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Australian Journal ofOphthalmologj. (1981).9. pp. 113-1 15

PAINFUL THIRD NERVE PALSY: HOW NOT TO MISS AN INTRA-CRANIAL

ANEURYSM
JOHN L. CROMPTON FRACO, FRACS
Neuro-Ophthalmology Unit, Royal Adelaide Hospital

COLIN E. MOORE FRACO, FRCS

Neuro-Ophthalmology Unit, Royal Adelaide Hospltal

Abstract
Case histone$ of two patients, each of whom presented to an ophthalmologist with early signs of
aneurysm, are presented Prompt referral of aneurysm patients allows mvestigation, dmgnosis and
treatment before catastrophic neurological and ocular sequelae ensue
Patients presenting to an ophthalmologist with diplopia, ptosis or limitation of eye movement due to
third nerve paresis or paralysis should be carefully screened for the presence of intra-cranial aneurysm,
when pain IS an accompanying feature

Ctise Reports no impairment of sensation in the face. Fundus

Case 1: A 23-year-old single woman was referred
to an ophthalmologist because of severe
continuous left retro-orbitaf pain, associated with
dilated left pupil. Aneurysm was not suspected.
Eventually, partial left ptosis developed.
On the day of hospital admission, she was
wakened at 3.00 a.m. by more severe headache,
associated with complete ptosis. By morning the
headache had spread to the nuchal area and she
had vomited several times.
On hospital admission, moderate neck stiffness
was found. The left pupil was dilated compared
with the right, and showed only very slight reaction
to light. Left divergent squint was present, 15-20'
on near fixation. The left eye elevated minimally,
and showed moderately impaired adduction and
depression. Diplopia, characteristic of third nerve
paresis, was present. The fourth cranial nerve was
not affected and no other cranial nerve
abnormality was detected. In particular, there was
examination was unremarkable.
Left percutaneous carotid arteriography
revealed a 9 mm saccular aneurysm projecting
posteriorly from the internal carotid artery just
below the origin of the posterior communicating
artery.
At operation the neck of the aneurysm was
shrunk with bipolar diathermy and a clip placed
across the neck. The sac was aspirated to relieve
pressure on the third nerve. Recovery was prompt
and the only abnormality persisting after operation
was a dilated left pupil.
The diagnosis was not made by the
ophthalmologist who was the specialist of first
referral. Fortunately, no serious ocular or general
disability resulted.
Case 2: A 29-year-old married female draftsman
had had periodic typically migrainous left-sided
headaches for a number of years. She then
developed for the first time severe headache of a

Repriiir i.cc/i/e.\r.c. Dr J. L. Crornpton. 104 Brougham Place. North Adelaide, South Australia. 5006

