Landon Carter Gray.

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Cuba, and the Dutch possessions in the China Sea. In these places
it is endemic, occasionally epidemic.

Clinical History. The symptoms of multiple neuritis consist
of motor and sensory symptoms in the upper and lower extremities,
the special nerves being rarely affected, and the trophic symptoms
being marked. The first symptoms to appear are the sensory ones.
The disease usually develops with pain of a burning kind affecting
the feet and hands, and with this are associated numbness, tingling,
or formication. This pain is usually moderate in d^ree, but occar
sionally becomes extremely severe. There is also at this time a sin-
gular tenderness of the nerves and muscles, and there may be some
hypersesthesia, and even, though rarely, ansesthesia. It is seldom,
however, that the tactile sense is entirely impaired, and when it is,
it is in areas. As the disease progresses there supervenes a paresis of
the affected limbs, and the seusory impairment may become more
marked, although seldom to any complete extent, there being usually
only delayed transmission of paii^ and temperature, some (fulness of
the muscular sense, and, as I have already said, impairment of the
tactile sense. The motor paresis, which may have been simply felt
as a sense of weariness or fatigue, passes on to actual paralysis, so
that the patient is usually paralyzed in from ten days to three weeks.
Paralysis may develop, however, in a few days, and it is probable
that some cases of acute ascending paralysis terminating fatally are
cases of multiple neuritis. The paralysis is very capricious in its
anatomical distribution, and may affect certain filaments in one nerve
trunk and leave the others unimpaired, and thus affect a number of
nerve trunks. The paralysis is a flaccid one, the tendon reflexes are
abolished, and atrophy supervenes in the course of a few weeks.
Electrical alterations are extremely variable. In some cases there is
simply diminished response to galvanism and faradism ; in others,
complete loss of response to faradism and I'esponse to a very strong
galvanic current ; in others the response is greater with the negative
pole ; in others, still greater with the positive pole; and in some there
is an actual reaction of degeneration. All sorts of abnormal mus-
cular deformities may result from the different forms of paralysis,
but a dropped foot and a dropped wrist are the most frequent, although
the claw-shaped hand and the different forms of talipes are frequently
observed. As has been said, vasomotor and trophic symptoms are
not so frequent as the sensory and paralytic ones Temporary oedema
in the feet and hands, coldness and cyanosis, profuse and offensive

Eerspiration, glossy skin, temporary inflammations of joints, and
ulbous fingers, are occasionally observed.
The onset is usually without fever or with slight fk^ver, but occa-
sionally there may be a chill and a teniperature of 103° to 104° F.,
and this may persist for several days. In other cases the temperature

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may not rise more than one-half or two d^rees. The pulse is asually
but slightly above the normal^ and it is only in the dangerous cases
that it rises above 120.

The disease is somewhat more common in males than in females.

Children are rarely affected, if at all. Most cases occur between
twenty and forty.

Prognosis. The prognosis in multiply neuritis is good, although I
have seen a number of cases in which permanent muscular deformity
had been left. Alcoholic patients in whom the general health has
been shattered usually become chronic or die, although it is surprising
to see the improvement that will take place in these cases when drink-
ing has been stopped and the general health has been built up. I
have in several instances known such a patient to be so completely
paralyzed as to be helpless in bed, and yet attending to his business
in the course of twelve weeks.

Diagnosis. The diseases from which multiple neuritis should be
differentiated are —
Simple neuritis ;
Numb fingers;

Myelitis of the anterior comua ;
Locomotor ataxia ;
Acute ascendfing paralysis of Landry.

Simple neui^is is confined to a nerve trunk, and the pain is not
burning, but sharp and stabbing. This limitation of the paralysis
and the character of the pain alone will serve to make the

Numb fingers is an affection that was first described by Putnam,
of Boston, and is observed in women between forty and sixty, con-
sisting of a tingling sensation in the finger-tips and fingers, or even
the hand, and rendering the movements of the hand awkward,
besides causing a feeling as if it were asleep. In some of these cases
there may be a slight d^ree of ansesthesia and analgesia, but usually
there are no objective changes.

lu myditia of the anterior comua^ the so-called essential infantile
paralysis, the affection is purely a motor one, there being no sensory
implication whatever, and the muscles affected are almost invariably
limited to a group in one limb, generally in the leg or around the
shoulder or in the upper part of the arm. The entire lack of sen-
sory symptoms and absence of any tendency to implicate other mem-
bers will usually, therefore, make the differential diagnosis.

