because they were made by careful and competent observers, and the
lesions were so marked and limited in character as not to allow of any
other interpretation than that given. If we admit the validity of the
evidence, we have proved conclusively that, from a clinical and a
pathological standpoint, binocular homonymous lateral hemianopia may be
produced by lesions of the optic tract, of the posterior part of the
thalamus opticus, and of the occipital lobe of the brain of the side
opposite to the defect in the field of vision; and that, therefore,
there must be a partial, and not a total, crossing of the fibres of the
optic tracts at the chiasm. Moreover, as Foerster has most pertinently
remarked, such a state of affairs does not violate the physiological
law of the total crossing of other nerves, because in the binocular
field of vision the partial crossing causes all objects to the right of
the point of fixation to be seen by the left hemisphere, while those to
the left of it are seen with the right hemisphere. While this problem
appears sufficiently plain, and the view above advocated is adopted by
the majority of writers of the present day, it is by no means equally
satisfactory when looked at from a purely anatomical or physiological
standpoint. Newton[184] in 1704 had already appreciated the importance
and difficulty of the subject, and in {777} the hope that others might
further investigate it asked the question whether the fibres from the
right sides of both retinæ do not so unite at the chiasm as to go
together to the right side of the brain, those from the left side of
each retina pursuing a similar course to the left hemisphere. He
further remarks that "if he is correctly informed that the optic nerves
of such animals as have a binocular field of vision join at the chiasm,
while those of the animals who have no binocular vision, such as the
chameleon and some fishes, do not so join."[185] Since his day the
majority of authors have adhered to this view, until Biesiadecki,[186]
by careful anatomical studies and lectures, attempted to prove that in
both men and lower animals there is a total crossing of the fibres at
the chiasm. Twelve years later Mandelstamm,[187] by clinical
observations of nasal hemiopia and dissections of the chiasm,
maintained the same view. In the same year Michel[188] supported the
same doctrine, and since then Schwalbe[189] and Scheel[190] have each
advanced the same view. However, Von Gudden,[191] also basing his
opinions upon dissections, takes the opposite ground, and has since
endeavored by a series of experiments, in which he enucleated one eye
of young rabbits and dogs, to prove[192] that if the animals were
allowed to live until central atrophy set in there is a partial atrophy
of both optic tracts, more marked on the side opposite to that of the
enucleated eye, because the crossed bundle is by far larger than the
direct.
[Footnote 184: _Optiks_, London, 1704, p. 136.]
[Footnote 185: _Loc. cit._]
[Footnote 186: "Chiasma Nervorum Opticorum der Menschen und der
Thiere," _Sitzungsberichte der Wiener Akadamie_.]
[Footnote 187: _A. f. O._, xix., 2, pp. 39-58.]
[Footnote 188: _Ibid._, xix., 2, pp. 59-84.]
[Footnote 189: _G. u. S._, vol. ii. p. 324.]
[Footnote 190: _Klin. Monatsblätter f. Augenheilkunde_ (extra number
2), 1874.]
[Footnote 191: _Arch. f. Psychiatrie_, vol. ii. p. 21.]
[Footnote 192: _A. f. O._, xx., 2, p. 226, and also _Ibid._, xxv., 1,
p. 1, 1879.]
From similar experiments on rabbits, Mandelstamm[193] maintains that
there is a total crossing at the chiasm, and Michel,[194] who repeated
Von Gudden's experiments, arrived at the same conclusion.
Brown-Séquard[195] asserted that a medial cut of the chiasm in rabbits
produces amaurosis of both eyes, which would indicate that there is
total crossing, while Nicati[196] a year later showed that a median
section of the chiasma in young cats did not produce blindness of each
eye, the animal following with the eye and the head the movements of a
light held at a considerable distance from the eyes.[197] The condition
of the optic nerve and brain obtained from the human subject, where by
accident or by disease one of the eyes has been destroyed long before
death, seems in the main to speak for partial decussation. Thus,
Biesiadecki, while maintaining total decussation, could only conclude
from such specimens of degenerated nerves and tracts that the greater
part of the fibres of the atrophic nerve went to the tract of the
opposite side. Woinow[198] demonstrated preparations to the Ophthalmic
Society at Heidelberg where the left eye had been blind for forty
years, and the atrophy, which had travelled up the left nerve, was
plainly visible in both optic tracts. Schmidt-Rimpler[199] also showed
atrophy of both tracts {778} more marked in that of the opposite side,
and Manz[200] found atrophy of both tracts after atrophy of the nerve
of one side; Plink[201] reports a similar state of affairs; while
Popp[202] and Michel[203] from analogous specimens draw conclusions
favorable to the total crossing.
