oscillatory or rotatory movements of the eyeballs. The oscillatory are
due to rapid alternate contraction of the straight muscles, while the
rotatory indicate either similar actions of the oblique muscles alone
or in conjunction with the straight. The oscillatory motions are
usually horizontal, but instances of vertical nystagmus occur, as in
the case recorded by Soelberg Wells.[217] Nystagmus may be either
congenital or acquired; the latter variety being much the more frequent
form of the affection. Congenital nystagmus is usually associated
either with cataract or imperfect development of the optic nerve and
retina. It is a very frequent accompaniment of albinism and pigmentary
retinitis. We often see the acquired form arise during the first few
months of life, when the child in its effort to see is hindered by
corneal or lenticular opacities resulting from ophthalmia neonatorum.
One of the most interesting of the acquired forms is that which occurs
amongst coal-miners, rendering a considerable number of those thus
affected unfit for work. At first the symptoms are that the lights in
the mines and the objects on which the patients endeavor to fix their
attention begin to dance, this being accompanied by a sensation of
dizziness and discomfort. In the first part of the attack they
disappear when work is stopped, and the miners come up into the
daylight; but if work be persisted in they become permanent and
exaggerated. When the nystagmic motions have ceased, they may often be
called into activity by placing the patient in a dark room and getting
him to direct his eyes to a candle held above the horizontal line of
the field of vision. The motions are usually lateral, or in some cases
the centre of the cornea describes an ellipse or circle which causes
the patient to see a ring of light. It has been observed to occur much
more frequently in those working in shafts where there is a good deal
of fire-damp; which has caused some writers to assert that the
nystagmus has been dependent upon the action of the gas. This view
would seem to receive some support from an instance reported by Bright
of nystagmus, in a case of suffocation from the fumes of burning coals,
which he attributed to cerebral pressure. In these cases it is more
probably due to fatigue of the eye and its nerve-centres in the
endeavor to see in the dim light and strained position which the miner
is often obliged to maintain, which is intensified by the enfeeblement
of the nerve-centres due to the action of the gas: these, associated
with the diminution of the light caused by the wire gauze of the
safety-lamp, would further increase the strain in those obliged to work
in the shafts pervaded with fire-damp. The statements of Dransart,[218]
founded on the examination of a large number of miners, probably give a
correct idea as to the frequency of the affection. He states that among
12,000 workmen employed by one company, there were 30 under treatment
for nystagmus, which would give about two and a half patients per
thousand. In any form of nystagmus the motions of {784} the eyes
usually become more rapid when they are used for near work. According
to Nagel,[219] excessive convergence will at times cause a temporary
cessation of all nystagmic motion; and he further proved this by
putting extra strain on the interni by means of prisms with their base
out. The true pathology of the various forms of nystagmus is still
imperfectly known. Arlt[220] supposes that there is a rapid repetition
of reflex movements in the endeavor to attain distinct vision in those
forms which develop on account of corneal and lenticular opacities. He
explains this by the supposition that the retinal impression is
strengthened by the same retinal areas being rapidly and repeatedly
subjected to the action of the rays of light from the same object,
while a longer period of fixation would cause retinal fatigue and blur;
showing the same principle by reminding us that our perceptive powers
for a test object, upon first being brought into view at the periphery
of the field of vision, are much stronger when the object is shaken
than when it is brought quietly toward the fixation-point. Some forms
of the affection, however, are manifestly due to fatigue of the
nerve-centres, and have been by some authors placed in the same
category as writers' cramp. For its causation we would naturally look
for the anatomical changes either in the cortical centres for the
eye-muscles or in the nuclei of the third and sixth pairs. Vulpian[221]
states that wounds of the medulla in dogs cause nystagmus, and Schiff
asserts that wounds of the white substance of the cerebellum near the
peduncles give rise to the same phenomenon; while Ferrier has produced
it by the influence of electricity on the cerebellum of apes. Cohn[222]
records a case of gunshot wound of the right parietal bone (near the
angular gyrus) which produced nystagmus. Merkel's case, occurring in a
patient with embolism of the artery of the fissure of Sylvius, would
also point to lesion near the angular gyrus. Stintzing[223] gives a
case where there was thrombosis of the basilar and Sylvian arteries.