Locomotor ataxia is a chronic disease, is charax3terized by sudden,
atrocious, stabbing or lightning-like pains, which come in very tem-
porary paroxysms and are seldom continuous, and there is ataxia,
either preceding the pains or succeeding them ; whilst the muscular
strength is unimpaired, and glossiness of skin, tapering fingers, and
muscular tenderness are absent. Atrophy of the optic nerve is
often present.

In acute ascending paralysis the sensory symptoms are usually
entirely lacking, and the paralysis is the salient symptom, beginning
in the lower extremities, ascending in a few days, or even hours,

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to the upper extremities, and often causing bulbar symptoms. Death
generally ensues in a week or two, sometimes in a day or two.

Treatment. The treatment of multiple neuritis should be at first
by absolute rest in bed in the acute cases, and in the chronic cases there
should be such rest for at least a period of one to four weeks. The pain
can best be relieved by means of warm applications and salicylate of
soda and quinine. I shall never forget the lesson that I was first taught
as to the value of hot applications by seeing the comfort and ease that
was given to a youth afflicted with this disease by immersion of his
feet in a tub of hot water, which had been done at his own sugges-
tion. Swathing the feet in cotton, over which in its turn should 1)€
placed a strip of gutta-percha or oil-silk, will give great comfort At
certain periods of the day, however, especially toward night, when
the pain is apt to be worse, the patient may often obtain great relief
by putting the feet and hands in hot water for about half an hour,
and then loosely tying around them a piece of muslin soaked in a
mildly alkaline solution (10 grs. bicarb, soda to 1 oz. water), with
perhaps the addition of some chloroform. Gently rubbing the limbs
with oil is often useful also. Salicylate of soda in doses of 2 to 3 or
5 grains, three or four times a day, with 2 or 3 grains of quinine at
the same time, is generally the best treatment. I have repeatedly
observed another curious fact in regard to treatment to which I have
never seen attention called. In several of my patients in whom the
pain could not be controlled, and in whom the disease was progress-
ing, removal from the locality in which they had been attacked to
another would often effect a marvellous change. As my first cases
were observed in a malarious, low-lying district, I supposed that
there might be some malarial element about this, but I have since
observed it in several other cases in which the disease had com-
menced in a non-malarious neighborhood, so that I now look upon
this as a very important matter in the treatment, at least of the cases
which we see in and around New York. If there is an actual
malarial history, quinine or Warburg's tincture should be used in
sufficient doses. In the alcoholic cases some skill is required in the
withdrawal of the alcohol, and I always reduce it very carefully,
making use of quinine as a stimulant in its place, and I proportion
the doses of quinine to the needs of such a patient, so that in some
cases I give as much as 5 grains of quinine every two or three hours
whilst in others I give only 2 grains three times a day. If quinine
produces any cinchonism in the doses that are necessary to adequate
stimulation in place of the alcohol, I conjoin w^ith it mild doses of
the bromide of potash, 10 grains three or four times a day. When
the alcohol is entirely, withdrawn, I place the patient upon a malt
liquor, either a heavy English or German beer ; and after using this
for some time, I taper off with an alcoholic malt extract, i. €., a malt
extract in which the diastase is combined with alcohol. When the
pain has passed off, galvanism of the affected muscles and faradism
will be found to be extremely useful. Massage will often be of
use at this stage, but it should be very gently done without any
griping whatever of the muscles, bearing in mind that its object is

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(»iily to facilitate the passage of blood through the muscular tissue
without mechanical irritation of it. Strychnine, y^ to A- grain, three
times a day, will also be useful in this chronic stage, and also arsenic,
best in the form of Fowler's solution, two or three drops three times
a day. As improvement goes on and all tenderness dies away, and
the muscles begin to return to their normal bulk, Swedish movements
may be employed in addition. In the cases that have had a syph-
ilitic history, iodide of potash in large doses, with inunctions of
mercury should be used.


Bernhardt, Zeltscbr. f. klin. Med.. 1886. p. 863, with bibliography of alooholic paralysis.

Briwac, Comptes-rendus de I'Acad. des Sci., t. cil. p. 439.

Brisaaud, Des Paralysies Toxiqaes, with general bibliography. Paris, 1886.

British Medical Journal, 1886, ii. p. 977 ; 1887, p 1.

Broeck, Centralbl. f. Nervenheilk., 1885, p. 31.

Ocupari, Zeitschr. f. kiln. Med., y. 537.

Charcot, 6az. des Hdp., August 28, 1884.

Dana, C. L., Brain, January, 1887, with bibliography of arsenical paralysis.

D/jmne, Arch, de Physiol , 1878; 1883, p. 72 ; 1884. p. 230.