[Footnote 193: _Ibid._, xix., 2, p. 47.]
[Footnote 194: _Ibid._, xxiii., 2, p. 227.]
[Footnote 195: _Archiv de Physiologie_, 1872, p. 261, and 1877, p.
656.]
[Footnote 196: _Ibid._, 1878, p. 658.]
[Footnote 197: Cats have a larger binocular field of vision, and are
better subjects for experiments than rabbits.]
[Footnote 198: _Klin. Monatsblätter f. Augenheilkunde_, 1875, p. 425.]
[Footnote 199: _Ibid._, 1877, "Bericht der Ophth. Gesellschaft," pp.
44-48.]
[Footnote 200: _Klin. Monatsblätter f. Augenheilkunde_, 1877, "Bericht
der Gesellschaft," pp. 49, 50.]
[Footnote 201: _Arch. f. Augenh. und Ohrenheilkunde_, vol. v.]
[Footnote 202: Inaug. Diss., _Embolie der Art. Centralis_, Regensberg,
1875, p. 20.]
[Footnote 203: _A. f. O._, xxiii., 2, p. 243.]
The above cases are amongst the most decisive which have been reported,
and are quite sufficient to show how great the conflict of opinions is
among good observers. The observations and experiments on the subject
of sight-centres in the cortex cerebri are also conflicting: thus,
while Ferrier places the cortical sight-centre in the angular gyrus,
and maintains that its destruction will produce blindness, Luciani and
Tamburini agree as to the locality of the sight-centre, but maintain
that its destruction produces hemianopia; while Munk places the
sight-centre in the occipital lobe, and asserts that its loss causes
hemianopia and not contra-lateral blindness. In the case of hemianopia
reported by Keen and Thomson,[204] where a bullet wound of the left
occipital lobe produced right hemianopia without other apparent lesion,
the writer has had an opportunity of personally examining it and of
confirming their conclusions. The conclusions which he arrived at,
associated with the knowledge which he obtained in Stricker's
laboratory by witnessing experiments upon dogs and apes, where portions
of the occipital lobes were destroyed, have convinced him that cortical
lesions of the occipital lobes produce hemianopia. On the other hand,
chiefly on clinical grounds and from the study of hystero-epilepsy,
Charcot concludes that the band of uncrossed fibres in the chiasm bends
again somewhere in the region of the geniculate bodies to join the
crossed bundle once more in the cortical centre. According to this
theory, destruction of the cortical centre should produce total
amaurosis of the opposite eye, and lesions between the chiasm and
geniculate bodies would produce homonymous hemianopia, while pressure
in the crossing-point of those fibres (which in the chiasma are
uncovered and run from the geniculate bodies to the opposite cortical
centre) would give paralysis of the temporal halves of both retinæ.
[Footnote 204: _Trans. A. O. Soc._, 1871.]
As regards pure crossed amblyopia, the scheme of Charcot is scarcely
borne out by his clinical facts. The latest theories of those cases
which were investigated by Landolt and himself showed, as they
reported, marked amblyopia on the opposite side from the lesion, but
associated with contraction of the field of vision in the eye of the
same side. The question, however, is so vast, and so much remains to be
learned concerning the brain-centres and their communications with the
optic tracts, that it can scarcely be considered sufficiently ripe for
an exhaustive discussion in a paper like the present.
