A CASE OF ACUTE 
BULBAR PARALYSIS, 
WITH REMARKS ON ITS PATHOLOGY 
AND DIAGNOSIS. 
BY 
ERNEST W. AUZAL, M. D. 
REPRINTED FROM THE 
Neto Yortt J&etttcal journal 
for March 1896. Reprinted from the New York Medical Journal 
for March If 1896. 
A CASE OF ACUTE BULBAR PARALYSIS, 
WITH REMARKS ON ITS PATHOLOGY AND DIAGNOSIS. 
By ERNEST W. AUZAL, M. D. 
The number of contributions to medical literature on 
the subject of acute bulbar paralysis is a limited one. For 
our knowledge of its pathological anatomy and symptoma- 
tology we are indebted chiefly to the descriptions given by 
Leyden, Hallopeau, Liclitheim, Erb, Schwalbe, Senator, 
Hughlings Jackson, Oppenheim, Gowers, and Etter, whose 
cases have, for tbe most part, afforded an opportunity of 
post-mortem examination. In the majority of instances the 
pathological changes had their origin in the blood-vessels 
which had become obliterated by thrombosis or, exception- 
ally, by embolism. Multiple foci of softening, of varying 
extent, were most frequently found. In rarer cases haemor- 
rhages (from vascular disease or traumatism), compression 
by tumor, or an acute or subacute polioencephalitis inferior, 
constituted the lesions that gave rise to the paralysis. The 
gravity of lesions of the medulla oblongata is easily under- 
stood when it is remembered that within a narrow space it 
not only gives passage to the fibres that connect the brain 
with the spinal cord, but that it also contains the centres 
Copyright, 1896, by D. Appleton and Company. 2 
ACUTE BULBAR PARALYSIS. 
of most of the cranial nerves, and especially those which 
control the cardiac and respiratory functions. 
The case I am about to describe is of considerable 
clinical interest, presenting, as it does, a well-defined and 
practically typical picture of acute unilateral bulbar pa- 
ralysis. It demonstrates, in addition, the efficacy of treat- 
ment with the iodides which I regard as no less valuable 
(in smaller doses) in angeio-sclerosis than in syphilitic en- 
darteritis and the sclerotic changes following it. 
Mr. J. S. D., thirty-nine years of age, unmarried, vocal 
teacher, was referred to me on the 17th of last October, and 
gave the following history: 
Both parents, as well as seventeen brothers and sisters, are 
still living and in good health. He had measles, whooping- 
cough, and varioloid in his childhood. In 1877 he had a 
sunstroke, in 1886 rheumatic gout, and in 1889 a mild attack 
of influenza. For the greater part of his life, up to three 
years ago, he has suffered from what he calls bilious head- 
aches. His occupation has never exposed him to mental or 
physical overwork, but his habits have, he admits, not infre- 
quently led to alimentary excesses, especially during his oper- 
atic career. He has always used stimulants very moderately, 
however, and has never been addicted to the use of tobacco. 
Denies ever having been infected with syphilis. 
Three weeks before coming under my observation he was 
seized during the night with a dull pain in the back of the 
head and neck, with dizziness and ringing in the right ear. 
Dimness of vision, together with an indisposition to mental 
and bodily exertion, had been coming on, he thinks, for three 
or four months. He found that the dizziness disappeared 
when he was in the recumbent posture, but that his whole 
body swayed sideways when he turned over on the left side. 
Three days later he noticed some embarrassment in swallow- 
ing and a numbness of the right foot. 
These troubles continued unchanged until the morning of 
the tenth day following, when he awoke with a numbness ACUTE BULBAR PARALYSIS. 
3 
and tingling in tlie right hidf of his face and in the right arm 
and leg. The lips and tongue felt stiff, and the difficulty in 
swallowing had become more pronounced. His discomfort 
was increased by difficulty in speech, shortness of breath, and 
by seeing objects double. He also noticed that his head was 
inclined somewhat to one side, and that the bach of his neck, 
the right arm and leg were weak. Walking had become so 
unsteady that he was unable to get about unless he was sup- 
ported. For a day or two his mind was somewhat confused, 
so that he did not remember clearly afterward what he had 
said or done during that time. Nausea or vomiting has at no 
time been present, and there has been no fever. Sleep has 
been poor since he was taken ill. 