DvboU, Corre8p.-bl. f. Schweizer Aerzte, 1883, No. 18.

Eloy, Union M6dicale, September, 1886.

Erb, Neurol. Centralbl.. 1883. p. 481.

Etdan, Berl. kUn. Woch., 1886. p. 95.

Francotie, Revue de M6declne, 1836, No. 5.

Freund, Wiener med. Woch., 1886, p, 167.

GombauU, Progrfes Medicale, 1886. No. 23 ; Arch, de Neurol., 1., 1880.

Oowert, Diseases of the Nervous System, vol. i. p. 91.

OuUmann, Deut. med. Woch., 1884, No. 19.

Hitter, Berliner klin. Wochenschr.. 1881, p. 605.

irirt, Neurol. Centralbl., 1884, p. 481.

Homen, Centralbl. f. Nervenheilk., 1885, p. 813.

Hosatin, Munch, med. Woch., 1836. p. 41.

Joffroy, A., Arch, de Physiol, norm, et path., 1879, pp. 172-198.

Kander9, Wien. med. Woch., 1885, No. 52.

East, Arch. f. Psych., xii. p. 266.

Kruche, Deut. med. Zeit., 1884, p. 229.

Lancet. 1886, 11. p. 380 ; 1887, i. p. 28.

Leyden, Ceber Poliomyelitis und Neuritis.

Lower\feld, Arch. f. Psych., xv.. 1881 ; also Aerzte Intell.-bl., 1885, No. 6 ; also Neurol. Centr.,
1885, p. 149.

Mills, a K., " Multiple Neuritis and Some of Its Complications," International Magazine,
February, 1892.

Oppenheim, Deut. Arch. f. kiln. Med., xxxvi. p. 563.

Zeitschr. f. kiln. Med., 1&S6, p. 860.

PUre*, Archives de Neurologic, 1882, v., ri.

PUreset VaiUard, Revue de Medeciue, 1885, p. 987; 1836, p. 574; Arch, de Neurol., 1886 and

Remak, Centralbl. fiir Augenhellkunde, June, 1886 ; Verhandlung des Congresses far innere
Medicin, 1884 ; Neurol. Centralbl., 1885, p. 813.

Roger, L'Encephale, 1885, No. 2.

Rosa, Medical Chronicle, January, 1887. \,

Roth, Corresp.-bl. f. Schweizer Aerzte, July 1, 1883.

Roaenbach, Centralbl. f. Nervenheilk., 1885, p. 375.

Schultz, Neurol. Centralbl., 1885, p. 433.

Strut>€, Berliner Dissert.. Ueber Multiple Neuritis, 1881.

Strumpdl, Neurol. Centralbl.. 1884, p. 241.

StrumpeU und MUbii^, Munch, med. Woch., 1836, No. 34.

Teaaier, Lyon Medical, 1879, xxxli. p. 417.

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Synonyms : Bell's palsy. Prosopalgia.

The symptoms of facial paralysis are an iDabilify to shut the eye,
lagophthalmus, a loss of power of the facial muscles in the affected
side, so that the naso-labial fold is lost, a puffing out of the cheeks in
whistling, aud sometimes a deviation of the uvula and sofl palate.
Very ofteu, too, there is an alteration of taste on one side of the
anterior portion of the tongue, which, as we have already seen
(page 142), is supplied by the lingual nerve, deriving its gustatory
fibres from the chorda tympani, whilst the sense of taste in the pos-
terior portion of the tongue supplied by the glosso-pharyngeal is
unaltered. Reaction of degeneration or lesser dectrical changes are
also usually found in the affected muscles.

The causes of facial paralysis are exposure, a so-called rheumatic
diathesis, disease of the middle ear, traumata, certain febrile diseases,
lesion of the nucleus of the facial in the medulla oblongata, in the
fibres of the facial in the pons, or in the centre of the facial in the
motor area of the cortex, and spinal lesions. The most frequent of
these causes is exposure, as to a high wind, to the draught from a
window, to great excesses of temperature, or to bad weather. It has
been supposed that the rheumatic diathesis — ^as evidenced by the
predisposition to rheumatism in different parts of the body — is also
a cause, but although this does occur, it is not so frequently as
is generally imagined. A frequent cause is disease of the middle
ear, such as caries of the petrous portion of the temporal bone, or
those chronic middle-ear troubles which are so frequently left as
sequelse of scarlatina or diphtheria. Trauma can also be a cause,
either from a blow upon the ear, a fracture at the base, or the
pressure exerted upon the infant's head in difficult or instrumental
delivery. Certain febrile diseases may predispose to facial palsy,
such as diphtheria, variola, typhus, scarlet fever. The lesions of the
&cial nucleus of the pons and the motor area producing facial
paralysis need only be mentioned in this place as a reminder. Such
spinal lesions as locomotor ataxia and Landry's paralysis are occa-
sionally accompanied by a facial paralysis.

