Chapter L: J. Lautenbach, in a recent communication to the Philadelphia (6)

Autopsies.—Until 1863 only five autopsies had been made upon persons affected with infantile paralysis.[70] As the disease was never, of itself, {1132} fatal, opportunity for pathological investigation did not present itself, while attention was still vividly attracted to the paralysis. When this had become a chronic infirmity, and patients had succumbed to intercurrent disease, the opportunity must have occurred, but was not then utilized.

[Footnote 70: I believe the first list of modern autopsies was made by myself in a paper read before the New York County Medical Society, Dec. 22, 1873. The paper was not published until May, 1874, and in the mean time Seguin's lecture on “Infantile Paralysis” was published in the _N. Y. Med. Record_, Jan. 15, 1874, with a tabulated list of 25 autopsies, necessarily almost identical with mv own—cases 9 and 10 are really identical. A case by Roth is included; 4 negative autopsies are omitted. In 1880, Seeligmüller, in his elaborate essay in _Gerhardt's Handbuch_, published a list of 32 cases, including the above, and adding to them the following: Case by Müller, 1871; 4 cases by Leyden, 1875 (_Arch. de Psych._); 1 case by Raymond, 1874 (_Gaz. méd. de Paris_); 1 case by Demme, 1876 (_B. med. Bericht über das Jennerischt Kinderspital zu Bern_); 1 case by Eisenlohr, 1876 (_Tageblatt des Hamburger Naturforscher Versammlung_); 1 case by Schultze, 1877 (_Virch. Arch._, Bd. lviii.).

To this list we may now add 3 cases by Turner, Humphrey, Taylor, 1881 (_Path. Trans. London_); 2 cases by Dejerine, 1878 (_Progrès méd._), giving a total of 37 cases with detailed histories and autopsies.]

The first cases affording autopsies in which the spinal cord was thoroughly investigated, belonged, however, precisely to this class of extremely chronic lesions, which should be regarded as showing rather the results of the morbid process than that process itself. Omission to observe this distinction has been the occasion of several misinterpretations of the pathological appearances.

Premature Theories.—In the entire absence of evidence it is a little remarkable that such high authorities as Rilliet and Barthez,[71] West,[72] Vogel,[73] Eulenburg,[74] should have pronounced dogmatically that the disease was essential—_i.e._ unaccompanied by any structural lesion whatever; and that Bouchut,[75] on the strength of most incomplete examination, should have built up a theory of myogenic paralysis. It is still more remarkable, after the published autopsies of Rinecker,[76] Laborde,[77] Cornil,[78] Prévost,[79] Charcot and Joffroy,[80] Parrot and Joffroy,[81] Vulpian,[82] Roger and Damaschino,[83] that Politzer in 1866,[84] Brown in 1871,[85] Barwell in 1872,[86] Kétli,[87] Adams in 1873,[88] should still adhere to this doctrine. They are, however, entirely in the minority, and all recent monographs and works published with a view to presenting the state of science assume the spinal nature of infantile paralysis to be established beyond possibility of controversy.[89]

[Footnote 71: _Traité des Maladies des Enfants_.]

[Footnote 72: _Diseases of Children_, Am. ed., 1860.]

[Footnote 73: _Diseases of Children_, trans. from 4th ed., 1870.]

[Footnote 74: _Arch. Virchow_, Bd. xvii. 1859.]

[Footnote 75: _Deutsche Klinik_, 1863.]

[Footnote 76: _Gaz. méd._, 1864, Soc. de Biol., 1864.]

[Footnote 77: _De la Paralysie de l'Enfance_.]

[Footnote 78: _Gaz. méd._, 1866, Soc. de Biol., 1866.]

[Footnote 79: _Arch. de Phys._, 1870, p. 134.]

[Footnote 80: _Ibid._, p. 310.]

[Footnote 81: _Ibid._, p. 316.]

[Footnote 82: Bouchut is said by Simon (_loc. cit._) to be alone in his theory; Kétli, however, agrees with him. Eulenburg, in 1872, in his systematic treatise, assigns a central origin to infantile paralysis, but offers no opinion in regard to its nature.]

[Footnote 83: _Gaz. méd._, 1871.]

[Footnote 84: _Jahrbuch für Kinderkrankheiten_, 1866.]

[Footnote 85: _Compend. für Kinderkrank._, p. 161.]

[Footnote 86: _Lancet_, 1872.]

[Footnote 87: _Jahrbuch für Kinderkrank._, 1873.]

[Footnote 88: _Treatise on Club-foot_.]

[Footnote 89: See Seguin, _loc. cit._, 1874; Erb, _Ziemssen's Handbuch_, Bd. xi.; Seeligmüller, _Gerhardt's Handbuch der Kinderkrankheiten_; Ross, _Treatise on Diseases of Nervous System_, vol. ii.; Hammond, _Diseases of Nervous System_, 6th ed., 1881, etc. etc.]

The following table contains a summary of the seven autopsies in which the spinal cord is said to have been examined with negative results. Of these, the only really important case is the third, in which a microscopic examination, made by so competent an histologist as Robin, was said to have discovered no lesion of the cord.

{1133} The foregoing autopsies may be tabulated as follows:

TABLE I.—NEGATIVE AUTOPSIES.

No.: 1

Year: 1850 or '51?

Name of Author and Patient: Rilliet and Barthez.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: l. o.

Electric Reaction: ?

Appearances at Autopsy: Negative.

Reference in Literature: _Gaz. méd. de Paris_, 1850 (or '51?) p. 681.

No.: 2

Year: 1850 or '51?

Name of Author and Patient: Rilliet and Barthez.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearances at Autopsy: Negative.

Reference in Literature: _Ibid._

No.: 3

Year: 1867

Name of Author and Patient: Bouchut and Robin. (Angélique Lermain).

Age at time of Paralysis, of Autopsy: 1½, 3

Nature of Symptoms: Suddenly after 3 days' fever.

Limbs Paralyzed: both u.

Electric Reaction: —

Appearances at Autopsy: Negative microscopically.

Reference in Literature: _Union méd._, 1867, No. 130, p. 187.

No.: 4

Year: 1873

Name of Author and Patient: Adams.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Treatise on Club-foot_, p. —.

No.: 5

Year: 1873

Name of Author and Patient: Elischer and Kétli.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Jahrb. Kinderheilk._, 1873.

No.: 6

Year: 1873

Name of Author and Patient: Elischer and Kétli.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: —

Electric Reaction: —

Appearances at Autopsy: Negative.

Reference in Literature: _Ibid._

Heine, in the absence of autopsies, but arguing from clinical symptoms alone, already inferred the existence of a spinal lesion as cause of the paralysis, and believed that it consisted in congestion, or even in hemorrhagic exudation, capillary or massive, which should compress the cord and result in partial atrophy. The same opinion is advanced in 1844 by Brunnière,[90] also by Vogt,[91] in 1868 by Salomon[92] and Radcliffe.[93] The autopsies contained in the following table, in all of which vascular lesions are prominent, might be invoked in support of this view:

TABLE II.—AUTOPSIES SHOWING VASCULAR LESIONS OF CORD.

