A CONTRIBUTION TO THE 
PATHOLOGY OF THE LAR- 
YNGEAL AND OTHER CRI- 
SES IN TABES DORSALIS. 
BY 
IRA VAN GIESON, M. D. 
REPRINTED FROM 
The Journal of Nervous and Mental Disease, 
July, 1890. 
M. J. Rooney & Co., Printers, 
Corner Broadway and 35th Street. 
NEW YORK. A CONTRIBUTION TO THE PATHOLOGY OF 
THE LARYNGEAL AND OTHER CRISES 
IN TABES DORSALIS* 
By IRA Van GIESON, M. D., 
First Assistant at the Laboratory of the-Alumm Association of the College of Physicians 
and Surgeons, N. Y. 
FOR the opportunity of presenting this case of tabes, 
in which laryngeal crises, one of them proving fatal, 
are associated with a chronic neuritis of the roots of 
the vagus and accessory portion of the eleventh nerves on 
both sides, I am indebted to Dr. W. Gill Wylie, of New 
York, who gave me the autopsy material with the follow- 
ing clinical history : 
“Mr. Van D—, a large, robust, healthy man, denying 
syphilis, had not been sick except with chills and fever, 
until four or five years previous to his death, when he grad- 
ually became uncertain in his gait, and began to lose the 
proper co-ordinative use of the muscles of the legs. Very 
gradually this condition grew worse, so that he could not 
stand upright very well and his arms became ataxic. Vision 
became impaired and he could see with only the lower half 
of the retina. He did not suffer pain. The bladder, bowels 
and digestion remained in good order until a short time 
before death. During the latter stages of the illness, the 
man had at times attacks of choking. He finally became 
insane, and died in one of the choking attacks. In this fatal 
attack there was apparently a paralysis of the laryngeal 
muscles.” 
Microscopical Examination.—The brain and first two seg- 
ments of the spinal cord were removed at the autopsy. 
Sections of the cord show the characteristic lesions of tabes 
in the posterior columns. The sclerosis cannot be traced 
° Read at the New York Neurological Society, November 5, 1889. 2 
IRA VAN G IE SON. 
upward beyond the point where the nuclei of the posterior 
columns become well developed. The nuclei of spinal 
accessory and vagus, and the ascending roots of the vagus 
are normal. The ganglion cells and fine nerve fibres in the 
motor cortex are normal. 
The root fascicles of the vagus and spinal accessory 
nerves on both sides were removed from the medulla and ex- 
amined separately. Sections of these fascicles, (stained 
double with haematoxylon and acid fuchsine, and by Wei- 
gert’s method) show the lesions of a chronic diffuse neuritis, 
—areas of neurogliar increase with the atrophy of the nerve 
fibres. There is an increase of nuclei in the sclerotic por- 
tions of the fascicles, and a few small round cells lie about 
the blood-vessels in one or two places in the damaged por- 
tions of the fascicle. (Some caution is required in deciding 
about degenerated areas in the vagus and spinal accessory 
nerve roots because both of these roots contain bundles of 
fine medullated fibres destined to pass to the sympathetic 
system ; these fibres have a more abundant connective-tis- 
sue matrix than the surrounding fibres, and in oblique sec- 
tions, stained by Weigert’s method, bundles of these fibres 
look like sclerotic patches). The neuritis does not affect 
all of the fascicles uniformly, some are but very slightly 
involved by it, and the roots of the right side are much 
more extensively involved than those of the left side. The 
hypoglossal and trigeminal roots are normal except that in 
the latter a few small round cells accompany some of the 
coarser endoneural septa. 
Laryngeal crises in tabes were first described by Fereol1 
in 1876, and Cherchvesky2 in 1881 collected 18 cases and 
divided them, depending upon the duration of the attack, 
into mild cases, lasting about 90 seconds ; medium cases, 
lasting from five to ten minutes ; and severe cases, lasting 
several hours. The mechanism of is not uni- 
form in all cases or all stages of the attacks, they occur in 
two ways. An analysis of the published cases admits of 
their division into two forms : 1. A spasmodic form. 2. A 
paretic form. 
In the first form, some of the attacks, probably as a rule TABES DORSALIS. 