Oglesby[224] relates two cases where nystagmus came on suddenly with
dilatation of the pupils, the autopsies showing a clot which pressed on
the medulla. Fienzal[225] also gives a case where there was a tumor in
the left peduncle of the brain. It is often seen during epileptic
convulsions. According to Raehlmann,[226] the motions of both eyes are
under the control of psychic centres which regulate them according to
the necessities of vision: for Willbrand[227] it is a sign of weakness
of the voluntary cortical centres which fail to regulate the reflex
activity of the middle brain and cerebellum. The latter author shows
that the extent of the field of vision is increased in the direction of
the oscillations in those cases where direct vision is not much
impaired, while there is marked contraction of the field in cases where
the direct visual acuity is much diminished. He also states that there
is contraction of the field in the nystagmus of miners, which is
greater during the intervals of the paroxysm than during their
occurrence, and, further, that the contraction is greater where the
case is one of long standing.
[Footnote 217: _Lancet_, 1871, p. 662.]
[Footnote 218: _Annales d'Oculistique_, 7, 82, p. 177.]
[Footnote 219: _Graefe u. Saemisch_, vol. vi. p. 226.]
[Footnote 220: _Krankheiten des Auges_, Bd. iii. p. 335.]
[Footnote 221: _Comptes Rendus de la Société de Biologie_, 1861 (quoted
by Robin, p. 157).]
[Footnote 222: _Schussvorletzungen des Auges_, p. 19.]
[Footnote 223: _Jahresbericht f. Ophth._, vol. xiv. p. 306.]
[Footnote 224: _Brain_, vol. iii., 1880.]
[Footnote 225: _Trans. Internat. Congress_, at Milan, 1881, p. 126.]
[Footnote 226: "Nystagmus und seine Aetiologie," _A. f. O._, xxiv., 4,
p. 237 (1878).]
[Footnote 227: _Klin. Monatsblätter f. Augenheilkunde_, vol. xvii.,
1879, pp. 419-438 and 461-480.]
{785} In some rare cases nystagmus may be produced at will.
Raehlmann,[228] Lawson,[229] Benson,[230] all report cases of the
voluntary type. In one of those given by Lawson the patient (a
gentleman in good health) "first made his eyes steady, and then set
both into rapid lateral motion--so rapid that the outline of the cornea
was completely lost to view." Zehender[231] observed it in a case of a
twelve-year-old boy, where he was able to produce it by the
instillation of a strong solution of eserine. Charcot states that
ordinary nystagmus is a valuable symptom of disseminate sclerosis, and
that it is present in about half of these cases, while it is
exceptional in locomotor ataxy. "In some patients the look is vague
until the eyes are made to fix some object, when the nystagmus
develops."
[Footnote 228: _Loc. cit._]
[Footnote 229: _R. L. O. H. Reports_, vol. x. p. 203.]
[Footnote 230: _Ibid._, vol. v. p. 343.]
[Footnote 231: _Klin. Monatsblätter f. Augenheilkunde_, vol. xviii.,
1879, p. 127 (note).]
According to Hammond, in disseminate sclerosis, nystagmus may be the
only symptom for the period of a year before other symptoms develop.
Moos[232] speaks of oscillatory movements of the eyes in Menière's
disease, and Schwalbach[233] describes them in a case of purulent
catarrh of the middle ear where they could be produced either by
syringing or by pressure on the mastoid process.
[Footnote 232: _Arch. f. Augenheilkunde und Ohrenheilkunde_, vii. 2, p.
508.]
[Footnote 233: _Deutsches Zeitschrift f. prakt. Med._, No. 2, 1878.]
Affections of the Fifth Pair.
HERPES FACIALIS.--Herpes facialis frequently appears on the lips and
angles of the mouth, and occasionally in the eye and its appendages.
When upon the conjunctiva or cornea, it commences as clear watery
vesicles, usually in groups, which soon burst and leave open ulcers
looking very much like abrasions or scratches of this membrane. They
usually occur in successive crops after fevers, especially pneumonia,
although at times they may appear without any assignable cause. They
are also slow to heal, but are not dangerous to the eyesight, except
where they give rise to purulent infiltration leading to hypopyon.
HERPES ZOSTER OPHTHALMICUS.--Herpes zoster ophthalmicus is a far more
formidable affection. The eruption, as is well known, follows the
distribution of the divisions of the ophthalmic branch of the
trigeminus, and when the eyeball is affected the sight is always
threatened. Clear watery blisters form on the cornea, which soon burst,
the exposed tissue taking on purulent infiltration, while pus is not
infrequently deposited in the anterior chamber. These ulcers are slow
to heal under the most careful treatment, which, as a rule, consists in
washing with disinfecting solutions and applying a bandage, etc. There
is almost always iritis, as evidenced by the sluggish pupil and at
times by marked synechiæ.