No.: 7

Year: 1829

Name of Author and Patient: Klein.

Age at time of Paralysis, of Autopsy: 5, 5

Nature of Symptoms: Persistent cerebral symptoms.

Limbs Paralyzed: l. o.

Electric Reaction: ?

Appearances at Autopsy: Congestion of pia around roots of left brachial plexus.

Reference in Literature: Quoted by Heine.

No.: 8

Year: 1855

Name of Author and Patient: Brund.

Age at time of Paralysis, of Autopsy: 1, 5

Nature of Symptoms: Meningitis?

Limbs Paralyzed: r. u.

Electric Reaction: ?

Appearances at Autopsy: Chronic spinal klepto-meningitis.

Reference in Literature: —

No.: 9

Year: —

Name of Author and Patient: Hammond.

Age at time of Paralysis, of Autopsy: 4 yrs. stand.

Nature of Symptoms: —

Limbs Paralyzed: l. u.

Electric Reaction: ?

Appearances at Autopsy: Encysted clot in left ant. column, lower dorsal cord.

Reference in Literature: _Journ. Psych. Medicine_, 1867.

[Footnote 90: _Krankheiten des Gehirns und Ruckenmarkes_.]

[Footnote 91: _Lahmung der Kinder_, p. —.]

[Footnote 92: _Jahrb. f. Kinderheilk._, 1865.]

[Footnote 93: _Reynolds's Syst. of Medicine_.]

The first really modern autopsy, that made by Cornil in 1863, agrees with the two earliest on record in disclosing only an atrophy of the cord. Some of the other cases, contained in Table III., note in addition sclerosis of the lateral columns.

In all the remaining autopsies on record are noted atrophy of the anterior gray cornua and more or less extensive destruction of the ganglionic cells.

In a certain number of cases the atrophy seemed to be the unique lesion. But it never was confined to the ganglionic cells, but included the reticulum of gray fibres in which these were imbedded, and which {1134} was replaced by a reticulum of connective tissue. These cases were all examined many years after the occurrence of the paralysis.

TABLE III.—AUTOPSIES SHOWING ATROPHY OR SCLEROSIS OF WHITE COLUMNS OR ROOTS.

No.: 10

Year: 1825

Name of Author and Patient: Hutin.

Age at time of Paralysis, of Autopsy: 7, 49

Nature of Symptoms: Convulsions.

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy of cord from below 8th dorsal nerve to thickness pencil, and of nerves.

Reference in Literature: Quoted by Heine, p. 151.

No.: 11

Year: 1842

Name of Author and Patient: Lunget.

Age at time of Paralysis, of Autopsy: ?, 8

Nature of Symptoms: ?

Limbs Paralyzed: r. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy and brown discol. of ant. roots of lumbar and sacral nerves going to sciatic.

Reference in Literature: _Anat. et Phys. du Syst. nerveux_, i. p. 358.

No.: 12

Year: 1863

Name of Author and Patient: Recklinghausen.

Age at time of Paralysis, of Autopsy: ?, ?

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy of ant.-lateral columns.

Reference in Literature: _Deutsche Klinik_, 1863, Jan. 3.

Seel. says also atrophy of cells; Seguin and J., tubercles.

No.: 13

Year: 1863

Name of Author and Patient: Cornil.

Age at time of Paralysis, of Autopsy: 2, 49

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Atrophy antero-lateral columns.

Seeligmüller says also atrophy of ganglion-cells, as if quoting Charcot.

Reference in Literature: _Soc. de Biol., Comptes Rendus_, 1863.

Infiltration of gray and white corpuscles, with abundant amyloid corpuscles, especially in anterior gray cornua. These through entire extent of cord—cells—intact. Paraplegia, but walks by muscles of thigh and pelvis; leg and foot atrophied.

No.: 14

Year: 1864

Name of Author and Patient: Laborde and Bouvier.

Age at time of Paralysis, of Autopsy: 1, 2

Nature of Symptoms: ?

Limbs Paralyzed: all four.

Electric Reaction: noted.

Appearance at Autopsy: Atrophy antero-lateral columns; nerve-fibres atrophied and varicose.

Reference in Literature: Laborde, _De la Paralysie de l'Enfance_, pp. 109-119.

No.: 15

Year: 1864

Name of Author and Patient: Laborde and Cornil.

Age at time of Paralysis, of Autopsy: ⅔, 2

Nature of Symptoms: ?

Limbs Paralyzed: b. u.

Electric Reaction: ?

Appearance at Autopsy: Sclerosis of ant.-lateral columns.

Ganglion-cells normal; sciatic neuritis.

Reference in Literature: Laborde, _loc. cit._, p. 104.

The first group is contained in the following table:

TABLE IV.—AUTOPSIES SHOWING ATROPHY OF THE ANTERIOR CORNUA AND GANGLION-CELLS.

No.: 16

Year: 1866

Name of Author and Patient: Prévost.

Age at time of Paralysis, of Autopsy: ?, 78

Nature of Symptoms: ?

Limbs Paralyzed: L. u.

Result of Autopsy: Atrophy of left anterior cornu, especially of ganglion-cells.

Reference in Literature: _Comptes Rendus, Soc. Biol., Gaz. méd._, 1866.

No.: 17

Year: 1870

Name of Author and Patient: Charcot and Joffroy.

Age at time of Paralysis, of Autopsy: 7, 32

Nature of Symptoms: Sudden.

Limbs Paralyzed: All esp. l. u.

Result of Autopsy: Atrophy of cells ant. horns and ant. lateral columns.

Reference in Literature: _Archives de Phys._, 1870.

No.: 18

Year: 1870

Name of Author and Patient: Parrot and Joffroy.

Age at time of Paralysis, of Autopsy: —, 3

Nature of Symptoms: Unknown.

Limbs Paralyzed: B. l.

Result of Autopsy: Atrophy and partial sclerosis of anterior cornua and ant. lat. columns.

Reference in Literature: — {1135}

No.: 19

Year: 1870

Name of Author and Patient: Vulpian.

Age at time of Paralysis, of Autopsy: ?, 66

Nature of Symptoms: ?

Limbs Paralyzed: L. l.

Result of Autopsy: Atrophy of ganglion-cells, sclerosis of antero-lateral columns.

Reference in Literature: _Archives Physiol._, 1870.

No.: 20

Year: 1871

Name of Author and Patient: Müller.

Age at time of Paralysis, of Autopsy: 4, 34

Nature of Symptoms: Fall from bed.

Limbs Paralyzed: L. lower.

Result of Autopsy: Atrophy of ganglion-cells ant. cornua; sclerosis of anterior roots.