3 
the earlier and less severe ones, are of a purely spasmodic 
character. The larynx is perfectly normal and the crises 
result from a contraction of the glottis abductors. Attacks 
of this kind, which may last for months or years are well 
illustrated by Landgraf’s3 case, which was under careful 
observation several months, and the author using the laryn- 
goscope, was assured of the reflex spasmodic nature of the 
crises. McKenzie3 and Cherchvesky2 each give two cases 
of crises in which the larynx was normal. 
The second form of the laryngeal crises includes the ma- 
jority of the recorded cases The crises in these cases are 
reported as due to a paresis or paralysis of the abductors. 
This is the so-called posterior paralysis of the Germans— 
posticus-laehmung Gerhardt. (Virchow’s Archiv., xxiii., 
1863). The writer thinks that in the great majority of these 
cases of posterior paralysis producing crises, are not due to 
the exclusive paralysis of the abductors, as is intimated by 
the term posticus-laehmung or posterior paralysis, but are 
due to a weakening or paresis of both adductors and abduc- 
tors, and that in this paresis of both sets of glottis muscles 
the action of the abductors is impaired more than that of the 
adductors. How the function of the abductors becomes 
more impaired than that of their opponents in paresis of 
both sets of muscles, so that in cases of laryngeal crises, 
the abductors appear to be exclusively paralyzed, may be 
better understood by considering the experiments of Semon 
and Horsly, Hooper and Donaldson. 
Semon and Horsley (Brit, Med. Jour., 1886, p.405) have 
shown in a large number of experiments on dogs and mon- 
keys (20 experiments stimulating the uncut nerve; 12 ex- 
periments stimulating the divided nerve), that electrical 
stimulation of the recurrent laryngeal nerve quite uniformly 
caused adduction of the glottis, except when the animals 
were deeply narcotized. The same result occurred even 
when the larynx was removed from the animal. These 
experiments show that although the crico arytaenoidei pos- 
tici are larger than any other of the intrinsic laryngeal mus- 
cles, yet under ordinary circumstances, they are not power- 
ful enough to resist the combined forces of their opponents, 4 
IRA VAN G IE SON. 
the adductors. When animals are deeply narcotized, stim- 
ulation of the recurrent produces the opposite effect—ab- 
duction of the vocal cords. (Hooper, N. Y. Med. Jour., 
July 4, 1885 ; June 6, 1886, Semon and Horsley, l. c.) ; Don- 
aldson, (Amer. Jour. Med. Sci., July, 1886), operating on 
dogs, found that the abductors responded to a weaker cur- 
rent than the adductors ; an initial weak current in the re- 
current nerve becoming gradually stronger produced at 
first abduction, which gradually gave way to adduction of 
the cords. 
A peculiar feature of the posterior crico arytaenoidei, 
discovered by Semon and Horsley, is that these muscles 
lose their electrical excitability long before any of their 
antagonists, when the laryngeal muscles are individually 
stimulated. They become fatigued and die sooner than the 
other muscles. In other words, a greater degree of de- 
structive metamorphosis is coincident with their activity. 
A still farther distinction between the abductors and the 
adductors is the morphological distinction pointed out by 
Simonowsky, (Inter. Centralbl. f. Laryngol., Vol. ii., p. 346), 
and Gruetzner (Breslauer Aertz. Ztschrift., 1883, No. 18), 
that the abductors belong to the red muscles of Ranvier ; 
whereas the adductors, at least the thyreo-arytaenoideus, 
belong to the so-called white muscles. (This histological 
distinction however is not definitely settled, for the re- 
searches of these anthors were incomplete when published). 
Semon, (Berlin Klin. Wschrft., 1883, No. 46; Archiv. of 
Laryngol., Vol. ii., p. 197), from a study of laryngeal pa- 
ralyses of neural origin, made the statement that in cases 
of injury or organic disease of the centres or trunks of the 
motor laryngeal nerves, the abductor muscle or muscles 
succumb first. (Semon’s statement is also supported by 
Rosenbach, Breslauer Aerzt. Ztschrft., 1880, Nos. 2, 3; 
Berlin Klin. Wschrft., 1884, No. 17; Virch. Arch., lid. 99). 
The difficult thing to understand about Semon’s statement 
is why the abductors should be thus selected when the same 
motor nerve and nucleus supplies both adductors and ab- 
ductors. Why, for instance, should a chronic neuritis of 
the roots or trunk of the vagus containing the motor fibres TABES DOR SAL/S. 