Status Prcesens.—Patient is somewhat under medium 
height, fairly well nourished, of active, nervous temper- 
ament, and looks at least ten years older than he is. The 
radial and temporal arteries are rigid, the latter markedly 
serpentine. There exists some enlargement of the prsecordial 
area of dullness, and the second sound is accentuated, but 
otherwise no cardiac abnormity can be made out. The pulse 
is not altered in frequency or rhythm. On the part of the 
lungs and abdominal organs no morbid signs are to be detect- 
ed, and evidences of constitutional syphilis are wanting. 
The sphincters are intact. The urine is normal in quantity 
and contains neither albumin nor sugar. The existing ambly- 
opia does not appear to depend upon any changes of the optic 
papilla which an ophthalmoscopic examination shows to be 
in normal condition. The cephalalgia is occipital, extending 
down the neck, and not subject to exacerbation ; it has the 
character of a dull ache. Psychically, he presents nothing 
unusual beyond a great depression and an inclination to weep 
at the slightest provocation. 
The head is slightly inclined to the left. When the patient 
is standing or sitting it falls forward, and in order to straight- 
en it he has to resort to the use of his hands. The turning of 
the head to either side is not impeded, however, and passive 
movements are readily executed. The vertigo is increased by 
turning it to the left. 4 
ACUTE BULBAR PARALYSIS. 
The movements of the right external rectus are weak, and 
efforts to turn the eye outward give rise to nystagmic twitch- 
ing. Diplopia is marked. The pupils are equal and moder- 
ately contracted; they react to light and accommodation. 
The frontal muscles contract symmetrically, hut, owing to 
weakness of the orbicularis palpebrarum, the right eye can 
not be closed as firmly as ihe left; the right naso-labial fold is 
somewhat effaced ; the corner of the mouth, slightly opened, 
hangs down a little on the same side and permits a constant 
dribbling of saliva, especially when he is lying down. The soft 
palate appears lower on the right and slightly drawn toward 
the opposite side, but the uvula is not deflected. 
Owing to paralysis of the right half of the tongue, degluti- 
tion and speech are interfered with. Food can be moved 
about in the month only with difficulty, and articulation is in- 
distinct, particularly as regards the pronunciation of the 
labials and linguals. It is only with the aid of a draught of 
water or by pushing it backward with the finger that he is 
able to transfer his food to the pharynx. When at rest within 
the buccal cavity the tongue shows nothing abnormal, but 
deviates to the right when protruded. The voice is somewhat 
raucous and dyspnoea is still complained of. The muscles 
supplied by the motor portion of the fifth nerve are intact. 
There exists a feebleness of the extremities of the right 
side. Muscular exertion, even the most moderate, is followed 
by great fatigue which can not he wholly attributed to the 
dyspnoea from which he is suffering. No tremor, either of 
the tongue or extremities, is present. 
The sensory disturbances consist in numbness and tingling 
of the right half of the face and corresponding mucous mem- 
branes, as well as of the right arm and leg. Objectively, no 
alteration of sensation is discoverable beyond a trivial hyp- 
iesthesia on the same side. Except in the right half of the 
tongue, the tactile sense is not affected, and there is no dis- 
sociation of sensibility. 
The sense of taste is impaired in the right half of the 
tongue, the patient being unable to distinguish with certainty 
sweet, bitter, and acid substances. The soft palate, tonsil, ACUTE BULBAR PARALYSIS. 
5 
and upper pharynx are somewhat anaesthetic on the right 
side. Hearing is diminished in the right ear, hut the sense of 
smell is not affected. 