Reference in Literature: Quoted by Seeligmüller, _Gerhardt's Handbuch_, Tabeln.

No.: 21

Year: 1873

Name of Author and Patient: Lancereaux and Pierret.

Age at time of Paralysis, of Autopsy: 2, 18

Nature of Symptoms: ?

Limbs Paralyzed: L. upper.

Result of Autopsy: Atrophy of external group cells in ant. cornua; general atrophy of left half of lumbar cord.

Reference in Literature: Petitfils, _Thesis on Atrophie aigue des Cellules motrices_, 1873, p. 33.

No.: 22

Year: 1875

Name of Author and Patient: Raymond.

Age at time of Paralysis, of Autopsy: ?, 75

Nature of Symptoms: ?

Limbs Paralyzed: R. arm.

Result of Autopsy: Atrophy of ganglion-cells in right ant. horn cerv. region.

Reference in Literature: _Gaz. méd de Paris_, No. 19, 1875.

No.: 23

Year: 1879

Name of Author and Patient: Taylor.

Age at time of Paralysis, of Autopsy: 1½, 3

Nature of Symptoms: 3 days' fever.

Limbs Paralyzed: L. leg.

Result of Autopsy: Atrophy of left ant. cornua; disappearance of ganglion-cells; no lesion in white column.

Reference in Literature: _Trans. Path. Soc. London_, 1879.

No.: 24

Year: 1875

Name of Author and Patient: Dejerine.

Age at time of Paralysis, of Autopsy: —, —

Nature of Symptoms: —

Limbs Paralyzed: R. foot (congenital equinus).

Result of Autopsy: Atrophy of ant. horn right side; atrophy external group of motor-cells.

Reference in Literature: _Arch. Phys._, 1874.

No.: 25

Year: 1879

Name of Author and Patient: Humphreys.

Age at time of Paralysis, of Autopsy: 1½, 3½

Nature of Symptoms: ?

Limbs Paralyzed: L. leg.

Result of Autopsy: Atrophy of left half lumbar cord; disappearance of medial group cells both sides; antero-lateral on left side.

Reference in Literature: _Trans. Path. Soc. London_, 1879.

In the remaining cases the ganglion-cells of the anterior cornua had also disappeared; but in addition to this atrophy excited distinct evidence of more or less extensive inflammation. This table includes one case of autopsy at two months (Roger's); one at six weeks after paralysis (Turner's).

TABLE V.—AUTOPSIES SHOWING EVIDENCE OF MYELITIS, TO WHICH THE ATROPHY OF THE GANGLION-CELLS WAS CONSECUTIVE.

No.: 26

Year: 1866

Name of Author and Patient: Echeverria.

Age at time of Paralysis, of Autopsy: 3, 10

Nature of Symptoms: Fever.

Limbs Paralyzed: R. arm, R. leg.

Appearance at Autopsy: Granular pigmentation anterior cornua, diffuse myelitis.

Reference in Literature: Quoted by Seguin, _loc. cit._

No.: 27

Year: 1866

Name of Author and Patient: Echeverria.

Age at time of Paralysis, of Autopsy: 2, 2½

Nature of Symptoms: Febrile diarrhœa.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Ibid.

Reference in Literature: _Ibid._

No.: 28

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 1-5/6, 2

Nature of Symptoms: Scarlatina with second attack.

Limbs Paralyzed: L. arm, then both legs.

Appearance at Autopsy: Foci of softening throughout cord. Atrophy ganglion-cells and nerve-fibres. Dilatation, fatty degen. vessels. Sclerosis ant. columns. Atrophy ant. roots.

Reference in Literature: _Gaz. méd. de Paris_, 1871.

No.: 29

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 2, 2½

Nature of Symptoms: Variola.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Foci of softening in ant. cornua. Fatty degen. blood-vessels, circumscribed myelitis.

Reference in Literature: _Ibid._

No.: 30

Year: 1871

Name of Author and Patient: Roger and Damaschino.

Age at time of Paralysis, of Autopsy: 2, 3

Nature of Symptoms: Fever.

Limbs Paralyzed: Ibid.

Appearance at Autopsy: Foci of softening, as above.

Reference in Literature: _Ibid._

No.: 31

Year: 1873

Name of Author and Patient: Roth.

Age at time of Paralysis, of Autopsy: 1, 2

Nature of Symptoms: Ibid.

Limbs Paralyzed: Ibid.

Appearance at Autopsy: Focus myelitis on both sides. Disappearance ganglion-cells, abundant exudation corpuscles.

Reference in Literature: _Virch. Arch._, 1873, Bd. lviii. {1136}

No.: 32

Year: 1868

Name of Author and Patient: L. Clarke.

Age at time of Paralysis, of Autopsy: 1, 32

Nature of Symptoms: After inoculation.

Limbs Paralyzed: Both arms.

Appearance at Autopsy: Extensive myelitis ant. and central part gray matter. Disappearance ganglion-cells.

Reference in Literature: _Med.-Chir. Trans._, li. p. 219.

No.: 33

Year: 1876

Name of Author and Patient: Schultze.

Age at time of Paralysis, of Autopsy: 3, 22

Nature of Symptoms: Acute disease.

Limbs Paralyzed: Both legs.

Appearance at Autopsy: Atrophy lumbar cord ant. lat. columns. Atrophy ganglion-cells. Abundant exud. corpuscles. Proliferation neuroglia.

Reference in Literature: _Virch. Archiv_, Bd. lxviii., 1876.

No.: 34

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 2, 60

Nature of Symptoms: Fall from table.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Circumscribed cicatrix with complete destruction gray substance. Amyloid degeneration. Atrophy ant. roots.

Reference in Literature: _Archiv f. Psych._, 1876, Bd. vi.

No.: 35

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: ¾, 1¾

Nature of Symptoms: Suddenly.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Atrophy ganglion-cells. Cellular diffused infilt. (myelitis) gray subst'ce.

Reference in Literature: _Ibid._

No.: 36

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 4, 58

Nature of Symptoms: Sudden over night.

Limbs Paralyzed: L. leg.

Appearance at Autopsy: Amyloid infiltration ant. horns, atrophy ganglion-cells left lumbar horn. Diffuse atrophy gray substance.

Reference in Literature: _Ibid._

No.: 37

Year: 1876

Name of Author and Patient: Leyden.

Age at time of Paralysis, of Autopsy: 3, 20

Nature of Symptoms: Ibid.

Limbs Paralyzed: R. leg, L. arm.

Appearance at Autopsy: Sclerotic focus in right lumbar and in left cerv. region. Diffuse meningo-myelitis. Atrophy ant. lat. columns. Encapsulated myelitis.

Reference in Literature: _Ibid._

No.: 38

Year: 1876

Name of Author and Patient: Demme.

Age at time of Paralysis, of Autopsy: ?, 3½

Nature of Symptoms: ?