5 
for all of the laryngeal muscles (except the crico-thyroids) 
cause an earlier or more extensive paralysis in the abduc- 
tors than in any of the other muscles ? 
Unless the motor fibres of the abductors are relatively 
much more numerous than the adductor fibres—and this is 
not likely to be the case for the abductor group of muscles 
is more voluminous—there is no reason why a chronic neu- 
ritis of the vagus roots should not involve the adductor 
nerve fibres just as much as the abductor fibres. Probably 
the truth of the matter is, that with such a lesion, the abduc- 
tors suffer no greater loss of power than the adductors, but 
as the direction of the fibres in the abductors—the posterior 
crico-aryt?enoidei—seems to put them at a greater mechan- 
ical disadvantage in moving the arytamoid cartilages than 
the lateral muscles; a uniform diminution of absolute power 
in both the adductors and abductors, may produce a far 
greater impairment of the abductors than of the adductors. 
Experiments show that the equilibrium of the glottis in- 
clines in favor of the adductors in the normal larynx (except 
in conditions like ether narcosis), and if the adductors are 
stronger in the normal larynx under ordinary circumstances, 
we should expect their strength still more prominently 
asserted in the disturbed eqilibrium of the glottis, when 
both sets of muscles are paretic, for the substraction of a 
given amount of absolute power from each set of muscles 
would diminish the action of the abductors in a greater 
ratio than the adductors, which are larger, stronger, and 
work at the glottis from a better mechanical standpoint. 
Thus it may be that the predilection of the abductors 
to become paretic, as observed by Semon, is only apparent, 
and, as Gowers (Dis. Nerv. Syst., 1888, p. 692) suggests, it 
would be better to speak of this condition as loss or impair- 
ment of abduction, rather than as paralysis of the abductors 
or posterior paralysis, in the sense that the abductors are 
exclusively paralyzed. 
Believing that a good many of these so-called posterior 
paralytic forms—the second form of the crises—-are caused 
by a chronic neuritis of the motor laryngeal fibres in the 
roots (or trunk) of the vagus, it seems that they occur in 6 
IRA VAN GIESON. 
this way. The neuritis causes a (nearly equal) reduction of 
absolute power in both the constrictors and dilators of the 
glottis, which renders their equilibrium so unstable that 
with the slightest reflex or direct motor impulses the adduc- 
tors, working on a superior mechanical vantage ground, gain 
the ascendency, and a crisis results. In other words, the 
exciting cause of many of the crises of this form, is a reflex 
or direct motor sent through the recurrent nerve to a paretic, 
unstable group of antagonistic muscles with the balance of 
power in favor of the adductors, operates like the stimuli of 
the recurrent nerve in the experiments of Semon and 
Horsley. This excites a spasm of the adductors which is 
intensified or prolonged and induced the more readily per- 
haps, from the impairment of the function of the abductors 
being greater than that of the adductors, although both sets 
of muscles are paretic to a nearly equal extent. When the 
adductors become fatigued by their tonus, or should a con- 
dition like ether narcosis occur from the attack, the crisis 
gradually ceases. 
Such an explanation of this second form of the crises 
accounts for the sudden way in which they occur as attacks, 
and is supported by the fact that deadening the reflexes 
from the fauces pharnyx and larynx by cocaine and bromides 
are of benefit in many cases. 
Changes in the nerve roots and in the peripheral nerves 
are so frequently present in tabes, and central lesions in the 
medulla are so comparatively infrequent, that probably 
chronic neuritis of the roots—analogous to the neuritis of 
the spinal nerve roots—or trunks of the laryngeal nerves is 
quite uniformly the lesion producing the laryngeal crises. 
The neuritis of the roots of the tenth and accessory portion 
of the eleventh nerves in this case explains very well how 
the laryngeal crises of both kinds may occur, if some points 
in the laryngeal innervation are referred to. 
The superior laryngeal nerve is the sensory nerve of the 
larynx, and is composed as a rule entirely of fibres from the 
accessory portion of the spinal accessory. Vrolik (Kirke’s 
Handbook of Physiology, 1889, p. 614), found in the chim- 
panzee that the internal division of the spinal accessory TABES DORSALIS. 
