INTRACRANIAL ARTERIAL ANEURYSMS BY Joln Woodworth Henderson, MD, MS, PH.D.

114 Pages·2005·10.55 MB·English

INTRACRANIAL ARTERIAL ANEURYSMS
A STUJDY OF 119 CASES, WITH SPECIAI REFERENCE
TO THE OCULAR FINDINGS
BY Joln WoodworthHenderson, M.D., M.S., PH.D.*
THE PRESENT CENTURY lhas witnessed a rapid advance in the diag-
nosis and treatIment of intracranial disease. Beginning in 1923 wvith
Symonds's observations (i), increasing avareness of the diagnostic
picttire presented by patients wvith intracranial arterial aneurysms
lhas led steadily to earlier recognition and treatment of these
lesions. The ophtlhalmnologist may be acutely involved wvitlh the
problem of diagnosis, since many patients wvith intracranial
aneurysms complain first of ocular symptoms.
The topograplhical demnonstration of related visual field defects
by Jefferson in 1937 (2) and the clinical correlation of the ocular
signs and symptoms by WValsh and King in 1942 (3) wvere followved
in 1944 by Dandy's monograph (4). This publication wvas a mile-
stone in the diagnosis and treatment of intracranial arterial aneu-
rysms. The introduction of intracranial angiograplhy by Moniz in
1927 (5) offered an additional diagnostic aid, and his first arterio-
graphic diagnosis of intracranial aneurysm wras reported in 1933
(6). Acceptance of this metlhod in the United States vas slowv be-
cause of difficulties wvitlh the contrast media and fear of complica-
tions. WVithin the past fifteen years, however, the procedure has
gained favor, and in its improved form it is nowv in routine use in
most leading inedical centers.
Thle cases of XValsh and King (3), of Dandy (4), and ofJefferson
(2) wvere presented almost entirely without the aid of arterio-
graphic findings. No similar series has been analyzed from the
ophtlhalmologic viewvpoint since use of intracranial angiography
has becomie wvidespread. Tlherefore, it appears worth whliile to study
stucli a group of cases. This paper wvill be concerned vith that task.
*Associate Professor of Ophthalmology, University of Michigan, Ann Arbor,
Michigan.
350 John Woodworth Henderson
HISTORICAL BACKGROUND
IJntil the present century, recognition of intracranial aneurysms
occurred almost exclusively at necropsy. McDonald and Korb, in
1939 (7), wrote an excellent review in which they tabulated the
previous cases in the literature and credited Morgagni with the
first post-mortem description of carotid aneurysms in 1761. It is
probable that Jonathan Hutchinson in 1875 (8) achieved the first
successful ante-mortem diagnosis of an aneurysm. His patient gave
a picture of ophthalmoplegia and trigeminal involvement that was
classical for subclinoid aneurysm, and the diagnosis was confirmed
at autopsy eleven years later. However, there is in the literature a
remarkable article by Bartholow, of the Medical College of Ohio,
which appeared in 1872 (9). He described in detail the involve-
ment of the cranial nerves by aneurysms of the circle ofWillis, in-
cluding the findings of ptosis, convergent strabismus, and a dilated
pupil, as well as signs of involvement of the trigeminal nerve.
However, diagnosis was still made chiefly at post-mortem exami-
nation until 1923, when Symonds (i) published an outstanding
paper on the clinical study ofintracranial aneurysms. He described
5 cases in which the diagnosis of intracranial aneurysm was made
before death, with post-mortem confirmation in 2 of the 5. More
important, however, was his insistence on considering the findings
in cases of intracranial aneurysm as (1) neighborhood signs, (2)
signs of the disease causing the aneurysm, and (3) signs of leakage
from the sac. He emphasized that a history of an attack of sub-
arachnoid hemorrhage with signs of a tumor at the base of the
brain is sufficient evidence for the diagnosis of intracranial aneu-
rysm. In the same publication, Cushing (io) set forth criteria
which have not changed in the intervening years. In his words,
an aneurysm should always be considered in a differential diagnosis
when an apoplectic attack or a series ofattacks ofcomparatively sudden
onset is followed by symptoms pointing to the internal carotid in its
intracranial portion, namely, a unilateral oculomotor palsy with
ptosis, and occipito-frontal pain with lowered sensitivity of the upper
trigeminal skin field. Should there be in addition subhyaloid retinal
hemorrhages, and should the cerebrospinal spaces be found to contain
free blood (or . . . xanthochromia in the intervals between periods of
leakage), a diagnosis is reasonably certain.