Limbs Paralyzed: —

Appearance at Autopsy: Purulent focus in ant. cornua lumbar region. Atrophy ganglion-cells.

Reference in Literature: Quoted by Seeligmüller, _loc. cit._, p. 18.

No.: 39

Year: 1876

Name of Author and Patient: Eisenlohr.

Age at time of Paralysis, of Autopsy: ?, ¾

Nature of Symptoms: ?

Limbs Paralyzed: B. legs.

Appearance at Autopsy: Diffuse inflammation anterior horns and ant. lat. columns.

Reference in Literature: _Ibid._

No.: 40

Year: 1879

Name of Author and Patient: Turner.

Age at time of Paralysis, of Autopsy: 2½, 2¾

Nature of Symptoms: ?

Limbs Paralyzed: —

Appearance at Autopsy: Myelitic disorganization gray substance ant. cornua lumbar cord.

Reference in Literature: _Trans. Path. Soc. Lond._, 1879.

No.: 41

Year: 1883

Name of Author and Patient: Archambault et Damaschino.

Age at time of Paralysis, of Autopsy: 30 m's, 31 m's, or 26 d'ys fr. début.

Nature of Symptoms: Malaise and prostration one day.

Limbs Paralyzed: Left leg and right arm.

Appearance at Autopsy: Focus red softening ant. horns left lumbar; right cervical region. Enormous enlargement vascular network, and distension blood-vessels; granular corpuscles in lymphatic sheaths; marked atrophy cells and of myeline sheaths of fibres in ant. roots; myeline balls in sheath; axis-cylinders disappeared. Lesions more or less marked throughout cord. Nerves not examined.

Reference in Literature: _Le Union médicale_, 1883.

No.: 42

Year: 1884

Name of Author and Patient: Money.

Age at time of Paralysis, of Autopsy: 2 yrs., 28 m's.

Nature of Symptoms: Fever and vomiting for a week.

Limbs Paralyzed: Paraplegia.

Appearance at Autopsy: Red area both anterior cornua lumbar region. Here distension and thrombosis vessels; infiltration leucocytes; absence multipolar cells.

Reference in Literature: _Trans. Path. Soc. Lond._, 1884.

No.: —

Year: 1884

Name of Author and Patient: Money.

Age at time of Paralysis, of Autopsy: Unknown, 7 yrs.

Nature of Symptoms: Unknown.

Limbs Paralyzed: Right leg.

Appearance at Autopsy: Wasting anterior horn almost throughout lumbar region. Atrophy cells chiefly in ant., ant.-lat., post.-lateral, and central groups, replaced by dense nucleated tissue.

Reference in Literature: —

It will be useful to add another table, which will group together the cases in which the autopsies were made within two years after the occurrence of the paralysis. Of these, all but the two made by Laborde, in which the cornua are declared to be healthy and the lesion limited to the {1137} white columns, show traces of destructive morbid processes in the gray substance of the cord, greatly predominating in the anterior cornua, but not absolutely limited to them, nor even to the part of the cord which corresponds to the paralyzed limb:

TABLE VI.

---------+-----------------+------------------+-------------
Case No. | Name of Author. | Date of Autopsy | Year of
| | after Paralysis. | Publication.
---------+-----------------+------------------+-------------
41 | Damaschino. | 6 weeks. | 1883
40 | Turner. | 26 days. | 1879
28 | Roger and | |
| Damaschino. | 2 mos. | 1871
42 | Money. | 4 mos. | 1884
27 | Echeverria. | 6 mos. |
39 | Eisenlohr. | 6 mos. |
29 | Roger. | 6 mos. | 1871
31 | Roth. | 9 mos. | 1873
35 | Leyden. | 11 mos. | 1876
14 | Bouvier and | |
| Laborde. | 12 mos. | 1864
30 | Roger. | 13 mos. | 1871
15 | Cornil and | |
| Laborde. | 16 mos. | 1864
12 | Recklinghausen. | 24 mos. | 1863
38 | Demme. | 24 mos. | 1876
23 | Taylor. | 18 mos. | 1879
25 | Humphrey. | 24 mos. | 1879
---------+-----------------+------------------+-------------

AUTOPSIES OF RELATIVELY RECENT CASES.—In cases relatively recent all macroscopic changes in the cord may be entirely wanting. There may be some degree of asymmetry in the surface of section, patches of white coloration in the anterior gray substance, or of gray or yellow color in the white columns; the anterior roots may be congested or even already atrophied.[94] On the other hand, there have several times been found foci of visible red softening, much more frequently at a point corresponding to the origin of the paralyzed nerves, but not absolutely confined to them, and sometimes existing at points where they have given rise to no symptoms whatever.[95]

[Footnote 94: Roger's first case, No. 28 of Table V.]

[Footnote 95: Case 1st of Roger, Tab. V.]

Microscopic Lesions.—In striking contrast with this paucity of macroscopic lesions are the interesting structural changes revealed under the microscope. These lesions are usually comprised within circumscribed foci whose size may vary from a long diameter of 2 mm.[96] to one of from 10 to 30 mm.[97] Sometimes bilateral foci are found with monoplegic paralysis; thus one side or the other preponderates in the morbid process.

[Footnote 96: Case Roth, Tab. V.]

[Footnote 97: Case Schulze, Tab. V.]

In recent cases (Damaschino's, at twenty-six days; Roger's, at two months; Turner's, at six weeks) patches of red softening existed at the portions of the cord containing the nuclei of origin of the paralyzed nerves. In Turner's case the focus contained hemorrhagic extravasation, and the traces of this were clearly perceptible in Roger's first case. The blood-vessels are dilated; their lymphatic sheaths infiltrated with leucocytes and with granular corpuscles; their walls are thickened, pigmented, or fatty.

{1138} Leucocytes are often disseminated through the diseased area, and in one case (Demme) were accumulated into a focus of pus. Besides the leucocytes, the foci are often infiltrated with large round granular cells that seem to be transformed neuroglia-cells (Leyden). In one case neuroglia nuclei were accumulated in a ring around the focus, seeming to indicate the beginning of encapsulation.

The most striking lesion, however, and the one which is common to the most recent as well as to old cases, is the deformation, atrophy, and final disappearance of the large ganglionic cells of the anterior cornua. The first change consists in granular pigmentation;[98] then the prolongations disappear, leaving the body of the cell shrunken and deformed; at last the whole cell disappears. Sometimes all the cells of an anterior horn have disappeared throughout the entire depth of the focus; quite as often, in certain sections at least, the atrophy is limited to certain groups, as the external,[99] or the external in one focus, the antero-lateral in another, situated on the opposite side of the cord.[100]

[Footnote 98: Case of Echeverria, Tab. V.]

[Footnote 99: Case by Schultze (this is a case of ancient lesion), Tab. V. (_Virch. Arch._, Bd. lviii.).]