7 
passed directly to the larynx without fusing with the vagus. 
The supposed motor supply of the superior laryngeal nerve 
to the crico-arytaenoidei postici is denied by Schech (Lit. of 
Biol., ix., p. 258). Stimulation of the central end of the 
superior laryngeal produces decided closure of the glottis 
(Krause, Virch. Arch., Bd. 98). The recurrent laryngeal 
nerve, supplying all of the muscles except the crico-thy- 
roids, as a rule derives its motor fibres from the vagus; 
occasionally this nerve varies in its composition, and its 
motor fibres come partly from the vagus and partly from 
accessory vagus. The recurrent nerve also contains a few 
sensory fibres, the centripital path of which is not definitely 
known. 
The statements of Bischoff, Longet, Bernard and Mor- 
ganti (references given in Donaldson’s paper), to the effect 
that the accessory portion of the spinal accessory is prin- 
cipally a motor nerve are quite untenable at present. If 
the superior laryngeal was chiefly motor, stimulation of its 
central end ought not to produce such a pronounced reflex 
closure of the glottis ; this experiment indicates that the 
superior laryngeal is more a sensory than a motor nerve. 
A study of the central termination of the accessory portion 
of the spinal accessory seems to show that it is mainly a 
sensory nerve. Recurrent motor fibres like those of the 
vagus passing to the nucleus ambiguus may be seen in the 
adult medulla, passing in from the very uppermost roots of 
the accessory portion ; but as the sections pass down to the 
middle and lower levels of the roots of the accessory por- 
tion, these recurrent fibres become fewer and fewer and dis- 
appear, so that it is doubtful if recurrent motor fibres like 
those of the vagus, exist in the middle and lower roots of 
the accessory portion. I think from this that all of the 
root strands of the accessory portion are sensory fibres 
from the larynx and pharynx, except the uppermost strands 
nearest the vagus, which contain motor fibres for the crico- 
thyroids and inferior constrictor, and a vicarious motor sup- 
ply for the pharyngeal and recurrent branches of the vagus, 
which nerves seem to be subject to occasional variation in 
their composition, as they sometimes have a portion of their 8 
TRA VAN GIESON. 
usually almost exclusively vagal supply of motor filaments 
replaced by motor fibres from the accessory portion.4 
A chronic neuritis of the roots (or trunk) of the acces- 
sory portion of the spinal accessory, irritating the laryngeal 
sensory fibres, would be responded to by motor impulses 
passing down the vagus which would cause, as in electric 
stimulation of the motor laryngeal fibres, adduction of the 
cords. This lesion would account for the first form of the 
crises. If this neuritis should be sufficiently destructive 
anaesthesia of the larynx would result. Krause and Frankel 
each report a case of anaesthesia of the larynx in conjunc- 
tion with tabetic laryngeal crises. 
An early irritative stage of the chronic neuritis in the 
vagus roots (or trunk) might also cause crises of the first 
form, by stimulating the motor laryngeal fibres and produc- 
ing direct spasms of the adductors. A later destructive of this 
neuritis might induce paresis or paralysis in both the abduc- 
tors and adductors. But with this condition abductorial 
impairment is greater than adductorial, and this coupled 
with the experimental facts that the abductors are unable 
to resist the forces of their antagonists in the normal larynx 
and become fatigued sooner, suggests as an explanation of 
the second form of crisis, that at certain times with reflex 
or direct motor stimuli, (which might not be of sufficient 
intensity to provoke a spasm in the normal larynx), the 
adductors get the balance of power and their tonus may be 
enhanced by the greater degree of metabolism in the abduc- 
tors. When both the vagus and accessory vagus are dis- 
eased together, the conditions are favorable for the produc- 
tion of violent crises of the second form. 
Review of Some of the reported Cases of Laryngeal Crises 
in Tabes.— Krause5 collects eight cases which were exam- 
ined laryngoscopically. The vocal cords were quite uni- 
formly in the median or adduction position. Three of 
Cherchvesky’s cases had paralysis of the left cord, and in 
one case there was paralysis of the abductors on both sides. 
4 References to other less definitely settled points In laryngeal innervation 
are given by Lennox Browne, The Throat and its Diseases, 1887, p. 477. TABES DORSALIS. 