According to Foerster, temporal hemianopia always develops slowly
without any concomitant paralytic symptoms: it does not have constant
boundaries, and is now progressive and again retrogressive. He cites
cases which he has observed for years where at first small negative
scotoma appeared just outside of the fixation-point, and increased till
there was a total loss of the temporal fields. The line of division
between the blind and seeing sides of the field of vision is not
sharply defined and {779} not accurately vertical. In some cases there
is a gradual invasion of the sound side. Although it is usually assumed
that some pressure in the anterior or in the posterior angle of the
chiasm is the cause, yet the writer does not know of any post-mortem
examination of a case. Mauthner[205] gives short histories of 23 cases
of temporal hemianopia, besides 11 cases relating to nasal hemianopia
(or, according to his classification, hemianopia heteronyma medialis)
from various authors, in most of which the ophthalmoscope showed either
the presence of a neuritis or an atrophy of the nerve. There were two
autopsies in the cases of nasal hemianopia related by Mauthner--those
of Schule and Knapp--one of which showed an enlargement of the third
ventricle and infundibulum, with atrophy of the nerves, and the other a
high degree of ætheromatous degeneration of arteries at the base of the
brain. Any cause which would produce simultaneous pressure on the outer
angles of the commissure would give rise to nasal hemianopia. Little is
known regarding hemianopia above or below the horizontal line: both
Mackenzie and Graefe mention its occurrence, and Knapp, Schoen, and
Mauthner give interesting cases. The writer has seen a case in a woman
of fifty-five years otherwise apparently in good health. The upper part
of each field was wanting, and the line of division ran slightly above
the fixation-point, it being nearly horizontal. The optic nerves did
not present any marked departure from their normal appearance, and
central vision was fair (20/x1). The only autopsy of a case of superior
hemianopia with which the writer is familiar is that reported by
Russell,[206] in which there was a tumor involving the bones of the
base of the cranium. The patient had upper hemianopia, confined to the
right eye, followed by total blindness, coming on first in the right
and then in the left eye. Genuine binocular hemianopia of the superior
or inferior variety is probably produced by some symmetrical affection
of the optic nerves between the chiasm and the eyes.
[Footnote 205: _Gehirn und Auge_, 1881, pp. 373-381.]
[Footnote 206: _Med. Times and Gazette_, No. 47, 1873 (rep. _Nagel's
Jahresbericht_, 1873, p. 361.)]
In apparently healthy individuals transient hemianopia is not an
unfrequent occurrence, and may either develop with or without other
cerebral symptoms. It is usually followed or accompanied by headache,
or more rarely by vertigo, tinnitus aurium, difficulty of speech, etc.
Even in intelligent patients, who have not been drilled by their
medical adviser to carefully analyze their symptoms, it is not
recognized as half-vision, but here, as in the permanent variety of the
affection, it is described as a dimness or blindness of the eye on the
side in which the field of vision is defective. Some cases of transient
hemianopia are accompanied by peculiar zigzag flickerings of light in
the defective portions of the field of vision, which have given it the
name of scotoma scintillans. We are fortunate in having an accurate
description of this form of the affection by so competent an observer
as Foerster, who has frequently experienced it in his own person. In
his case the phenomena last from fifteen to twenty-five minutes, and
commence with the appearance of dimness in both eyes, which gradually
increases to a defect of the field of vision lying to one side of the
fixation-point. This is soon followed by a flickering which commences
in a zone around the scotoma, and increases centrifugally until it
assumes the form of an arc with the convexity outward, {780} the
flickering rarely extending beyond the vertical line which separates
the two halves of the field of vision. When it has reached the outer
limits of the field, it generally diminishes and fades away. From a
consideration of the celebrated case of Wollaston, it is probable that
transient hemianopia may be caused by some temporary congestion of a
brain tumor, but in the majority of instances it is certainly allied to
functional disorders like migraine. Transient hemianopia has been
observed in several members of the family of one of the writer's
patients, all of whom are subjects of consecutive neuralgic headaches.
Leber has observed the same thing. Brewster and Quaglino have
attributed it to a retinal anæmia, but a careful ophthalmoscopic
examination in two well-marked cases (that of Foerster and one related
by Mauthner) failed to show any retinal changes. In some cases the
well-marked hemianopic character of the attack speaks for its
intracranial origin, which may be temporary derangement of the
circulation, possibly in the optic tracts. Dianoux tells us that in his
case the attack could be cut short by keeping the head down between the
legs. In some of the cases which the writer has seen it may be cut
short by a liberal dose of whiskey.
Affections of the Third Pair.