[Footnote 100: Case by Taylor, Tab. IV. (_Path. Trans._, London, 1879.)]

In a case rendered celebrated by Charcot it is stated that in many sections of the cord atrophy of ganglionic cells constituted the unique alteration, the tissue immediately surrounding the place whence they had disappeared being perfectly healthy. It is on this appearance that has been built up the theory of a primary idiopathic atrophy of the ganglionic cells as the characteristic lesion of infantile paralysis. But in other portions of the same cord Charcot himself describes destruction of the gray reticulum imbedding the cells; and this destruction is insisted upon in many other observations. In other words, there is a general disintegration of the gray nervous tissue of the anterior cornua which contain the focal lesion. The normal tissue is then replaced by a reticulum of conjunctive fibres, more or less dense according to the age of the case.

These focal lesions of the cord explain admirably, as will be seen, the permanent symptoms of the disease. But of great importance for understanding its initial period is the fact that structural changes—similar to, but less severe than, those just described—have beer found diffused throughout the cord. In several cases hyperæmia, partial atrophy of ganglionic cells and nerve-fibres, infiltration with exudation corpuscles, in the anterior cornua and even central gray canal from the lumbar to the cervical region.[101] In Damaschino's case, besides the focal lesions which corresponded to the paralyses of the right arm and left leg, were others corresponding to the left arm and right leg where no paralysis existed.

[Footnote 101: See cases by Leyden, Roth, Schultze, Clarke, Damaschino.]

This case (1883) is also interesting in bringing out another lesion not usually noticed. This is the breaking up into balls of the myeline in the medullated tubes, both of the anterior intraspinal nerve-roots and of such fibres as traversed the anterior nerves. In balsam preparations these myeline drops are dissolved; but in osmic acid and glycerin preparations they appear as black balls all over the field. The lesion is identical with that already described by Dejerine (1875) in both nerves, roots, and white columns. The columns of Clarke have always been found intact.

{1139} In the recent cases no lesions of the white columns have been observed—a fact upon which reposes the doctrine that such lesions, when existing, are secondary to those of the cornua.

SECOND GROUP OF CASES.—The next group of cases contains 16, where the autopsy was made more than two years after the début of the paralysis.

TABLE VII.—AUTOPSIES SHOWING LESIONS OLDER THAN TWO YEARS.

---------+-----------------+------------------+-------------
Case No. | Name of Author. | Date of Lesion. | Year of
| | | Publication.
---------+-----------------+------------------+-------------
11 | Longet. | 7 yrs. | 1842
27 | Echeverria. | 7 yrs. | 1866
43 | Money. | 7 yrs. | 1884
16 | Lancereaux. | 16 yrs. | 1873
38 | Leyden. | 17 yrs. | 1876
33 | Schultze. | 19 yrs. | 1876
17 | Charcot and | |
| Joffroy. | 25 yrs. | 1870
20 | Müller. | 30 yrs. | 1871
22 | Clarke. | 31 yrs. | 1868
10 | Hutin. | 42 yrs. | 1825
13 | Cornil. | 47 yrs. | 1863
36 | Leyden. | 54 yrs. |
34 | Leyden. | 58 yrs. | 1876
19 | Vulpian. | 64 yrs. | 1870
22 | Raymond. | 70 yrs. | 1875
16 | Prévost. | 76 yrs. | 1866
---------+-----------------+------------------+-------------

The date of these lesions varies from seven to seventy-six years. In two or three cases, where the autopsy was made on very old people, the early history of the disease was unknown, but the probable date of the paralysis was calculated.

In this group of cases patches of atrophy, semi-transparent and grayish in color, focal or diffused, are clearly perceptible to the naked eye. As a rule, the atrophy is unilateral, and sensibly affects the entire half of the cord. In some cases of paraplegia, however, there is a bilateral, symmetrical shrinkage of the entire lumbar cord, which has been reduced to the size of a quill.

The atrophy involves, first and most markedly, one or both anterior cornua; second, the anterior nerve-roots arising from them; third, the antero-lateral columns.

In both the latter localities the microscope will often find individual nerve-tubes wasted and deprived of their myeline. The atrophied patches are generally sclerosed as the seat of a proliferated neuroglia, coloring deeply with carmine. In Laborde's cases, published at the very beginning of what may be called the anatomical period, the atrophy and sclerosis were said to be limited to the antero-lateral columns and the nerve-roots, while the cornua remained intact. In all more recent observations, however, the lesion of the white columns and roots has been found strictly proportioned to that of the gray horns. The sclerosis extended into the latter, constituted by a reticulum of connective-tissue fibres, sometimes fine, sometimes so matted together as to form a dense felt-like substance, sometimes offering the ordinary aspect of sclerosis.

Amyloid corpuscles have been found infiltrated in great numbers {1140} through both the gray and white substance in these old cases (case by Cornil),[102] seeming to replace the infiltration with exudation corpuscles observed in the more recent ones.[103] When the lesion is distinctly circumscribed the focus is often surrounded by a zone of embryonic cells, seeming to indicate a reactive proliferation on the periphery.[104]

[Footnote 102: _Loc. cit._, _Soc. Biol._,1863.]

[Footnote 103: Seguin (_loc. cit._) observes that the opinion is gaining ground which ascribes these to a transformation of the neuroglia corpuscles.]

[Footnote 104: Case by Schultze, _loc. cit._]

As in the relatively fresh cases, the circumstance which has attracted the most attention is the atrophy of the ganglionic cells from the sclerosed patches of the anterior cornua. The completeness with which these have disappeared in any focus seems to be proportioned to the completeness of the paralysis in the corresponding limb. Partial atrophy or disappearance of spinal groups of cells from the cornua may sometimes be correlated with paralysis of special muscles.[105]

[Footnote 105: Thus in Schultze's case, already quoted, the external group of cells had disappeared from the focus in one gray horn, and the extensors of the foot were alone paralyzed. This seems to confirm the opinion advanced by Spitzka, that this external group of motor-cells corresponds to the extensor, the internal groups to the flexor muscles.]

Study of the pathology of infantile paralysis is not completed when the above series of spinal lesions has been enumerated. Most various interpretations have been made of these lesions as they have been successively discovered. Thus, after the theory of congestion came the theory of primary sclerosis, built upon Laborde's two autopsies;[106] then the theory of primary atrophy of ganglionic cells;[107] then the theory of myelitis;[108] finally, a theory of complex and variable lesion.[109]

[Footnote 106: Laborde, _loc. cit._; Cornil, _loc. cit._]

[Footnote 107: Charcot, _Leçons sur les Maladies du Syst. nerveux_; Prévost, _Soc. Biol._, 1864; Joffroy, _Arch. de Physiol._, 1870; Petitfils, “De l'Atrophie aigue des Cellules matrices,” _Thèse de Paris_, 1873.]