9 
Wegener’s8 two cases had paralysis of the left abductors. 
Frankel’s6 case had paralysis of one cord and paresis of the 
other. Fournier (Lecons sur le periode prae ataxique de 
tabes d’origine syphilitique, Paris, 1885), reports five cases 
of one-sided laryngeal paralysis in tabetics who had no 
crises. Kahler’s case had paralysis of the left cord, and 
crico-arytaenoideus posticus and dysphagia. Crises in this 
case could be elicited at times by causing the patient to 
swallow a glass of water. 
Krause7 reports two cases, in one of which anaesthesia 
of the larynx was present, but there was good laryngeal 
reflex irritability so that every touch of the larynx with the 
sound elicited a crisis. In the second case laryngeal irrita- 
bility was absent; the larynx could be sounded without 
awakening crises. In both cases crises could be produced 
by irritating the nasal fossae. Oppenheim10 presented two 
cases having gastric crises. In one of the cases, the crises 
was of a purely spasmodic character for several years, but 
subsequently the crises assumed the features of the second 
form associated with loss or impairment of abduction. The 
voice became rough and the crico-arytaenoidei postici and 
the thyro-arytaenoideus became paretic. Pulse anomalies 
were also present in this case. 
In the second case, the crises were very violent and one 
of them proved fatal. (Microscopical examination in this 
case showed neuritis of the vagus and accessory vagus roots) 
Besides the fatal crisis recorded in this paper, a third fatal 
crisis is instanced by Keller, (quoted by Cherchvesky). 
Krishaber15 had to do tracheotomy in an urgent case of 
tabetic laryngeal crises. 
In a third case of Oppenheim’s11 there were spasmodic 
pharyngeal attacks followed by movements of swallowing. 
A fourth case, by the same writer, had paralysis of the right 
cord which remained immobile when the right recurrent 
nerve was stimulated electrically, while the left cord re- 
sponded to stimulation of the left recurrent. 
Landgraf’s3 case of purely spasmodic crises of the first 
form is very interesting in connection with the fact, that 
two years afterward the patient developed paralysis of the IRA VAN GIE SON 
sterno-cleido-mastoid and trapezius on one side. (Reported 
by Martius, Berlin Klin. Wochenschrift, No. 8, 1887). This 
would indicate that the spasmodic reflex crises were caused 
by a neuritis of the accessory portion of the eleventh nerve, 
which subsequently extended to the spinal portion of the 
nerve. McBride’s13 case of tabetic crises also had paresis 
of the sterno-cleido-mastoid and dysphagia, frequent heart 
action, and finally Cheyne-Stokes respiration, indicating 
neuritis of both the vagus and spinal portion of the spinal 
accessory. 
In Weil’s14 case, the crises, which as a rule do not appear 
until the tabetic symptoms are well established, were the 
initial symptoms of the disease, and enhances the sug- 
gestion of Buzzard and Semon, of testing the knee-jerk in 
all cases of laryngeal paralyses. Weil regarded the case 
as one of posterior paralysis. (Jeleneffy, Berlin Klin.W-sch- 
rift, 1888, p. 728, reviewing Weil’s case, and finding that the 
crises were often originated by peripheral stimuli, questions 
whether there really was posterior paralysis). Weil instan- 
ces Krishaber’s,15 Lhoste’slfi and Morgan’s17 cases as of pos- 
terior paralysis similar to his own. 
Some writers have reported cases of laryngeal cases due 
to ataxia of the laryngeal muscles. The consideration of 
ataxia of the glottis muscles is exceedingly complicated. 
A central lesion would be indicated in laryngeal ataxia 
rather than lesions in the roots or trunks of the laryngeal 
nerves, which are believed by the writer to be the cause of 
the crisis in the majority of the cases. If such cases of 
laryngeal ataxia-producing crises exist, it must be very 
difficult to distinguish them from the other two forms 
alluded to in this paper. 
Summary of the Lesions in the Reported Cases.—Jean1 
found atrophy of the left vagus, accessory, and recurrent 
laryngeal nerves and left thyro-arytamoideus. Kahler 's: 
thickening of the ependyma involving the right vagus 
nucleus, and principally the nucleus of the right accessory 
vagus nerve. (The paralysis in this case could be explained 
by the damage done to the recurrent or motor fibres, pass- 
ing to the nucleus ambiguus, by the lesion in the sensory TABES DORSALIS. 
vagus nucleus.) Demange19: lesions similar to those in 
Kahler’s case. Landouzy and Dejerine: atrophy of the 
vagus roots and nucleus of the vagus accessory nerve. 