The gait is titubating, with a tendency to stagger toward 
the right. It is so marked that walking is impossible without 
assistance. When he is asked to stand with his eyes closed, 
the ataxia is so great as to cause him to fall (to the right). In 
order to avoid staggering he enlarges his basis of sustentation 
by widely separating his feet and keeps a fixed point in view 
in front of him. Being conscious of the extent and direction 
of the movements he executes in walking, he does not watch 
his feet as he would do were the ataxia of the locomotor 
type. The inco-ordination does not extend to the upper ex- 
tremities. 
The cutaneous and tendon reflexes are not altered; there 
is no exaggeration of the masseteric reflex. 
Under the use of iodide of potassium, appropriate diet, 
and galvanization, at a later period, of the nucha and through 
the mastoid processes, as advocated by Strlimpell and Oppen- 
heim, the symptoms have gradually subsided, so that now, 
five months since the beginning of treatment, only slight 
numbness and tingling of the tips of the fingers of the right 
hand remain. The vision has been completely restored and 
his lacrymose frame of mind has given place to one of com- 
parative impassibility. 
The varying distribution of the vascular supply of the 
medulla oblongata has made it impossible so far to separate 
into syndromal groups the disturbances that arise from 
arterial obstruction. But the frequent anomalies of arterial 
distribution do not form the only obstacle to such a sepa- 
ration ; it is largely upon the multiplicity and situation of 
the points of obstruction and the shape, which is often 
irregular, of the necrobiotic (or haemorrhagic) foci that the 
symptomatology depends. That mere narrowing of the 
lumen of a vessel, altered by atheromatous or endarterilic 
processes, may, by retarding the blood current and favoring 6 
ACUTE BULBAR PARALYSIS. 
coagnlative adhesions, be the cause of morbid symptoms is 
readily apparent. The possibility of compression by rigid, 
dilated, and frequently tortuous sclerotic vessels is another 
factor to be taken into account. 
According to Charpy, the floor of the fourth ventricle 
derives its blood supply from two different sources : the 
upper half, which contains the nuclei of the facial, abducens, 
and trigeminus, receives its nutrient vessels from the ba- 
silar artery ; the lower half is supplied by the ventricular 
branches of the anterior and posterior spinal arteries which 
are given off by the vertebral. An occlusion of the basilar 
would therefore, when not compensated by collateral circu- 
lation, give rise to bilateral lesions, whereas an obliteration 
of one of the vertebral arteries would be productive of uni- 
lateral lesions. 
Duret, whose elaborate researches on this subject, pub- 
lished in 1873, have in the main been confirmed by those of 
Adamkiewicz, divides the vessels of the medulla oblongata 
—all of them branches of the vertebral artery—into (1) the 
radicular arteries, which divide into two branches—one ac- 
companying the nerve root to the periphery, the other fol- 
lowing it to its nucleus ; (2) the median (or nuclear) arteries, 
of which some, coming from the anterior spinal, supply 
the nuclei of the spinal accessory, hypoglossal, and infe- 
rior facial, while others supply the pneumogastric, glosso- 
pharyngeal, and auditory nuclei, aud others again, given off 
by the basilar, pass across the fibres of the pons to reach 
the nuclei of the superior facial, abducens, patheticus, and 
motor oculi; (3) arteries of the remaining portions of the 
medulla oblongata, which take their origin from the ver- 
tebral, anterior spinal, and inferior cerebellar arteries, and 
are distributed to the olivary bodies, pyramids, lateral 
tracts, and corpora restiformia. The last two receive their 
supply from the inferior cerebellar branch. ACUTE BULBAR PARALYSIS. 
7 
How are we to interpret the complexus of symptoms I 
have described ? The mode of onset and character of the 
disease, the evidences of arterio sclerosis presented by the 
patient, and the steady improvement under treatment jus- 
Diagram showing arrangement i f nuclei in floor of fourth ventricle (right side'). 