P A I N i . U L T H I R I ) N E R V E P A L S Y : H O W N O T TO MISS A N I N T R A - C R A N I A L A N E U R Y S M 113

different kind, centred around her left eye and
orbit and upper jaw. Two weeks later her husband
noted that her left pupil was dilated. Sinus X-rays
organized by her family doctor were normal. She
then was examined by a dentist and an
orthodontist, both of whom found no pathology.
The original family doctor recommended that she
return to work, where she again suffered very
severe left-sided headaches, so she consulted a
second local doctor. Despite ptosis of the left upper
lid she was again advised to return to work. The
patient requested referral to an ophthalmologist,
but this was not arranged by the local practitioner
as “his eye specialist was at golf‘.
She returned to work but became so distressed
by pain that she consulted her mother’s general
practitioner, who referred her at once to an
ophthalmologist. A CT scan was obtained within
two days, which was normal. Carotid angiography
was booked for the following week but was
brought forward on request.
On the day prior to angiography, the headaches
intensified, and after losing consciousness for a
short period she awoke with paraesthesiae of her
right arm and leg. She then became unconscious
again. She was admitted to the Royal Adelaide
Hospital in deep coma with extensor responses in
both upper limbs, fixed dilated left pupil and
bilateral large sub-hyaloid haemorrhages.
The combination of orbital and retro-ocular
pain followed by progressive third nerve palsy,
coma and sub-hyaloid haemorrhages are
pathognomonic . of ruptured posterior
communicating aneurysm. This diagnosis was
confirmed by angiography which also revealed a
left-sided subdural haematoma.
In the Intensive Care Unit she was ventilated
and given high dosage of steroid and intravenous
glycerol to combat cerebral oedema. An initial
episode of ventricular fibrillation was recognized
soon after admission and treated promptly and
effectively. She regained consciousness after four
days, when examination revealed nominal
dysphasia, almost complete left third palsy with
partial left fourth and sixth nerve palsies, relative
right homonymous hemianopia and massive
sub-retinal and sub-hyaloid haemorrhages. Seven
days after admission she had focal seizures
114
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involving her right arm. In the meantime she was
treated with anticonvulsant drugs and epsilon
aminocaproic acid in order to’ inhibit further
rupture of the aneurysm.
Left fronto-temporal craniotomy was performed
three weeks after admission and the posterior
communicating artery aneurysm was clipped. Her
post-operative course was stormy and necessitated
the insertion of a Richmond screw to monitor
intra-cranial pressure. Slow recovery of
consciousness occurred. Massive sub-hyaloid
haemorrhages had burst through into the vitreous
on each side with less than 6/60 vision in the right
and 6/6 in the left eye where the haemorrhage was
largely in the nasal vitreous. In the succeeding
weeks the left ptosis recovered but gross aberrant
regeneration of her third nerve occurred.
Because of long-term anticonvulsant
medication, the patient is unable to hold a driving
licence for the next three years.
Comment
The patient with intra-cranial aneurysm may
present because of pressure on neighbouring
structures, for example, diplopia and pupillary
paresis from pressure on the oculomotor nerve, or
visual impairment from optic nerve or chiasmal
compression. This is the ideal time for diagnosis,
before rupture with subarachnoid haemorrhage
and systemic collapse.
The ophthalmologist may well be the specialist
to whom the patient is initially referred, so he
should be alert for signs indicating the presence of
aneurysm.
There are numerous diagnostic types of third
cranial nerve paresis.’ The presence of a trunk
lesion (involvement of pupil, eyelid and other
ocular muscles) with peri-ocular pain suggests
posterior communicating artery aneurysm or
diabetes mellitus as causes. Pupillary involvement
is almost invariable in the former because of the
dorsal location of the pupillary fibres in the nerve
trunk (see diagram). Walsh and Hoyt have said
that isolated internal ophthalmoplegia as the
presenting sign of posterior communicating
aneurysm is “exceptionally rare”.* In their
experience “unilateral paralysis of the third nerve
with pupillary involvement in an individual who
AUSTRALIAN J O U R N A L OF O P H T H A L M O L O G Y

Diagram of the relationships of the right
oculomotor nerve (111) viewed from above. The
intimate relationship of the osterior communicating
artery aneurysm to the ocuLmotor nerve is shown.
(ACA anteriorcerebral artery, ON optic nerve,
A Co A anterior communicating artery, OC optic
chiasm, A ch A anterior choroidal artery, OT optic
tract, PS pituitary stalk, MCA middlecerebral artery,
P Co A posterior communicating artery, TENT
tentorium cerebelli, PCA posterior cerebral artery,
SCA superior cerebellar artery).
has complained of sudden severe pain in and
about the eye always suggests carotid aneurysm”.
The pupil almost always is spared in diabetic
oculomotor palsy, probably because of the central
axial location of the causative le~ io n .~
PAINFUL THIRD NERVE PALSY: HOW NOT TO MISS AN INTRA-CRANIAL ANEURYSM
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These patients with third nerve paresis and pain
around the eye should be urgently and properly
investigated. Neurological assessment, skull X-ray,
carotid angiography and CT scan should be
performed without delay. Angiography is the
investigation of choice because of accuracy of
diagnosis4and provision of information regarding
feeding vessels and neighbouring circulation.
Computerised tomography, while useful as a
screening procedure, should not be the only
investigation, as aneurysms less than 4 5 mm in
diameter in the anterior part of the circle of Willis
will be missed by the first and second generation
scanners because they cut thicker brain “slices”.
Later generation Scanners with thinner “slices” will
be much more accurate in this regard. Larger
aneurysms in the posterior part of the circle of
Willis will also escape CT scan detection because
of their proximity to bone.
Vitreous and optic pathway haemorrhage with
visual loss and subarachnoid haemorrhage with
resultant epilepsy and death can result if diagnosis
of intra-cranial aneurysm is delayed. Early
diagnosis should allow a curative neuro-surgical
procedure thereby preventing serious visual and
general disability.
Acknowledgement
The assistance of Mr P. R. Oatey, F.R.A.C.S.
(art-work) is gratefully acknowledged.
References
Kestenbaum, A: “Clinical Methods of
Neuro-Ophthalmologic Examination”, Grune &
Stratton, New York, 1961,p . 275 et seq.
Walsh, F B, Hoyt, $ F: “Clinical Neuro-
0 hthalmology” Williams & Wilkins, Baltimore; Third
Elition, 1969,Vol. 1, 252.
Asbury, A K,Aldredge, H, Hershberg, R, Miller Fisher
C: “Oculo-motor Palsy in Diabetes Mellitus: A
Clinico-Patholo ical Study”, Brain 1970, 93: 555.
Perrett, L V,B u i J W D: “The accuracy of Radiolog in
Demonstratin Ru tured Intra-cranial Aneurysms”, grit
J Radiol, 32: E5, 1$59.
I15