While a few words on the pathology of the third and sixth nerves tend
to throw light on our knowledge of cerebral localization, they will
also spare a good deal of needless repetition in the detailed
discussion of the eye symptoms which accompany many well-marked
diseases. Complete paralysis of the third nerve may be caused by
pressure on its filaments at the base of the brain without other
symptoms. Where it occurs with hemiplegia of the opposite side of the
body and other cerebral symptoms, it is usually due to pressure on the
nerve where it runs beneath the cerebral peduncle: according to
Nothnagel,[207] this localization of the disease is still more certain
when paralysis of the facial and hypoglossal nerves exists on the same
side as the hemiplegia (that is, on the side opposite to the third-pair
paralysis). Hughlings-Jackson[208] remarks that the symptoms are only
positively diagnostic of a lesion in the neighborhood of the peduncle
when they appear simultaneously, but when they are concentric to each
other they may be due to an affection of the cranium. Ollivier and
Little[209] have each related a case where this group of symptoms has
not originated in any lesion in the peduncle, but has been caused by an
abscess of the middle and posterior lobes, which secondarily involved
these parts.
[Footnote 207: _Topische Diagnostik der Gehirnkrankheiten_, p. 198,
1879.]
[Footnote 208: In Russell Reynolds's _System of Medicine_, vol. ii.,
1872.]
[Footnote 209: Robin, _Des Troubles oculaires dans les Maladies de
l'Encephale_, p. 95.]
DOUBLE THIRD-PAIR PARALYSIS.--Double third-pair paralysis is rare, but
might be produced by any cause acting on both peduncles. Kohts gives a
case where such paralysis was caused by a tumor of the size of a
cherrystone limited exactly to the posterior tubercles of the
quadrigeminal body. Nothnagel remarks that paralysis of corresponding
branches of the third pair point to the corpora quadrigemina as the
seat of lesion. On the other hand, Panas[210] relates a case of
absolute {781} immobility of the eyes where the only demonstrable
lesion at the autopsy was a meningo-encephalitis in the lower part of
the cerebellum. Robin describes a case of double third-pair paralysis
where there were ptosis and dilatation of the pupils, with a loss of
all power to move the eyes except downward and outward. The diagnosis
was that of an interpeduncular syphilitic gumma: there was complete
recovery. In the above case it is interesting to note that while the
paralysis of the left eye occurred previous to that of the right, the
eye last attacked was the first to regain its motions.
[Footnote 210: Cited by Robin, _loc. cit._, p. 74.]
PTOSIS.--Paralysis of the branch of the third pair which supplies the
levator palpebræ, when it exists without any lesion of the other
branches or where it is coincident with hemiplegia of the opposite
side, is frequently held to indicate a cerebral lesion, which may be
either cortical or have its seat in the nucleus of the nerve. According
to Grasset,[211] when the lesion is cortical it is situated in the
parietal lobe in advance of the angular gyrus. The localization is by
no means well made out. Coignt[212] has shown that it is not always
crossed, for in 5 out of 20 cases mentioned by him it existed on the
same side as the paralysis. Steffen[213] gives a case of double ptosis
with sluggish pupils where there was complete control over the muscles
moving the globe, the autopsy showing a tubercle in the tubercular
quadrigemina which had entirely effaced their normal structure.
[Footnote 211: Robin, p. 104.]
[Footnote 212: _Thèse de Paris_.]
[Footnote 213: _Berliner klin. Wochenschrift_, No. 20, 1884.]