IIT, motor oculi; IY, patheticus ; Vm, motor nucleus of trigeminus (locus 
caeruleus); Vs, sensory (descending) root of trigeminus; VI, ahducens; 
VII, facial; VIII, auditory ; IX, glosso-pharyngeus ; X, vagus ; XI, spinal 
accessory ; XII, hypoglossus. 
tify the conclusion that it was caused by thrombotic ob- 
struction of the right vertebral artery. It would account 
for the involvement, more or less pronounced, of the hypo- 
glossal, vago-accessory, glosso-pharyngeal, auditory, abdu- 8 
ACUTE BULBAR PARALYSIS. 
cens, facial, and sensory trigeminus, as well as for the hemi- 
paresis and hemiparaesthesia of the right side. The accom- 
panying diagram will serve to recall the arrangement of the 
nuclei in the floor of the fourth ventricle. It is safe to 
conclude, from the absence of any appreciable source of 
embolism and from the existence of prodromal symptoms 
for some length of time, that the obstruction was not due 
to an embolus, which, besides, rarely passes into the verte- 
bral artery, and in that event is more apt to plug the left 
branch. 
It is obviously impossible to locate with accuracy the 
seat of the lesion that led to the right liemiparesis. Wheth- 
er, in unilateral affections of the medulla oblongata, the 
hemiplegia is direct or alternate depends not alone upon 
the situation of the diseased focus relative to the motor 
decussation—i. e., upon its situation above or below this— 
but also upon the seat of the obstruction (in cases of throm- 
bosis or embolism) above or below the point at which the 
anterior spinal artery is given off. The direct hemiparesis 
may have been due in this instance to an encroachment 
upon the motor fibres below their decussation, or, what ap- 
pears to me more probable, to a lesion of the direct pyram- 
idal tract above that poiut. The latter view seems the 
more acceptable in the light of the recent discovery of 
Jacobsohn (Neurol. Ctrlbl., 1895, No. 8, p. 348), who has 
found that the fibres of the direct pyramidal tract are not 
intermingled with those of the crossed pyramidal tract, but 
that in their entire course through the medulla oblongata 
they occupy the lateral angle of the pyramids. There is 
no satisfactory evidence showing that they cross at suc- 
cessive levels of the spinal cord and enter the anterior 
cornua of the opposite side; such a conception has always 
seemed to me, on physiological grounds at least, open to 
doubt. Competent observers have of late called it into ACUTE BULBAR PARALYSIS. 
9 
question, and advanced the opinion that the fibres termi- 
nated in the gray matter of the same side. If, as has been 
believed hitherto, they do not reach below the middle or 
lower dorsal region, my conjecture would leave the paresis 
of the lower extremity still unexplained. Quite recently, 
however, at a meeting of the Society de biologie, Dejerine 
and Thomas (Bulletin medical, 1896, No. 13; Medecine 
moderne, 1896, No. 13) have been able to demonstrate, by 
a series of sections treated according to Marchi’s method, 
that the column of Tiirck can be traced as far as the root 
of the fourth sacral nerve. From the lower dorsal region 
downward it appeared in the sections no longer in the shape 
of a comma, but is a small mass in front of the anterior 
commissure. 
How great the difficulty in accounting for unilateral 
paralysis or ana3sthesia in pontine or bulbar affections can 
be is shown by the case of Langdon [Brain, 1895, lxxii), in 
which compression by a tumor (fibro-cystoma of pons and 
cerebellum) above both the motor and sensory decussations 
produced motor and sensory disturbances on the same side. 
The author attempts to account for them by assuming that 
they were “ due to a contre-coup effect—i. e., to pressure 
by the tumor of the right periphery of the medulla against 
the comparatively acute margin of the foramen magnum at a 
point above (before) the motor decussation and also above 
(after) the sensory (fillet) decussation.” Another case in 
point is that reported by Senator [Arch. f. Psych, u. Ner- 
venkrh., 1882, xi, p. 713), in which a focus of softening in 
the left half of the medulla oblongata, one centimetre in 
its longest diameter, caused, among other symptoms, crossed 
hemiana3sthesia affecting the left face and right extremities. 