Oppenheim: neuritis of the vagus and accessory vagus 
roots and degeneration of the recurrent laryngeal nerve. 
The pharyngeal crises—dysphagia, with or without spas- 
modic deglutory movements, which occasionally are in 
company with the laryngeal crises—may be accounted for 
by a chronic neuritis of the roots (or trunks) of the ninth, 
tenth, or accessory portion of the eleventh nerves ; but it is 
difficult to explain these crises in detail, owing to the com- 
plicated and apparently variable distribution of these nerves 
to the pharyngeal plexus. The simplest account of the 
pharyngeal plexus is given by Schwalbe (“Lehrbuch,” 1878, 
p. 874). All three of the nerves of the eighth pair send 
both sensory and motor branches to the pharynx. The 
principal sensory conductor is the glosso-pharyngeal, which 
also sends motor fibres to the stylo-pharyngeus, and middle 
constrictor. The principal motor nerve is the vagus. The 
accessory fibres to the pharynx are sensory, except those 
to the inferior constrictor, and except when accessory fibres 
replace the motor vagus fibres in the pharyngeal branch 
of the vagus. A chronic neuritis in the roots or trunks of 
one or more of these nerves might produce reflex or direct 
pharyngeal movements, or a degree of paresis of some of the 
muscles, giving rise to dysphagia. 
The gastric crises might occur in two ways : Reflexly— 
for instance, by a neuritis involving the sensory pharyngeal 
filaments ; directly, by a neuritis of the upper three cervical 
nerve roots, or of the vagus accessory roots or of the trunk 
of the vagus, which is the path of the viscero-motor fibres 
upon which depend peristaltic contraction of the thoracic 
oesophagus, stomach, and small intestines (Gaskell, “Jour, 
of Phys.,” vol. vii.). 
The bronchial crises—spasms of the larger bronchi, with 
attacks of rough coughing—might be caused by a neuritis 
of the vagus which carries bronchial sensory fibres, and the 
viscero-motor fibres supplying the smooth muscles of the 
bronchi. 12 
IRA VAN GIESON. 
The cardiac crises — anginoid attacks, and the pulse 
anomalies occurring in tabes—might be caused by a vagus 
neuritis interfering with the cardio-inhibitory fibres. Cardiac 
disturbances might also occur from the cord lesion in the 
upper dorsal region, whence, according to Gaskell, the 
cardio-augmentor fibres issue in the anterior roots. 
The reason of the other tabetic visceral symptoms may 
be made clearer by referring to the researches of Gaskell 
{loc. cit.) on the distribution and origin of the sympathetic 
fibres. The fibres of the sympathetic arise in the spinal 
cord and lower medulla, and issue thence, as finely medul- 
lated fibres in the anterior and posterior roots, in three great 
channels, viz.: The cranio-cervical outflow, in the vagus, 
in the spinal accessory passing to the vagus through the 
ganglion trunci, and in the upper three cervical nerve roots; 
the thoracic outflow, situated between and including the 
second dorsal and second lumbar nerve roots ; the sacral 
outflow, from the second and third sacral nerves. The 
cranio-cervical outflow contains the cardio-inhibitory fibres 
and the viscero-motor fibres for the stomach and circular 
fibres of the small intestine. The thoracic outflow passes 
upward to the cervical sympathetic trunk and ganglia, 
medially to the praevertebral ganglia (semilunar and mesen- 
teric) and splanchics, and downward to the hypogastric 
plexus. The thoracic outflow contains the viscero-motor 
nerves for all parts of the body, glandular nerves, viscero- 
inhibitory nerves, cardio-augmentor nerves, and viscero- 
motor nerves for the circular fibres of the hind-gut, and 
some of the vaso-dilator fibres. The sacral outflow, com- 
posing the nervi-erigentes, consists of fibres passing directly 
to the hypogastric plexus, whence they pass upward to the 
inferior mesenteric ganglion and downward to the bladder, 
rectum, and generative organs. The sacral outflow contains 
vaso-dilator fibres for the penis (stimulation of the anterior 
second and third sacral roots produces erections in rab- 
bits: Gaskell, “Jour, of Phys.,” vol. viii.) and vaso-dilator 
fibres for the lower extremities. This outflow also contains 
the viscero motor fibres for the bladder, uterus, and longi- 
tudinal muscles of the rectum. TABES DORSALIS. 