Intracranial Arterial Aneurysms 351
The following year, Kirby (ii) reported on a patient with a
supraclinoid aneurysm diagnosed at post-mortem, and reviewed
4 cases which he found in Cushing's writings, including the origi-
nal one that had stimulated Symonds's interest. In 1929 Pfingst
and Spurling (12) drew the attention of the American Ophthal-
mological Society to the role played by intracranial aneurysms in
the production of ocular palsies. After reviewing the literature,
these authors described 2 cases which had come under their obser-
vation, but without post-mortem or surgical confirmation.
With the appearance of Jefferson's article in 1937 on involve-
ment of the visual pathway by intracranial aneurysms (2), the in-
terest of ophthalmologists was quickened. Jefferson analyzed 66
previous cases from the literature and added 12 cases of his own
with visual field findings. His discussion of localization by means
of visual field defects has not been improved upon since that time.
The cases were grouped according to involvement of the visual
radiation and cortex, compression of the optic tract, involvement
of the optic nerves, and effects upon the chiasm. The visual path-
way was affected in 12 of 53 cases of his personal series (22.6 per-
cent). The following year he published an outstanding paper de-
tailing the syndromes produced by subclinoid or cavernous sinus
internal carotid aneurysms (13).
Widespread knowledge among ophthalmologists in this country
has been fostered by the outstanding article of Walsh and King
in 1942 (3). They presented in detail the ocular signs of intra-
cranial saccular aneurysms and noted the diagnostic importance of
aberrant oculomotor nerve regeneration. By experimental work
they demonstrated that collateral arterial circulation prevented
blindness in the trapping operation.
Since that time many reports have appeared in the ophthal-
mologic literature, including the paper of Igersheimer on binasal
hemianopsia (14) and the report of Alpers and Schlezinger on
posterior communicating arterial aneurysms (15). A tremendous
neurosurgical bibliography has ensued, and for this the reader is
referred to Hamby's recent book on intracranial aneurysms (16).
CASE MATERIAL
The series of i19 cases comprising this report has been compiled
from the records ofthe University Hospital fromJanuary, 1937, to
35 Joh/n Woodztworth Henderson
I
October, 1954. Before this period the diagnosis of intracranial
arterial aneurysm wvas seldom made, and no records wvere obtained
through the diagnostic code before 1937, although the code in its
present form began in 1926. This fact reflects the growving interest
in the diagnosis followving the introduction of systematic intra-
cranial angiograplhy in the University Hospital in January of 1941,
as reported by List, Burge, and Hodges (17). All the patients in
thie series wvere treated clinically, eitlher for stubarachnoid hemor-
rhage whliichi led to fatal outcome before diagnostic studies couild
be instittuted, or for an aneurysmn of proved diagnosis. The ma-
jority wvere studied arteriograplhically, and many received active
treatment. In all cases the diagnosis vas confirmed either by intra-
cranial angiography, by sturgical exposure, by autopsy findings, or
by varying combinations of these three forms of evidence.
The series studied includes only those cases in which an arterial
aneurysm arose from the intracranial carotid artery, the basilar
and vertebral arteries, or from the branches of the circle of WVillis
interconnecting them. Angiomaita and other arteriovenous anom-
alies, as vell as carotid-cavernous fistuilas, have been excluded. No
cases have been included from the routine autopsy records, since
it is knowvn that a definite percentage of such lesions is found in-
cidentally atpost-mortem.
The distribution of the aneurysms is presented in Figure 1.