Could the syndrome observed in the patient have 
originated in an extrabulbar lesion, such as an aneurysm 
of the vertebral artery or a neoplasm ? A growth of this 10 
ACUTE BULBAR PARALYSIS. 
kind, when it compresses the cranial nerves and the pyram- 
idal tract of the same side below its decussation, may 
produce peripheral paralysis of the cranial nerves with 
hemiplegia on the same side, but, in view of the clinical 
history, especially the acute development of the headache 
and the absence of vomiting, it is unlikely that this was 
the case. Moreover, the prompt results of the treatment 
speak against the existence of an aneurysm or any other 
form of tumor, except a gumma, which would, however, 
have required far more energetic medication than my pa- 
tient has been subjected to. 
A striking feature of the case was the extreme inco- 
ordination. As a result of his experiments on the frog, 
Foster, in his Text-book of Physiology, long ago expressed 
the opinion that in the mammal as well as in the frog the 
medulla oblongata was largely concerned in the co-ordina- 
tion of movements. Anatomico-clinical facts have since 
made it evident that it contains a region whose lesion 
produces disturbance of equilibration. It is probable that 
this region is to be found in the bulbar endings of the pos- 
terior columns of the spinal cord. Oppenheiin (Lehrbuch 
der Nervenkrankheiten, 1894, p. 606) is inclined to place it 
in the interolivary tract, and perhaps in the corpus resti- 
forme. Ataxia of the “cerebellar type” has been ob- 
served in connection with a lesion of the corpus olivare. 
The case of Senator’s, previously cited, in which a focus of 
softening was found in the left half of the medulla ob- 
longata, showed a marked tendency to fall to the left. 
Dinkier (Deutsche Zeitschr. f. Nervenkrh., vii, 1895, p. 465) 
has reported a case of acute haemorrhagic polioencephalitis 
inferior, the result of cranial traumatism, in which, in ad- 
dition to a train of symptoms indicative of bulbar involve- 
ment, there were a staggering gait and an occasional tend- 
ency to fall. The patient succumbed two years and a half ACUTE BULBAR PARALYSIS. 
11 
after lie had received the injury, and the autopsy revealed 
numerous small extravasations in the floor of the fourth 
ventricle, particularly noticeable in the nuclei of the fifth, 
eighth, and tenth nerves, and a cellular infiltration of the 
walls of the blood-vessels. Haemorrhages existed also in 
the posterior cornua of the cervical spinal cord, but with 
the exception of a diffuse cerebro-meningeal hyperaemia no 
other lesions were found in the nerve centers. It is inter- 
esting to note in this connection that several authors, like 
Luciani, Dupuy, Eisenlolir, Bristowe, and Bruns, contrary 
to the view generally held, do not regard inco-ordination 
as pathognomonic of disease of the cerebellum, whether 
this involves the vermis or not. Their experiences are in 
accord with those of Friedeberg (Berliner Min. Wochenschr., 
1895, No. 38), who found that, out of nine cases of cere- 
bellar disease the diagnosis of which was verified by the 
autopsy, only two showed an ataxic gait. 
While a paresis of the right sterno cleido mastoid and 
trapezius muscles—the latter in so far as its clavicular por- 
tion, innervated by the spinal accessory, is concerned— 
would explain the oblique position of the head, it is not 
sufficient to account for the weakness of the posterior 
cervical muscles which, next to the difficult deglutition, 
dysarthria, and inco-ordination, seemed to the patient the 
most formidable symptom. There was no evidence that 
the drooping of the head was due to an involvement of 
both trapezii. 
Together with the proneness to general muscular ex- 
haustion, it recalls the form of bulbar paralysis without 
anatomical lesions, which has been studied by a number of 
observers, chief among them Wilks, Erb, Oppenheim, 
Shaw, Goldflam, Hoppe, and, more recently, by Pineles, 
Jolly, Murri, and Striimpell, of whom the last named has 
published an exhaustive paper treating of this topic a short 12 
ACUTE BULBAR PARALYSIS. 
time since (Deutsche Zeitschr. f. Nervenhkr., 1896, viii, p. 
