CHAPTER IX_Lead poisoning and lead absorption

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. |

+----------------------+------+-----+------+----+-----------------+

| | | M.A.| |M.A.| |

|R. Deltoid (anterior |K.C.C.| 8 |A.C.C.| 8 | |

|L. Deltoid (anterior |K.C.C.| 6 |A.C.C.| 9 | |

|R. Deltoid (posterior |K.C.C.| 6 |A.C.C.| 9 | |

|R. Supinator longus |K.C.C.| 6 |A.C.C.| 10 |Reaction brisk |

|L. Supinator longus |K.C.C.| 5 |A.C.C.| 6 |Reaction brisk |

|R. Extensor communis |No reactions either A.C.C. or K.C.C.[15] |

|L. Extensor communis |K.C.C.| 8 |A.C.C.| 12 |Brisk, but feeble|

|R. Extensor primi |K.C.C.| none|A.C.C.| 13 |Brisk |

| internodii pollicis| |at 13| | | |

|L. Extensor primi |K.C.C.| 6 |A.C.C.| 12 |Reaction brisk |

|R. Extensor carpi |K.C.C.| 8 |A.C.C.| 8 |Brisk Contraction|

|L. Extensor carpi |K.C.C.| 8 |A.C.C.| 12 |Brisk Contraction|

|R. First interosseous |K.C.C.| 8 |A.C.C.| 6 |Contraction slow |

|L. First interosseous |K.C.C.| 6 |A.C.C.| 6 |Brisk contraction|

|R. Second interosseous|K.C.C.| 8 |A.C.C.| 10 |Brisk contraction|

|L. Second interosseous|K.C.C.| 6 |A.C.C.| 8 |Brisk contraction|

|R. Third interosseous |K.C.C.| 9 |A.C.C.| 6 |Brisk contraction|

|L. Third interosseous |K.C.C.| 6 |A.C.C.| 8 |Brisk contraction|

|R. Fourth interosseous|K.C.C.| 8 |A.C.C.| 6 |Brisk contraction|

|L. Fourth interosseous|K.C.C.| 10 |A.C.C.| 9 |Brisk contraction|

+----------------------+------+-----+------+----+-----------------+

+----------------------+---------------+-----------------------------+

| Muscle. | Faradism. |Remarks. |

+----------------------+---------------+-----------------------------+

| | | |

|R. Deltoid (anterior |Good |Evidently extensor communis |

| portion) | |digitorum on right side is |

|L. Deltoid (anterior |Good |completely degenerated. First|

| portion) | |interosseous on right side |

|R. Deltoid (posterior |Good |show reactions of degenera- |

| portion) | |tion. On left side extensor |

|L. Deltoid (posterior |Good |communis digitorum shows |

| portion) | |normal but feeble contrac- |

|R. Supinator longus |Good |tions |

|L. Supinator longus |Good | |

|R. Extensor communis |No reaction | |

| digitorum | | |

|L. Extensor communis |Feeble reaction| |

| digitorum | | |

|R. Extensor primi |Good | |

| internodii pollicis| | |

|L. Extensor primi |Good (but less | |

| internodii pollicis|than right) | |

|R. Extensor carpi |Good | |

| ulnaris | | |

|L. Extensor carpi |Good | |

| ulnaris | | |

|R. First interosseous |No reaction | |

|L. First interosseous |Good | |

|R. Second interosseous|Slight reaction| |

|L. Second interosseous|Good | |

|R. Third interosseous |Slight reaction| |

|L. Third interosseous |Slight reaction| |

|R. Fourth interosseous|Slight reaction| |

|L. Fourth interosseous|Good | |

+----------------------+---------------+-----------------------------+

ELECTRICAL REACTIONS IN LEAD PARALYSIS. (CASE 2.)

+---------------------+----+---------------+---------+--------------+

+---------------------+----+---------------+---------+--------------+

|R. Extensor communis | 9 |Slow reaction |No | |

|L. Extensor communis | 9 |Slow reaction |No | |

+---------------------+----+---------------+---------+--------------+

ELECTRICAL REACTIONS IN CASE OF RECOVERED WRIST-DROP. (CASE 3.)

+---------------------+----+---------------+---------+--------------+

+---------------------+----+---------------+---------+--------------+

+---------------------+----+---------------+---------+--------------+

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.

REFERENCES.

[1] TANQUEREL: Traité des Maladies de Plomb ou Saturnines. Paris,

1839.

[2] LANCEREAUX: Gaz. Méd., 1862; Tribune Méd., 1896.

[3] MEILLÈRE, G.: Le Saturnisme, chap. iv.

[4] TELEKY: Deutsch Zeitschrift für Nerven Heilk., vol. xxxvii., 1909.

[5] DÉJERINE-KLUMPKE: Thesis on Des Polynephrites en Général et des

Paralysies et Atrophiques Saturnines en Particulier. Paris, 1889.

[6] TELEKY: _Ibid._

[7] TELEKY: _Ibid._

[8] GOMBAULT: Arch. Phys., 1873.

[9] MOEBIUS: Ueber einige Ungewöhnliche Fälle von Bleilähmung. Cent.

für Nervenheilk. 1886.

[10] TANQUEREL: _Ibid._

[11] SAJOUS: Archiv für Laryng., iii., 1882.

[12] MORELL MACKENZIE: Brit. Med. Journ., epitome, p. 1202, 1893.

[13] SEIFERT: Berl. Klin. Woch., 1884.

[14] LOCKHART GIBSON: Brit. Med. Journ., vol. ii., p. 1488, 1908.

[15] GALEZOWSKI: Jahr. f. Aug., p. 382, 1877.

[16] FOLKER: Brit. Med. Journ., ii., p. 1556, 1898.

[17] ROBERT JONES: Brit. Med. Journ., September 22, 1900.

[18] RAYNER: Journ. of Mental Science, 1880.

[19] SAVAGE: Clifford Allbutt’s Medicine, vol. vii., p. 657.

[20] GOODALL: _Ibid._, p. 693.

[21] ELSCHNIG: Wien. Med. Woch., Nos. xxvii, xxix., 1898.

[22] MANNABERG: Ber. Klin. Woch., 1896.

[23] BIKLER: Arch. für Augenheilk., b. xl., 1900.

[24] WEBER: Thèse de Paris, 1884.

[25] FOLKER: _Ibid._

[26] LOCKHART GIBSON: _Ibid._