There was a total of 125 such lesions in the 119 patients, including
4 patients with multiple aneurysms in entirely separate sites (Cases
12, 22, 83, and 102). Of the other cases, 3 showved multiple dilations
at the same site (Cases 19, 78, and 98) and therefore wvere not tabu-
lated as to different locations. Lesions were located on the midline
in 22 cases, on the anterior communicating artery in 17, and on
the basilar trunk or its branches in 5. Lesions vere lateralized in
102 cases, 6i wvith lesions located on the right side, and 41 on the
left. Thle origin of the aneuirysm in one case muist remain unspeci-
fied becauise the exact site couild not be determined even at post-
mnortem dissection. It definitely arose from the region of the circle
of WVillis (Case iio).
Altlhouighi it is known that certain aneuirysmiis take origin from
bifurcations of the vessels comiiprising the circle of XVillis, no at-
tempt wvas made to classify the cases on this basis. In most instances
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354 John Woodworth Henderson
Total Number
* ~~~Midline
Anterior Communicating 17
Basilar 5
Right side 6i
? ( Left side 41
UnspecifiedI
125
Lateralized Lateralized
Left Side Right Side
3 Subclinoid Carotid 2
14 Supraclinoid Carotid 24
II Anterior Cerebral 12
9 Middle Cerebral '3
3 Posterior Communicating 4
I Posterior Cerebral 3
o Superior Cerebellar I
O VTertebral 2
41 6i
FIGURE 1. DISTRIBUTION OF 125 ANEURYSMS IN 119 PATIENTS
arteriographic evidence pointed more strongly to one vessel of a
bifurcation than to the other, and where surgical exposure or post-
mortem evidence was available, one of two possible vessels was im-
plicated to a greater extent. In each case the choice of vessel has
been made on this basis rather than by making additional sub-
groupings.
The rostral half of the circle of Willis was involved by 105 an-
eurysms, while the caudal portion and its tributaries were affected
by only 19. The unspecified case (119) has not been included, but
it would most likely be listed as more rostral in location.
Age distribution in the 1 19 cases studied is presented in Table 1.
The highest incidence occurred in the age group thirty-one to fifty,
Intrtacranial Arter-ial Aneurysms 3355Z55
wvitlh the yotungest patient eiglht muonthis old anid the oldest seventy-
tlhree years. There wvere 104 patients of fifty years or younger, and
only 15 above the age of fifty.
The occurrence of aneurysmis by sex distribtution is slhown in
TABLE 2. DISTRIBUTION OF PATIENTIS IBY SEX
1iale Fenmale
Internal carotid
Subclinoid I 4
Supraclinoidb 12 23
Anterior communicating 13 4
Anterior cerebrala 14 8
Middle cerebral 14 7
Posterior communicatinga 2 4
Posterior cerebral 2 2
Basilar I 4
Superior cerebellar I 0
Vertebral I I
Unspecified I O
62 57
allIclL(des
one Negro patient.
bIncltides three Negro patients.
Table 2. There wvere 62 male patients as compared wvith 57 female,
an insignificant difference. However, if one ,groups the subclinoid
and supraclinoid internal carotid aneurysms, an incidence of 27
female versus 13 male patients is evident. If the anterior cerebral
and anterior communicating groups are examined, there appears
to be a preponderance of male patients. Twenty-seven aneuirysms
occurred in males, as contrasted wvith 12 in females.
Only 5 Negroes were included in the group, the remaining 114
patients all being of the wsvhite race.
The relationslhip of subaraclhnoid hemorrhage to the series is of
interest (Table 3). Of the 1i 9 cases, 94 showved evidence of bleed-
ing into the subarachinoid spaces either in the recent history, at the
timne of admission to the lhospital, or dturing the lhospital cotirse. In
most instan-ces this diagnosis wvas confirmed by lumiibar ptuncture,
and in only a fewv did the clharacteristic clinical history and findings
stuffice as evidence. There wvas no evidence of bleeding in the stub-
clinoid internal carotid group, wsvhich wvas to be expected, since
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Intracranial Arterial Aneurysms 357
suich aneuirysmis are slhielded from the stibarachnoid space vithin
the cavernous sinus. Of 35 supraclinoid internal carotid aneu-
rysms, 26 had bled, while all of thie middle cerebral and anterior
commtunicating lesions slhowved signs of subarachnoid hemorrhlage.