16). This progressive and habitually fatal disease is char- 
acterized by an abnormal tendency to muscular fatigue, and 
has for this reason been termed asthenic bulbar paralysis 
by Striimpell and myasthenia gravis pseudo-paralytica by 
Jolly. The paresis affects not only the muscles of mas- 
tication and deglutition, thereby producing dysphagia 
and dysarthria, but also those of the trunk, extremities, 
and notably of the back of the neck. Ptosis, diplopia, 
and disturbed innervation of the upper and lower facial 
nerves have been the rule in the cases on record, while 
sensory and psychical disorders have been absent or very 
slight. 
The absence of fibrillary tremor and atrophy, the presence 
of sensory disorders, and the fact that the symptoms attain 
their maximum within a very short period of time after their 
inception, sufficiently distinguish, I think, acute (bilateral) 
bulbar paralysis from the labio-glosso laryngeal paralysis 
of Duchenne. Its differentiation, however, from the labio- 
glosso- lar} ngeal paralysis of cerebral origin, or pseudo- 
bulbar paralysis, may be attended with difficulty. Before 
the bulbar symptoms make their appearance in the latter 
affection, repeated apoplectic attacks have generally oc- 
curred and, as a rule, the lower extremities have been found 
to be more affected than the upper, in which there is often 
a mere motor weakness. In two cases I had an opportunity 
of observing several months ago in Professor Raymond’s 
clinic at the Salpetriere a rapid amelioration of the hemi- 
plegic symptoms took place, while the bulbar phenomena 
remained unimproved. This is, indeed, the usual course of 
the malady, although cases have been reported in which 
the apoplectic seizure and hemiplegia were wanting, the 
bulbar symptoms appearing d'emblee. 
Pseudo-bulbar paralysis depends, in the large majority ACUTE BULBAR PARALYSIS. 
13 
of cases, upon symmetrical lesions of both cerebral hemi- 
spheres, the foci of softening being seldom cortical, hut 
mostly in or about the basal ganglia, notably in the external 
portion of the lenticular nucleus, the putamen (G-rasset et 
Rauzier, Maladies du systeme nerveux, 1894, ii, p. 26). 
They have also been found in the centrum ovale, cerebel- 
lum, and pons. Unlike acute bulbar paralysis, in which 
the psychical manifestations are limited to a tendency to 
weeping or, less often, to laughing (Oppenheim), it is al- 
ways associated with impairment of the intelligence, with 
varying degrees of dementia, confusion, excitability, or loss 
of memory. The general sensation as well as the special 
senses are almost always intact, although Oppenheim and 
Siemerling have noted optic changes. Cephalalgia, ver- 
tigo, disorders of the ocular muscles, and cardio-pulmonary 
troubles are absent, and laryngeal symptoms seem to he 
exceptional. 
When ushered in by an apoplectoid ictus, the bulbar 
form of disseminated sclerosis may assume the character 
of an acute bulbar paralysis, hut a consideration of the pa- 
tient’s age, the mode of evolution, and the presence of in- 
tention tremor will he sufficient to make the differential 
diagnosis. Ataxia occurs in this disease only when it is 
complicated with tabes. 
In the course of syringomyelia localized in the medulla 
oblongata, of which the chief symptoms are troubles of 
speech and deglutition, apoplectoid attacks are likewise 
not infrequent, and the disease may for this reason bear a 
close resemblance to acute bulbar paralysis. The further 
progress of the syringomyelia, its characteristic sensory 
disorders, and the muscular atrophies will remove the 
doubt. 
As regards the diagnosis from tabes dorsalis, a con- 
fusion is scarcely possible even when, as is sometimes the 14 
ACUTE BULBAR PARALYSIS. 
case, the vago-accessorius and sensory trigeminus are im- 
plicated and vertigo exists. The same may be said of 
those varieties of amyotrophic lateral sclerosis and acute 
ascending paralysis (Landry’s paralysis) which begin with 
bulbar symptoms. 
It is well to bear in mind, finally, that there is hardly 
an affection of the nervous system, acute bulbar paralysis 
not excepted, which hysteria may not simulate. 
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