[Footnote 108: Schultze, _Virch. Arch._, Bd. lxviii.; Roth, _Ibid._, Bd. lviii.; Henoch, _loc. cit._, p. 208; Ross, _loc. cit._, p. 125; Seguin, _loc. cit._, 1877; Erb, _Ziemssen's Handbuch_; Seeligmüller, _Gerhardt's Handbuch_; Roger and Damaschino, _Gaz. méd._, 1871; Turner, _Path. Trans. Lond._, 1879; Hammond, _loc. cit._]

[Footnote 109: Leyden, _Archiv für Psych._, Bd. vi., 1876.]

It was Prévost who first ascribed a predominant importance to the atrophy of the ganglionic cells of the anterior cornua; but it was in the hands of Vulpian, Joffroy, and more especially Charcot and his pupils, that the theory was fully developed. Infantile paralysis was ranked in a newly-formed group of diseases, all characterized by atrophy of these same cells, and differing from each other principally in the acuteness of the process and in its complications.[110] Seguin, in his original lecture in 1874, supported the same views, but in 1877 fully adopted that of myelitis. The objections to this theory are: 1st, that by it two diseases so different in their course, localization, electrical reactions, and form of paralysis as atrophic paralysis and progressive muscular atrophy are essentially identified on account of the identity of one lesion, the atrophy of the anterior ganglionic cells;[111] 2d, the presence of other lesions or of traces of them peremptorily proves the pre-existence of a complex {1141} morbid process which involves the ganglionic cells, but is neither limited to them, nor, necessarily, originates in them.

[Footnote 110: Thus, acute anterior poliomyelitis, subacute anterior poliomyelitis, progressive muscular atrophy, amyotrophic lateral sclerosis, bulbar paralysis.]

[Footnote 111: When this objection is accepted, Barlow's remark falls to the ground, that “the similarity of lesion found in two such different diseases as infantile paralysis and progressive muscular atrophy proves the failure of anatomical characters, taken alone, to serve as a basis of nosology” (_Brain_, April, 1879, p. 74).]

This inference was drawn by Roger from the hemorrhagic softening, dilatation, and degeneration of blood-vessels, infiltrations with exudation-corpuscles, and hyperplasia of conjunctive nuclei present in his case. Similarily, Schultze, in a case examined nineteen years after the occurrence of the paralysis, found traces of an extensive myelitis in the diffusion of the lesions,[112] in the exquisite cellular infiltration, the proliferation of the neuroglia, and the atrophy of axis-cylinders of nerve-fibres together with the cells; and inferred an anterior myelitis, diffused in the long axis of the cord, but limited to the antero-posterior region. Schultze defines Charcot's theory to be an hypothesis of such an acute atrophy of ganglionic cells as leads to a rapid melting down of these bodies, whereby reactionary inflammation is excited in the surrounding tissue. This implies that the dying cells are able to act like a virulent substance on the imbedding tissue, and of this, declares Schultze, “Charcot has offered no proof.”[113]

[Footnote 112: In this case of paraplegia without lesion of the upper extremity, to which we have several times alluded, there was bilateral atrophy of the lumbar cord, atrophy of the right anterior nerve in the dorsal and lower cervical region, also in the cervical enlargement.]

[Footnote 113: It might be said that the fall of the fever as soon as the paralysis is declared and the motor cells presumably melted down should contradict the idea that their dying substance acts as an irritant upon surrounding tissues.]

A third objection has been brought forward by Leyden, and is really an enlargement on the second. It is, that various lesions or morbid processes may underlie the same clinical history. In four autopsies of cases presenting all the clinical history of acute anterior poliomyelitis this author has found three different lesions. In one an extensive lepto-meningitis, together with irregular focal sclerosis of the white columns, evidently depended upon the latter, and in turn caused sclerosis of the anterior cornua with consequent destruction of their cells.[114] In two other cases an anterior poliomyelitis was accompanied by diffused lesions of the central canal. Finally, in a fourth case the lesions were limited to the anterior cornua, as is most usual.

[Footnote 114: This case of Leyden's throws light on the two autopsies by Laborde with sclerosis of the white columns and intact cornua. It seems probable that a process originating in the cornua had then been arrested or had receded, while continuing its evolution in the white columns.]

The theory of acute atrophy of ganglionic cells is not sensibly different from that of a parenchymatous myelitis.[115] But all the objections which can be urged against the former theory apply to the latter also, with the exception that the hypothesis of inflammation suggests a cause for the otherwise inexplicable atrophy. Observation of the pathological appearances alone could not decide whether the irritation started in the parenchymatous or interstitial tissues. Reference to the etiology of the disease shows that of the two most frequent apparent causes, {1142} blood-poisoning and traumatisms, the first would indicate that the inflammation started in the connective tissue supporting the blood-vessels; the second suggests that the irritation began in the spinal elements constituting the origin of the nerves.

[Footnote 115: Hammond assumes such a form of myelitis in his classification of inflammations limited to the anterior part of the gray matter of the spinal cord:

1. Inflammation of motor and trophic nerve-cells: (_a_) Infantile spinal paralysis; (_b_) Spinal paralysis of adults; (_c_) Pseudo-hypertrophic spinal paralysis.

2. Inflammation of motor cells: (_a_) Glosso-labia-laryngeal paralysis.

3. Inflammation of trophic cells: (_a_) Progressive muscular atrophy; (_b_) Progressive facial atrophy (_Dis. Nerv. Syst._, 6th ed., p. 464).

We think this classification open to several fundamental criticisms.]

Whatever be the starting-point, however, it is very evident that the morbid process soon involves all the tissues contained in the gray matter of the anterior horns, and constitutes, therefore, a real anterior poliomyelitis.

A question of much interest is the relation to this of the lesions of the anterior roots and of the white columns. Is the atrophy of nerve-tubes a passive consequence of their separation from the ganglionic cells, the sclerosis a secondary consequence of this? or is the sclerosis the cause of the atrophy, itself the result of an irritation propagated downward from the myelitic focus, according to the usual law for secondary degenerations in motor tracts? or, finally, is it a residuum of a leucomyelitis (or of the white substance), complicating by simple extension the inflammation of the gray substance?

Review of the autopsies recorded would indicate that the lesions in question are brought about sometimes in one, sometimes in another, of these ways—sometimes even, as in Leyden's case, by extension from a meningitis. That sclerosis of the white columns is most frequently a secondary degeneration is indicated by the frequency with which it appears below the lesion of the cornua, by the rarity with which it is found above, and also by the general proportion between its intensity and that of the disease of the gray matter.

We have devoted so much space to consideration of spinal-cord lesions, because they are by far the most constant and the most important; after these rank the structural alterations of the muscles, which received for a while such a preponderance of attention.