The burning and pricking pain at the seat of eruption is marked, and
there is severe neuralgia in the temple, forehead, and side of the
nose. The intensity of the iritis varies considerably in different
cases, and, although some terminate favorably, having had but few and
slight symptoms, yet the one case reported by Noyes, where it led to
cyclitis, followed by shrinking of the eyeball, which ultimately gave
rise to {786} sympathetic irritation of the fellow-eye, shows how
serious its consequences may be. Permanent opacities of the cornea are
not infrequent. The disease is, fortunately, a rare one. It usually
comes on either in middle or declining life, although Wadsworth has
reported a case in a child four years old. The cornea becomes
anæsthetic, both in the ulcers and over the rest of its surface, a long
time often elapsing before any of its sensibility is regained.
Horner[234] was the first to demonstrate that the corneal ulcers
originated in vesicles, and the very great diminution of intraocular
pressure in the affected eyeball, and also to show the marked
difference in the temperature of the skin of the two sides. The
temperature on the affected side is usually one and a half to two
degrees higher than on the other side, while the cutaneous sensibility
is markedly diminished; as, for instance, the æsthesiometer might give
twelve lines on the healthy forehead as against twenty-two lines on the
diseased side, and the superciliary ridges and the upper eyelid on the
normal side might give respectively nine and five lines as against
seventeen and seven lines on the affected side. In the cases which the
writer has had an opportunity of studying he has found similar
variations in intraocular tension, temperature, and sensibility.
Hutchinson[235] thinks that the affection of the nasal branch is always
accompanied by inflammation of the eyeball, and says: "Thus far, I have
never seen inflammation of the whole side of the nose without
witnessing inflammation of the eye;" while Bowman[236] says that he has
"not found affections of the eyeball to occur, especially in those
cases of ophthalmic zoster in which the eruption followed the course of
the nasal branch." Wadsworth[237] gives a case where the entire side of
the nose was involved, the eyeball and conjunctivæ not being affected.
He suggests that possibly the explanation in these cases is an anomaly
of distribution described by Turner, where the side of the nose is
supplied by a long, slender infratrochlear branch. Bowman,[238]
although realizing that peripheral excitement of sensory nerves may
originate in a central or reflected source, and induce tenderness and
redness in the parts supplied by them, yet nevertheless holds that
ophthalmic zoster is a peripheral disease, having its primary seat in
the branches of common sensation, the nerves probably becoming inflamed
in the more superficial portions of their trunks, as the eruption
succeeding as an extension of vascular excitement to the cutaneous
tissue: he thus explains the tenderness of the skin before it reddens
and the often lasting alteration of sensibility. In reference to
whether the neuritis causing the eruption is an ascending or descending
one, the only two careful autopsies that give answer with which the
writer is familiar are those of Wyss and of Weidner, where both show
extensive changes in the nerve-centres. The latter, made five years
after the attack, showed cicatricial shrinking of the ganglion of
Gasser and of the root of the nerve between it and the medulla; while
that of Wyss, made within two weeks of the outbreak of the affection,
showed that the entire ophthalmic branch of the trigeminus was
thickened, reddened, softened, and surrounded by extravasation of blood
from the entrance of the orbit up to the ganglion of Gasser; while the
other branches of the trigeminus were normal in size and {787}
appearance. The Gasserian ganglion itself was enlarged and bright red,
while that of the other side of the head was yellowish-white. As is
well known, zoster in other parts of the body not infrequently affects
the two sides simultaneously; and there are recorded cases where it has
twice attacked the same locality, but the writer is not familiar with
any such facts as regards ophthalmic zoster.
[Footnote 234: _Klinische Monatsblätter f. Augenheilkunde_, 1871, p.
321.]
[Footnote 235: _R. L. O. H. Rep._, 1866, pp. 191-215.]
[Footnote 236: _Ibid._, 1867.]
[Footnote 237: _Trans. of Amer. Oph. Soc._, 1874.]