The prognosis will vary greatly, accordingly as the disease is due
to a peripheral lesion or to a central one ; in other words, whether it
is a neuritis or a neuritis due to a central lesiou. The neuritis is
usually of good prognosis. The degree of reaction of degeneration will
generally be a guide in the prognosis of these peripheral cases. If
there is but little alteration in the reaction of the galvanic and farad ic
currents, the prognosis is excellent, and the affection will pass away in
a few weeks. If there is a partial reaction of degeneration, i. 6., if
the faradic and galvanic response of the nerve has been greatly
impaired, but not entirely lost, whilst the muscles display qualitative
and quantitative alteration in the galvanic reactions as well as
increased response to mechanical excitation, the prognosis is fair, and
a cure will be obtained in the course of two or three months. If
there is a pronounced and complete reaction of deo:eneration, the

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prognosis is unfavorable, although even in some of these cases a
relative cure may be affected, leaving slight twitching and paresis in
the muscles. In the cases of lesion of the nucleus of the facial, as
in some cases of labio-glosso-laryngeal paralysis, the prognosis is
unfavorable. In lesions of the pons the prognosis is generally un-
favorable, except where the lesion is in the pons at the apparent or

Fio. 107.


Diagram of the facial nerve, its connections and branches.
(From Hbrmann's Physiology.)

F. The facial nerve. A. Auditory nerve.
1. The geniculate ganglion.

gup. Great superficial petrosal nerve connecting the facial and Meckel's

asp. Small superficial petrosal nerve connecting the facial with the Otic

ganglion and with the tympanic branch of the glosso-pharyngeal.
esp. External superficial petrosal connecting the &cial with the plexus on

the middle meningeal artery.
Chorda tympani, joining lingual nerve.
Nerve to stapedius muscle.

Communicating branch with the ganglion of the root of the vagus.
Posterior auricular nerve.

Branch to the stylo-hyoid and digastric muscles.
?. Temporo-fecial division ) ^ ^„^,^ „f expression.
?, Cervico-facial division )


V. Fifth nerve, at. Auriculo-temporal branch.

id. Inferior dental nerve. /. Lingual nerve.
MG. Meckel's ganglion.
OG. Otic ganglion.
SG. Submaxillary ganglion.
IM. Internal maxillary artery.
MM. Middle meningeal artery.
P. Pneumogastric nerve.
GP. Glosso-pharyngeal nerve.

t. Its tympanic branch (nerve of Jacobson).

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superficial origin of a nerve and is only a part of an intra-cranial
syphilis which is brought under vigorous treatment in the early
stage, when the prognosis may be fair. In lesions of the motor area
of the cortex implicating the centre of the facial, the prognosis will
vary according as it is syphilitic or not, being fair in the specific
cases that are brought imder treatment in the early stage, and bad
in almost all others.

The diagnosis of a facial paralysis is a matter of no difficulty, as
the open eye, the flattened face, and the cheek bellying out when any
marked expiratory efforts are made, are pathognomonic. But it must
be remembered that the causative lesion may be peripheral, in the
middle ear, at the base of the cerebrum, or in the nucleus of origin of
the nerve in the medulla oblongata. The course of the facial in the
internal capsule (pp. 38 and 125), as well as the cortical centre (Fig.
7), need not be considered in this process of differentiation, because
a lesion of either site would not involve the fibres to the eyelid on one
side, and the levator pcUpebrce superioris would not be paralyzed. A
peripheral site of the lesion may be diagnosed by exclusion of one in
the middle ear, the cerebrum, or the medulla. Fig. 107 will show the
relation of the facial nerve to the middle ear. Fig. 108 gives an

Fig. 108.