Hammond has studied the progress of these changes on the living subject by fragments of fibre successively removed with Duchenne's harpoon. In an incipient stage of degeneration the fibrillæ are found to be irregular and torn,[116] the transverse striæ dim; oil-globules are seen arranged according to the long axis of the fibre. In a more advanced stage the transverse striæ nearly disappear, the oil-globules are in large numbers, and fat-corpuscles are also abundant. Finally, the whole specimen is seen as a mass of air-globules. Six weeks later, however, these had in turn disappeared, and there remained a mass of connective tissue.

[Footnote 116: Though, from the method of removal, this appearance cannot be considered as certainly pathological.]

This series of changes, however, does not always take place, as Hammond himself recognizes. Laborde[117] first described a granular form of muscle atrophy, where the muscular substance gradually wastes away without ever becoming fatty, and leaving a transparent and hyaline sheath. The two forms of fatty and of simple atrophy can be distinguished by the naked eye. In the latter the muscle begins by being thinner or lighter and softer than usual, ultimately turning light brown. The fatty muscle becomes a homogeneous yellowish-white, diversified by occasional remnants of reddish fibres.

[Footnote 117: _Loc. cit._, p. 131.]

{1143} Proliferation of the interstitial connective tissue may be combined with either simple or fatty atrophy. A combination of abundant sclerosis and abundant fatty infiltration may lead to a pseudo-hypertrophy of the muscles.

“There cannot be the slightest doubt,” observes Erb, “that the lesions described constitute a degenerative atrophy similar to what may be caused by section or sense traumatism of a peripheric nerve.”

The peripheric nerves have been much less thoroughly studied than the spinal cord. Leyden first directed special attention to the nerves. He found the sciatic altered in two cases,[118] in the first by an interstitial neuritis; in the second by partial atrophy. In 1880 the same writer, in an extensive article on poliomyelitis and neuritis,[119] greatly extends his views as earlier expressed. Not only does he claim the coexistence of neuritis with spinal-cord disease in atrophic paralysis, but thinks that many cases of this, and also of other forms of paralysis, “lately supposed to originate in the spinal cord, may really begin in any part of the motor apparatus,” thence sometimes generalize throughout the whole apparatus, sometimes remain limited to the original portion affected. Thus, progressive muscular atrophy may sometimes begin in the nerves, sometimes in the muscles, and sometimes in the ganglionic cells of the cord; and this variety of origin explains the discrepancies of opinion which have been held upon the nature of this disease. Similarly, all forms of acute or chronic atrophic paralysis in either children or adults may begin in either the nerves or cord, thence become generalized to both, or remain limited to one part of the spinal motor system. Cases of atrophic paralysis which recover are probably not cases of poliomyelitis at all, but of multiple neuritis, rheumatic, traumatic, or infectious in nature. The regeneration of peripheric nerves is a well-demonstrated possibility, but not that of the cells of the cord. Lead-paralysis is usually confined to the nerves, but sometimes extends to the cord. In diphtheritic paralysis Buhl has found injection, thickening, and granular infiltration of nerves at the union of their anterior and posterior roots;[120] and as long ago as 1876, Dejerine, in a case of atrophic paralysis in a syphilitic woman, found varicose swelling of the medullary sheath in the nerves of the paralyzed lower extremities, together with heaping up of the myeline into large drops, colored black in glycerin and osmic-acid preparations. Coincidently, in the cord, at the origin of the same nerves, the number of motor-cells was diminished, and of those that remained the prolongations, and even the body, of the cell were atrophied.[121]

[Footnote 118: Cases 34 and 35 of Table V., quoted from _Arch. de Psychiatrie_, Bd. vi., 1876.]

[Footnote 119: _Zeitschrift für Klin. Med._, 1880.]

[Footnote 120: _Zeitschrift für Biol._, 1867.]

[Footnote 121: _Arch. de Phys._, 1876.]

These views of Leyden's are extremely interesting, and should stimulate future research into the condition of nerves in all cases of atrophic paralysis. It is quite incorrect to say, as Archambault and Damaschino have recently done,[122] that Leyden denies the existence of anterior poliomyelitis in such cases, especially in such as prove permanent. He only insists on the frequent coincidence of neuritis, on a varying point of departure for the morbid process, and on the probability that in cases of recovery this process has always remained peripheric.

[Footnote 122: _Le Union méd._, 1883, 7, 35, case quoted in Table V. It is much to be regretted that Damaschino, who strongly controverts Leyden's views, did not examine the nerves in his own most interesting case.]

{1144} The strongest objection to Leyden's theory is the absence in most recorded cases, either infantile or adult, of the usual signs of nerve inflammation, local pain, or tenderness. Autopsies of old cases are not able to differentiate an inflammation from an atrophic process in the nerves, followed by a secondary thickening of the endoneurium. This thickening was found in three cases examined by Edmonds in 1882, whose subjects had suffered from infantile paralysis in early life, and had had the paralyzed limb amputated at the age of fifteen or sixteen. Transverse sections were made from the internal popliteal nerves. The specimens showed some healthy nerve-fibres, presumed to be sensory; others much smaller, with the axis-cylinders wasted or degenerated; while strands of connective tissue traversed the nerve-bundles, resulting from hypertrophy of the endoneurium. The vessels showed inflammation of their coats, with proliferation of the endothelium.[123]

[Footnote 123: _Trans. Path. Soc. London_, 1883.]

The brain is usually normal, unless indeed the paralysis has affected children previously rendered idiotic by congenital atrophia cerebri. Sandie, however, examined one brain with an interesting positive result.[124] The brain was taken from a boy of fifteen paralyzed since the age of three in almost all his muscles, with even paresis of the muscles of the trunk and neck. The paralysis was more marked upon the right than on the left side. At the autopsy, in addition to atrophy of the muscles and of the motor nerves, with exquisite atrophy of the anterior columns and anterior cornua, was found a decided atrophy of the left central convolution, and, less marked, of the paracentral lobule. This was shown by comparative measurements with the opposite side of the same brain, and also with the corresponding convolution and lobule in two other brains. The child's intelligence had not been affected.

[Footnote 124: _Centralblatt f. d. Med. Wissensch._, No. 15, 1875.]

The arrest of development of the bones has been already mentioned, as well as that of their epiphyses and apophyses. The compact osseous tissue is atrophied: the medullary, on the contrary, abundantly developed and rich in fat.

PATHOGENY OF INFANTILE PARALYSIS.—In the pathological anatomy of infantile paralysis there are two principal facts to be correlated with its clinical phenomena—namely, the limitation of the myelitis to the anterior gray horns of the spinal cord; the destruction of the ganglionic nerve-cells in these gray horns. That the other lesions observed are subordinate to these is shown by their variableness as compared with the constancy of the anterior poliomyelitis. These lesions are, in the cord, the atrophy and sclerosis of the anterior nerve-roots and white columns; in the muscle, the fatty degeneration or simple atrophy of the fibre; in the nerve, breaking down, and finally atrophy of the myeline sheath, sometimes of the axis-cylinder; proliferation of the endoneurium.