Of the 22 anterior cerebral aneturysms, i8 hiad a positive history
and findings for bleeding. A high percentage of the other cases also
presented this picture.
The relationslhip of ftindtuscopic findinas to subaraclhnoid lhem-
orrhage is also presented in Table 3. Papilledema wvas found,
either monocular or binocuilar, in 24 of the 94 cases wvith sub-
araclhnoid bleeding. Nineteen of the cases wvith papilledema also
showved retinal hemorrhages, either superficial flame-shaped or
stubhyaloid in type, or both. In 14 cases hemorrhages wvere seen in
the ocular fundi wvithout an associated edema of the optic nerve
head. Therefore, 36 patients of the 94 wvith a suibarachnoid hemor-
rhiage had associated fundtuscopic findings, an incidence of 38.3
percent.
The relationslhip of intracranial angiography to the positive
diagnosis of an aneutrysm is slhowvn in Table 4. Diagnostic evidence
TABLE 4. RESULTS OF ARTERIOGRAPHY
Number of
Cases
Positive diagnosis, unconfirmed 34
Positive diagnosis, surgically confirmed 48
Positive diagnosis, autopsy confirmed 4
Negative diagnosis, surgically confirmed 5
9I
Percent of positive diagnosis 94.5
Diagnostic errors
Aneurysm disclosed, but wrong site
noted 6
MIissed ruptured anetrysm, found
another I
AMissedl clotted aneuLrysm 5
Complications after arteriography
Immmediate 3
Delayed 2
358 John Woodworth Henderson
by arteriography only wvas presented in 34 cases. In 48 cases a
positive angiographic diagnosis was confirmed by surgical ex-
posure. Of the 48 diagnoses, 9 wvere furtlher verified at post-mortem
examination. WVithin this surgically proved group were 7 cases
in whiclh errors wvere disclosed. In one patient (Case i8) three
successive angiograms lhad been performed. The first wvas reported
as negative; the second, six years later, disclosed an aneurysm, but
in the wvrong location. On the third attempt, four months later,
the lesion wvas demonstrated at the site confirmed by surgical ex-
posure. In a second patient (Case 22), a rtuptured aneurysm of
the right intracranial internal carotid wvas missed, btut a second was
demonstrated on the riglht middle cerebral artery. Both- wvere vis-
ualized at sturgery. In 5 other cases a positive diagnosis ofaneurysm
was given, but wvith errors in differentiating anterior communi-
cating locations from anterior cerebral locations, an understand-
able mistake since many wvere located at the junction of the tvo
vessels. These wvere all confirmed eitlher by surgical exposure, by
post-mortem examination, or botlh.
In 4 cases, a positive arteriograplhic diagnosis wvas clhecked by
autopsy findings alone. In '3 of the 4, the findings wvere confirmed,
and in the one case whliiclh wvas missed (Case 96), an anomnalous kink
in the riglht anterior cerebral artery wvas called an aneurysm of the
anterior communicating artery, wvliile a rtupttured aneuirysm of the
riglht middle cerebral branclh wvas found at post-mortem.
In r cases the presence of aneurysm wvas not demonstrated by
intracranial angiography, althouglh it wvas proved by exposure of
the lesion at surgery. In all of these, the aneurysm wvas seen to be
clotted fuill, and therefore not visualizable.
In stunmmary, arteriograplhy wvas performed in a total of 91 cases.
A positive diagnosis vas made in 86 of the 91 cases, or 94.5 percent.
There wvere minor errors in 7 of these patients, as pointed out
above, but a positive diagnosis wvas made. In only 6 cases wvas the
lesion missed entirely, and in 5 of the 6 tlhrombosis of the aneuirysm
prevented disclostire.
No angiograplhic exaimination was done in 28 cases. One of these
(Case 112) wvas diagnosed at surgery, while the remainder vere
fouind at atutopsy, the patients having (lied before definitive stuidies
could safely be started.