[Footnote 238: _Loc. cit._]
NEURO-PARALYTIC OPHTHALMIA.--In 1822, Herbert Mayo[239] showed that
section of the fifth nerve within the cranium produces insensibility of
the eye; and Charles Bell[240] in 1830, while recognizing this fact,
maintained that "when that sensibility is destroyed, although the
motions of the eyelids remain, they are not made to close the eye, to
wash and clear it, and consequently inflammation and destruction of
that organ follow." Since that time the subject has been a favorite
theme with both clinicians and physiologists, but opinions as to its
cause have been a good deal divided. While, perhaps, a majority, with
Bell,[241] Snellen,[242] Kondracki,[243] Gudden,[244] Senftleben,[245]
and others, hold that the inflammation of the cornea is of traumatic
origin, many writers--amongst whom may be mentioned Longet,[246]
Graefe,[247] Meissner,[248] Schiff,[249] and Eckhard[250]--assert that
it is caused by the impaired action of the trophic fibres of the nerve;
and again others, such as Ferrier,[251] Balogh,[252] and Buchmann,[253]
maintain that the inflammation is peripheral, consequent upon the
drying of parts of the cornea. Clinically, soon after the occurrence of
complete palsy of the trigeminus, there is an interstitial punctate
keratitis, which makes the cornea so cloudy that the motions of the
iris are with difficulty observed, this being accompanied by
conjunctival and ciliary injection. The symptoms, especially where the
paralysis is incomplete, are often much alleviated by maintenance of
careful closure of the lids and repeated washing of the eye, which
protects the enfeebled tissue from the action of foreign bodies.
Success is not, however, always obtainable, for occasionally, even with
the most complete protection of the eye, eventual sloughing of the
cornea cannot be prevented. This is not a usually-accepted doctrine,
but the writer is convinced[254] of its truth by a case seen within a
week of the commencement of the disease, in which the cornea was not
yet ulcerated, where the most sedulous care in cleansing the eye and
protecting it from external irritants did not prevent the necrosis and
perforation of the central part of the cornea. Since then other cases
of similar import have been published. Quaglino[255] gives an instance
where complete ptosis shielded the eye from all gross insults, but
where, nevertheless, a central slough of the cornea formed.
Laqueur[256] also found {788} that the cornea sloughed in spite of the
most careful protection. In all other cases where the cornea is exposed
to air and external irritants, as in lagophthalmos or excessive
exophthalmos, the case is quite different, the consequent inflammation
being much better borne. While this is a fact more or less familiar to
all clinicians, it is nowhere better shown than in the case of
Horner,[257] where there was caries of the petrous portion of the
temporal bone and complete paralysis of the facial nerve. Two years
later the trigeminus was attacked, and then for the first time
ulceration occurred in the hitherto sound cornea. Hirschberg[258]
describes neuroparalytic keratitis and panophthalmitis consequent upon
a neurectomy of the infraorbital nerve, and quotes Langenbeck as
relating a similar case after section of the supraorbital nerve.
[Footnote 239: _Anat. and Physiol. Commentaries_, London, 1822, No. 2,
p. 5.]
[Footnote 240: _Nervous System of the Human Body_, London, 1830, p.
207.]
[Footnote 241: _Loc. cit._]
[Footnote 242: _Virchow's Archiv_, Bd. xiii. S. 107, 1850.]
[Footnote 243: _Nagel's Jahresbericht_ (Lit. 1873), p. 266.]
[Footnote 244: _Idem._]
[Footnote 245: _Virchow's Archiv_, Bd. lxv. Heft. 1, pp. 69-99.]
[Footnote 246: _Anatomie et Physiologie du Système nerveux_, t. ii. p.
161, Paris, 1842.]
[Footnote 247: _Arch. f. Ophthalmologie_, Bd. i. Abth. i. S. 306-315.]
[Footnote 248: _Henle und Pfeuffer's Zeitschrift_ (3), xxix. p. 96
(quoted by Soelberg Wells).]
[Footnote 249: _Ibid._, p. 217 (also quoted by Wells).]
[Footnote 250: _Centralblatt f. Med. Wiss._ (cited by Nagel,
Literature, 1873).]
[Footnote 251: _Nagel's Jahresbericht_, (Lit. 1876), p. 51.]
[Footnote 252: _Ibid._]
[Footnote 253: _Ibid._, 1883, p. 153.]
[Footnote 254: Norris, "Case of Paralysis of the Trigeminus, followed
by Sloughing of the Cornea," _Trans. Amer. Ophth. Soc._, 1871, pp.
138-141.]
[Footnote 255: _Nagel's Jahresbericht_ (Lit. 1874), p. 26.]
[Footnote 256: _Klinische Monatsblätter f. Augenheilkunde_, 1877, p.
228.]
[Footnote 257: _Nagel's Jahresbericht_ (Lit. 1873), p. 267.]
[Footnote 258: _Berliner klinische Wochenschrift_, 1880, S. 169;
_Sitzung der Gesell. f. Psych. und Nervenkrankheiten_, 10 März, 1879.]