Consequence of Limitation of Myelitis.—Limitation of the morbid process to a portion of the motor tract, the anterior cornua, and exclusion of the posterior horns and roots, readily explain the predominant positive symptom of motor paralysis, together with the absence of sensory disturbance. The absence of muscular rigidity, spasm, active contraction, and of exaggerated reflexes is similarly explained by the immunity from the morbid process of the posterior white columns and the portion of the {1145} lateral columns immediately adjacent to them. The motor paralysis resulting from destruction of the anterior ganglionic cells of the cord is much more complete than that which depends on simple interruption of the motor tracts passing from the brain. The manner in which the motor tracts are connected by a succession of arching fibres with these cells already indicates that the latter are dépôts for the reinforcement of the motor impulses. We must believe, indeed, that the centrifugal impulses reaching the anterior cornua are not yet motor in character, but to become so must sustain a new elaboration in the ganglionic cells of this region. Evidently, the network of gray fibres connecting the arcuate strands of the antero-lateral columns with the cells become, in virtue of that fact alone, essential to the process. But it is also probable that the multiplied transmission of impressions, which lies perhaps at the basis of the process of their higher elaboration in ganglionic centres, is carried on in the larger network of gray fibres as well as in the smaller network contained in the ganglionic cells. Destruction of a portion of this network would therefore interfere with the elaboration of the motor impulse, in the same manner, though to a relatively less extent, as destruction of the ganglionic cells themselves.

Trophic Lesions.—The rapid wasting of the paralyzed muscles, with their degenerative electrical reactions, seems, however, to be an effect altogether peculiar to lesions of the ganglionic bodies.[125] According to Charcot, who has so especially formulated the laws of amyotrophic paralysis, all the ganglionic cells essential to the elaboration of motor impulses exercise a trophic influence upon muscles. The spinal cell, nerve-fibre, and muscle-fibre combine into a complex indissoluble unity or element. One part of this lesion of complex elements is necessarily followed by proportionate lesion of all its other parts.

[Footnote 125: The amyotrophic lateral sclerosis of Charcot exhibits in an exquisite manner the difference between paralysis without atrophy, caused by sclerosis of the antero-lateral columns, and paralysis with atrophy when the morbid process has extended to the anterior cornua.]

According to Erb, however, who extends Samuel's doctrine of special trophic nerves, it is not the motor cells which influence the nutrition of the muscle-fibres with which they are connected, but special trophic cells lying among the others in the anterior cornua. This theory is principally based on the existence of muscular atrophies of central origin (progressive muscular atrophy, bulbar paralysis), unaccompanied for a long time by paralysis.[126] Hammond cites as a converse example the anterior poliomyelitis “where the peripheric disturbance is, in the first place, solely one of motility; this is paralysis without atrophy. After a time, which may be as much as six months or even more, the trophic changes begin.”[127]

[Footnote 126: _Ziemssen's Handbuch_.]

[Footnote 127: _Loc. cit._, p. 429.]

But surely this is an exaggerated emphasis on the exception, rather than the true inference from the rule of rapid wasting in anterior poliomyelitis—a rule so general as to have originated the title atrophic paralysis. Erb gives an ingenious scheme (Fig. 55) of the mental relations of motor and trophic cells with cerebral and spinal nerve-fibres. It will be seen that isolated lesions of one or the other trophic apparatus might occur without paralysis of motor tracts, while simultaneous lesion of the trophic {1146} apparatus and of the ganglion-cells, or of the latter, involving the tracts coming from the trophic cells, would cause, as in anterior poliomyelitis, motor paralysis, muscular atrophy, loss of the reflexes, degenerative reaction in nerves and muscles.

Duchenne and Joffroy[128] also argue the existence of special trophic nerve-cells. The absence[129] of the nutritive lesions of the skin and cellular tissue which are so conspicuous when the gray matter around the {1147} central canal or posterior to it is involved,[130] the dependence of the nutrition of the motor apparatus, nerves, muscles, bones on the integrity of the anterior horns, are facts which, taken together, seem to indicate that the maintenance of nutrition depends on the unbroken continuity of the motor or sensory apparatus from the periphery to the ultimate central element, rather than on any special central cells endowed with trophic functions.[131] Erb's hypothesis, as his own scheme moreover denotes, demands not only trophic cells distinct from motor cells, but separate trophic cells for the muscles, for the motor, and for the sensory nerves.

[Footnote 128: “De l'Atrophie aigue et chronique des Cellules nerveuses,” _Arch. de Phys._, No. 4, 1870.]

[Footnote 129: Money, and also Gowers, have signalized a condition of the skin resembling myxœdema (_Tr. Path. Soc. London_, 1884, and _Brit. Med. Journ._, 1879).]

[Footnote 130: Mayer (Herman's _Handbuch Physiol._) sums up the great mass of evidence now accumulated, which demonstrates the trophic influence of the central gray mass of the cord upon the tissue.]

[Footnote 131: Nepveu (_La France médicale_, 1879) mentions some cases of infantile paralysis complicated with trophic lesions of the skin. The facts, if accepted, could only indicate an extension of the myelitis to the central and posterior regions of the gray columns. The relations between non-atrophic paralysis caused by interruptions of the motor tracts and muscular atrophy dependent on lesion of the anterior cornua are exquisitely shown in a case reported by Sander. An adult suffered from chronic motor paralysis, gradually increasing, in the right arm, with paresis of the lower extremities. In the hand, arm, and shoulder the paralysis was followed by gradual atrophy and diminution of the faradic contractility; in the lower extremities no atrophy occurred. At the autopsy was found a gliomatous tumor seated in the anterior cornua predominating on the right side, extending from the level of the sixth dorsal to that of the eighth cervical vertebra. The ganglion-cells were pigmented and compressed, not altogether destroyed. The lumbar cord was intact, and the non-atrophic paresis of the lower extremities evidently resulted from the interruption of the motor tract above.]

The peculiar grouping of nerve-centres within the cord that seems to be indicated by some of the groupings of infantile paralysis shows, as has been said, a probable divergence within the cord of nerve-fibres which run together in the same nerve-stem. The associations to be expected from the data of functional association and of clinical history are by no means fully decided. It is even a matter of dispute whether the tibialis anticus is functionally more associated with the flexors or with the extensors of the thigh, and whether its experimental irritation or clinical paralysis really coincides with that of the first or of the second group. This entire field of observation is new and promises fertile results.[132]

[Footnote 132: It is from this field that has come a new argument for the spinal nature of lead-paralysis, from its peculiar grouping, and from analogy with that of anterior poliomyelitis of the upper extremities (Remak, “Ueber die Local. Atropa. Spinal Lahm.,” _Archiv für Psych._, Bd. ix.; also, Ferrier, _loc. cit._).]