View of the inner wall of tympanum, enlarged. (Grit.)

excellent view of the inner wall of the tympanum. From these two
figures a clear idea can be obtained of the branches of the facial nerve
and its connection with the middle ear. A lesion in the aqueduct of
Fallopius, situated between 3 (Fig. 107), the stapedius nerve fila-
ment, and 2, the chorda tympani, will cause impairment of the sense
of taste in the corresponding anterior two-thirds of the tongue, as
well as diminished salivary secretion on the same side. If there is a
lesion between the nerve filament to the stapedius (3, Fig. 107) and
the geniculate ganglion (1), there will also be abnormal acuteness of
hearmg — hyperacusis. Implication of the geniculate ganglion itself

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adds paralysis of the soft palate and distortion of the uvula to the
symptoms. A lesion above the geniculate ganglion will cause most
of these symptoms — facial paralysis, lagophthalmus, lessened saliva,
paralysis of the soft palate, and deviation of the uvula; but there will
be no impairment of the sense of taste in the anterior portion of the
tongue, and there will probably be deafness, as the auditory nerve is
close by ; moreover, bone conduction, as tested by the tuning-fork,
will probably be increased {vide p. 141). A lesion at the base of
the cerebrum would be certain to involve the auditory (Fig. 21),
would be likely to implicate the neighboring cranial nerves, and
would be caused by an intra-cranial neoplasm, arterial disease, intra-
cranial syphilis, cerebro-spinal meningitis, or a trauma of the skull.
An isolated lesion of the facial nuclei in the' medulla oblongata would
be a clinical curiosity, as this nucleus is generally affected by disease
involving the nuclei of other cranial nerves, such as progressive
muscular atrophy, labio-glosso-laryngeal paralysis, and occasionally
Landry's paralysis. Disease of the pons Varolii (p. 127) might also
implicate the fibres of the facial. The diagnosis of a peripheral
lesion of the nerve must, therefore, be arrived at by exclusion of
disease in these different regions through which the facial passes in
its devious career.

The treatment of Bell's palsy will resolve itself into a treatment
of the lesion causing it. In the one case, therefore, the middle
ear must be* treated ; in another, the causative lesion at the base
of the cerebrum ; in a third, the affection at play in the internal
capsule, the centrum ovale, or the centre in the cortex ; and in a
fourth, the neuritis itself, although it should not be overlooked that
this neuritis must also be cared for even when it is induced by one
of the central lesions. A neuritis of the facial, however, is identical
with a neuritis of other nerves, so far as the art of therapeutics is
concerned, and my reader must, therefore, look to " Neuritis," page
173. As the latter deals mainly with the mixed nerves, though, its
suggestions for the relief of pain may be disr^arded. Fig. 80 will
show the motor points of the facial.


Synonyms : Hyperplastic neural growths or formations. Nerve

Neuromata are morbid growths upon the peripheral nerves. The
name seems to have first been used by Odier in the year 1803. They
are classified as —

Stump neuromata (Stumpf-Neurome or Trennungs-Neurome) ;
Painful neuromata {tubercula dolorosa) ;
Nerve-trunk neuromata {Stamm^Neurome) ;
Tendril neuromata {Ranken-Neurorne).
Stump neuromata are found in nerves which have been severed.
The first description was given by Lower in 1669. All severed
nerves have a tendency to become club-shaped at the central end.

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although the nersre fibres are not otherwise altered. They are found
at various times after section, from two up to many years.

The painftd tubercles {tubercula dolorosa) are small tumors gener-
ally lying upon small subcutaneous nerves, circumscribed, movable
in all directions, very painful upon pressure, and giving rise to neu-
ralgic attacks from cutaneous irritation. They were first described
by Cheselden in 1750.

Nerve-trunk neuromata {Stamm-Neurome) are, as the name denotes,
to be found upon the trunks of nerves, and are either single or

The tendril or plexiform neuromata {Ranken-Neurofne) consist of
a diffuse hypertrophy of several nerve trunks, branches, and fibrils
within a certain area. The first description was given by Robin
in 1854.

These different varieties are divided into two great classes : true
neuromata, consisting of such tissue as constitute morbid growths in
other places. They are either of medullated or non-meduUated
nerve fibre, and between tlie nerve fibres is a varying amount of
connective tissue. Of the false neuromata, fibromata are the most
common, although myxomata, gliomata, sarcomata, and carcinomata
are occasionally met with. Syphilomata are very rare, except on
the cranial nerves.

Causes. The neuromata of the stump are found either in sec-
tions of nerves that have been severed, or after amputations. The
age of patients suffering from painful tubercles ranges from youth
up to the sixtieth year, although the majority are found between the
twelfth and fortieth years. Women are more subject to them
than men. Most of them are found about the leg, next around
the mammae, less frequently about the upper extremity, next in
fi^uency about the head, and seldom in other parts of the body.
The trunk neuromata are seen most frequently from the tenth to the
fortieth year, although they are observed occasionally in childhood,
and even up to the eightietli year. There seems to be no difference
in the susceptibility of the sexas. The optic nerve is most prone to
single trunk neuromata, and after this the median and the ulna, next

Online LibraryLandon Carter GrayA treatise on nervous and mental diseases: for students and practitioners of ... → online text (page 18 of 84)