INJURIES OF THE FIFTH PAIR.--Although daily clinical experience shows
us how promptly irritation of the sensitive branches of the trigeminus
are followed by symptoms of reflex action in the eye--as, for instance,
a cinder in the conjunctiva will cause contraction of the pupil, or a
sharp pinch of the temple will at times cause pupillary
dilatation--nevertheless, instances of impairment of the eyesight due
to injury of the branches of the infraorbital or supraorbital nerves,
and to this alone, are of rare occurrence. Sympathetic ophthalmia is
the exception in which we too frequently see inflammation of one eye
cause severe and often irreparable damage to its fellow. Scattered
through ancient and modern surgical works there are many interesting
and well-attested cases of impaired vision, some of which should be
excluded on account of the want of proper evidence, which is now
obtained from testing of the acuity and field of vision and
ophthalmoscopic examination. Erichsen[259] cites cases from
Hippocrates, Fabricius Hildanus, and La Motte where amaurosis was
produced by a wound of the brow. Chelius[260] gives a case from similar
injury, while Wardrop[261] narrates three instances--one of wound of
forehead, one from a blow on it with a ramrod, and one from an injury
by a fragment of shell. The same author calls attention to the fact
that amaurosis is more readily caused by wounds and injuries of the
supraorbital and infraorbital nerves than from complete division of
them. The various neurotomies and neurectomies performed upon the
supraorbital branch since his day bear witness to the accuracy of his
deduction. The same author quotes Morgagni as saying that Valsalva has
seen amaurosis follow a wound of the lower lid which has been inflicted
by the spur of a cock. Morgagni relates a similar case where the injury
was inflicted by the broken glass from the windows of an upset
carriage; and Beer reports a similar case of amaurosis from wound of
the cheek. Guthrie[262] remarks that "when the eye becomes amaurotic
from a lesion of the first branch of the fifth pair of nerves, the
pupil does not become dilated; the iris retains its usual action,
although the retina may be insensible and the vision destroyed." More
recently, Rondeau[263] {789} gives two cases, one of which caused
lachrymation, photophobia, and eventual atrophy of the eye on the
affected side, followed, fifteen years later, by loss of the fellow-eye
from sympathetic ophthalmia, which had been produced by degenerative
changes taking place in the shrunken bulb; and a second, in which a
wound of the left brow became painful eight days after the receipt of
the injury, and where pains became more severe as the wound cicatrized:
in this latter case the left eye became foggy in three weeks, and soon
sight was entirely lost, whilst six weeks after the accident there was
dull pain in the right eye, with a sensation of cloudiness and a
gradual development of photophobia in it. By local bloodletting, which
caused the photophobia to rapidly yield, and a derivative and alterant
treatment, the patient's right eye was so far improved that fifteen
days later he could find his way about with the left eye, and could see
to read with the right. Ophthalmoscopic examination showed in the left
eye a serous swelling of the retina which entirely obscured the margin
of the discs and gave the whole fundus a grayish tint, the veins being
much enlarged and very tortuous. The right eye showed similar changes,
though less developed.
[Footnote 259: _Loc. cit._, pp. 233-261.]
[Footnote 260: South's translation of Chelius's _System of Surgery_,
vol. i. p. 430.]
[Footnote 261: _Morbid Anatomy of the Human Eye_, vol. ii. pp. 180,
181, London, 1818.]
[Footnote 262: Quoted by White-Cooper, _Injuries of the Eyes_, London,
1859, p. 92.]
[Footnote 263: _Des Affections oculaires Reflexes_, Paris, 1866, pp.
53, 54.]
Affections of the Sixth Pair.
The extremely limited distribution of the sixth pair of cranial nerves
renders the clinical study of their pathology comparatively simple. The
eye supplied by the paralyzed muscle turns inward to an extent
corresponding to the degree of loss of power in the paretic muscle plus
the energy of its opponent rectus internus. The image of the object
fixed by it falls, therefore, to the inner side of the macula lutea,
and, being projected outward, causes a double vision, in which the
image of the deviated eye appears to be in the temporal field of the
affected eye (homonymous diplopia). When the healthy eye is covered and
the patient endeavors to fix any near object with the paralyzed eye, it
will be found that (as in all other cases of peripheral paralysis
affecting any of the extra-ocular muscles) the secondary deviation of
the sound eye is considerably greater than the primary deviation of the
affected one; this being accounted for by the fact that the amount of
consentaneous innervation which is sufficient to cause a small motion
in the paretic muscle will produce a marked effect in the sound one.