OPHTHALMOPLEGIA INTERNA.--In those cases where affection of the orbital
ophthalmic ganglia can be excluded, paralysis of the pupillary and
ciliary branches of the third pair is, according to Jonathan
Hutchinson, due to an affection of the twig which runs through the
lenticular nucleus in the striated body. It is frequently associated
with paralysis of the internal rectus, and may be accompanied by
paralysis of the ciliary muscle. After diphtheritis there is often
paralysis of the ciliary muscle, with prompt reaction of the iris. The
writer is not aware of any recorded instance of apoplexy or other
sudden onset of disease which would enable us to localize exactly the
centre for pupillary contraction. According to Hughlings-Jackson, we
may have in apoplexy the most varied states of the pupil (normal,
dilated, or contracted) independent of the seat of lesion: he further
states that upon calling loudly to the patient there will sometimes be
a transient pupillary dilatation. When we look at the state of the
pupils as part of general symptomatology, we find a most perplexing
confusion and contradiction: in fact, notwithstanding the quantity of
material both in ancient and modern literature, we are far from having
any satisfactory account of the subject. This is partly due to our
imperfect knowledge of the anatomy of the brain and to the great
difficulty of estimating exactly pupillary changes, and partly
carelessness and want of a proper system of observation. The data have
for the most part been hastily compiled, without a minute statement of
concomitant symptoms or the stage of the disease in which they are
developed. Usually, they have been made without any proper means for
illuminating the pupil or apparatus for correctly magnifying and
observing its motions. In most cases the want of knowledge of the more
common sources of error, such as a difference in the size of the pupils
owing to difference in the refraction of {782} the eyes, posterior
synechiæ, or other intraocular changes, has invalidated the results.
ASSOCIATED MOVEMENTS OF THE HEAD AND EYES.--In many central lesions,
associated movements of the head and eyes are present, and, although
the exact channels through which they are propagated are for the most
part unknown, yet certain groups of these clinical symptoms are of so
frequent occurrence as to be recognized and admitted by almost all
observers. Vulpian and Prévost were the first to enter into a minute
study of these movements. Vulpian in his lessons on the physiology of
the nervous system (1866) states that "in cases of unilateral cerebral
lesion, whether it be situated in the cerebral hemispheres, the
striated bodies, the thalami optici, the cerebellum, or in the
different parts of the isthmus cerebri, whether the lesion be softening
or hemorrhage, there is often, immediately after the attack, a
deviation of the eyes at the time of development of the hemiplegia. The
deviation is in general transient, and may last either a few minutes or
hours or several days. The eyes are usually turned in a direction
opposed to that of the hemiplegia; thus, if the right side is
paralyzed, both eyes are turned toward the left. On regaining
consciousness the patient, if he tries to turn his eyes to the right,
may either be entirely unable to move them, or, what is more usual, may
succeed in bringing them to the middle of the palpebral aperture
without being able to turn them farther in that direction. Does this
phenomenon depend on a paralysis of the muscles which cause conjugate
motion of the eyes, or on a spasmodic contraction of their opponents,
over which they are unable to triumph?" He further states: "I incline
strongly to the latter view, as it is in accordance with what we
observe in animals. The analogy of the phenomena goes still farther:
often the head of the patient has made a more or less marked movement
of rotation on the neck--a movement as the result of which the face is
turned toward the non-paralyzed shoulder, and in the cases where we
cannot observe a deviation by turning back the head into its normal
position, an action which can often be only brought about by
considerable effort."
Prévost[214] has since formulated the following laws for cases of
hemiplegia: "I. When the hemiplegic looks toward his lesion and away
from his paralyzed side, the lesion is hemispherical. II. If he looks
toward his paralyzed side, the latter is situated in the
mesencephalon." This statement coincides with the facts reported by
Hughlings-Jackson, Charcot, and many other observers. Nothnagel[215]
admits that this is the rule, but quotes as an exception to it a case
of his own where, with right hemiplegia and head turned to the right,
the eyes were turned to the left, the autopsy showing an extensive
patch of softening in the left hemisphere which involved the frontal
convolutions, the central convolution, and the adjacent white
substance. In addition, he cites Bernhardt as giving other exceptional
cases which, in his own judgment, "considerably diminishes the
diagnostic value of the phenomenon." Landouzy and Coignt[216] have
attempted to define still more clearly the diagnostic value of the
associated movements of the head and eyes, and, while they admit the
correctness of these laws of hemiplegic paralysis, they add that in
convulsive {783} cases in which there are symptoms of irritative
lesions the above rules are reversed. To explain such cases they lay
down the following rules: first, that if the patient looks toward his
convulsed side the lesion is situated in the hemisphere of the opposite
side; and second, if he looks away from his convulsed side (or toward
the lesion) there is an irritant lesion of the mesencephalon.
[Footnote 214: _Thèse de Paris_.]
[Footnote 215: _Topische Diagnostik der Gehirnkrankheiten_, p. 580,
1879.]
[Footnote 216: _Thèse de Paris_, 1878.]