valve.
(b) The presence or absence of minute ulcerations, or even hæmorrhages along the intestine, even in the mucosa of the stomach.
(c) The presence of dark staining in the coats of the lower intestine, not altogether disappearing when washed under a gentle stream of water. Should there be any evidence of this staining, it is highly important to remove some of the fæces, as well as a portion of the intestine, for chemical examination.
7. The condition of the liver, which in poisoning by lead, as by alcohol, frequently shows a considerable amount of enlargement, and may even show patches of perihepatitis due to secondary causes. But the cirrhosis occurring in lead poisoning is not so great as in alcohol. In lead poisoning the liver as a rule is large and soft, and engorged with blood.
8. The kidney, for signs of interstitial rather than tubular nephritis, adherent capsule, and blood-stained exudate.
9. If paresis of any sort has been present during the illness, examination of the cord and brain should be made with especial care, and in addition the nerves on the affected side supplying the affected muscles should also be examined. In the brain definite small but coarse hæmorrhages may be occasionally observed, but as a rule the only signs to be found are injection of the cortical vessels, frequently over certain definite areas, and not involving the whole of the vascular system of the brain. Minute hæmorrhages may be also found in the spinal cord.
For the purposes of histological examination, a portion of the following organs should be removed and placed in a 5 per cent. formalin solution at once: Liver, spleen, kidney, intestine, the last-named specimen being selected from any area which shows injection, or ulceration, or dark staining.
Smears may also be made from the bone-marrow, as in prolonged anæmia of saturnine origin definite changes may at times be found in the bone-marrow cells.
Where paresis has existed, a portion of the particular nerve supplying the muscles should be obtained, and histological examination made, as well as a portion of the cord above the lesion, and where cerebral symptoms have been present, a portion of the brain, the portions taken being part of that showing engorgement of the vessels. For the nervous tissue generally, it is better to place some of the specimens in Müller’s solution, and others in spirit. Equal parts of Müller’s solution and formalin may be used if desired.
Material for Chemical Examination.
—For the purposes of chemical examination, any of the organs which appear to be mainly affected by chronic inflammation may serve, but it is usually important to examine the brain, kidney, and liver. If any dark staining exist in the intestine, a portion of this, together with the contained fæces, should be removed. It is better to tie ligatures round the intestine, and divide the coat between the ligatures, and place the whole of the specimen in dilute formalin. Specimens thus obtained should be sent off for examination at once. The whole of the organ need not necessarily be despatched for examination in every case, but if only a portion is sent, it is essential that the weight of the whole organ be accurately taken before any portion is removed, and the total weight noted with the specimen when sent.