These three regions’of the cord, whence issue the finely 
medullated fibres to the sympathetic system, correspond so 
closely with the situation of the cervical nucleus, the columns 
of Clark, and the sacral nucleus, that Gaskell thinks that 
the central origin of the sympathetic is partly in these 
nuclei. As the central tabetic lesions, or neuritis of the 
spinal nerve roots, may involve these portions of the cord, 
we may try to explain how some of the other visceral and 
trophic symptoms in tabes arise. 
The tabetic lesion in the second and third sacral seg- 
ments, interfering with the vaso-dilator fibres of the sexual 
organs, would account for some of the sexual disturbances 
and the clitoris crises. The paroxysms of rectal pain and 
tenesmus—rectal crises—if not caused by the lower dorsal 
portion of the cord lesion, involving the viscero-motor 
nerves of the circular rectal muscles, may be caused by the 
sacral portion of the cord lesion interfering with the motor 
nerves of the longitudinal muscle layer of the rectum. The 
vesical disturbances and crises, the urethral crises, and the 
weakness of the rectal and vesical sphincters may be caused 
by the lesion in the second and third sacral segments in- 
volving the viscero-motor fibres of these organs. 
As the vaso-dilator and vaso-motor fibres to the lower 
extremities pass out of the second and third anterior sacral 
roots and lower portion of the dorsal region respectively, 
lesions in these portions of the cord may account for the 
trophic disturbances in the lower limbs, viz.: Brittleness of 
the bones, atrophy of their heads, etc., arthropathies of the 
knee-joint, changes in the tarsal bones and joints, flattening 
the foot (tabetic foot of Charcot and Fere), temporary 
oedema without renal lesions, local sweating, perforating 
ulcer of the foot, unprovoked ulceration of the toes, bad 
growth of the nails, etc. 
Intestinal troubles are manifested by constipation, spas- 
modic attacks, and peculiar diarrhceal attacks, which Pierret 
supposed to be of vaso-motor origin. If not due to a vagus 
neuritis, the intestinal symptoms may be caused by the 
lesion in the dorsal cord. The constipation may occur from 
a destruction of some of the viscero-motor fibres to the gut. 14 
IRA VAN GIESON. 
The dorsal region of the cord probably contains the vaso- 
dilators of the guts. 
The lesion producing the nephritic crises is difficult to 
locate. The path of the viscero-motor fibres to the ureter 
is not known. According to Bradford (“Journal of 
Phys.,” vol. ix., p. 358) the renal vaso-motor fibres issue 
from the cord in the ninth, tenth, and eleventh anterior 
dorsal roots. The lesion in this portion of the cord might 
interfere with the renal circulation. 
LITERATURE OF CASES OF LARYNGEAL CRISES IN TABES. 
1 Fereol. - Sur quelques sympt. viscereaux laryngo-bronchiques de l’ataxie 
locomot. Gaz. hebd., October, 1876. 
2 ( herchvesky.—Contrib. a l’etude des crises laryngees tabetique. Kevue 
de Med., tome i., 1881, p. 541. 
3 Landgraf. Krankenvorstellung mit Tabes und Larynxkrisen. Berlin, 
klin. Wochenschrift, 1885. 
4 McKenzie.—Diseases of the Throat. 
5 Krause. --Berlin, klin. Wochenschrift, 1887, p. 652. 
6 Frankel.—Berlin, klin. Wochenschrift, 1886, p. 675. 
7 Krause.—Berlin, klin. Wochenschrift, 1887, p. 620. 
8 Wegener.—Inaug. Dissertat. Berlin, 1887. 
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12 Oppenheim.—Berlin, klin. Wochenschrift, 1886. 
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20 Martin. - De l’atax. locomot. prog. These de Paris, 1874. 
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25 Charcot.—Atax. loc. crise laryngee arthropathies. Gaz. des Hop., 
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