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Aneurysms and third nerve palsies.

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values. An EEG revealed a modified hypsarrhythmic pattern
consisting of high-amplitude disorganized background activity and superimposed multifocal spikes (Figure). Some decrease in seizure frequency occurred after corticotropin treatment was started, but increased again when corticotropins
were discontinued.
At 19 months of age, the patient was brought to our clinic
with recurring infantile spasms. He showed a developmental
delay of 12 months, no localizing o r lateralizing signs, normal
head size and other measurements, no depigmented skin lesions, and normal results from neurological and funduscopic
examinations. An EEG revealed epileptic abnormalities of
generalized polyspike and wave complex. A cranial computed tomographic scan revealed a large area of lucency with
a small high-density area in the right temporal lobe.
A low-grade astrocytoma in the right temporal lobe was
removed totally by right temporal craniotomy. The child was
maintained seizure free postoperatively on phenytoin. An
EEG five weeks after surgery revealed a normal sleep pattern
with no epileptogenic abnormalities or disorganized background activities. Throughout the following year, the child
was seizure free and continued to progress developmentally
at a normal or near normal rate. At 2 years and 7 months of
age, neurological examination showed no abnormalities.
It has been suggested that the infantile spasm syndrome
consists of three necessary characteristics: the spasms themselves, developmental delay or neurological deterioration,
and hypsarrhythmia as a specific EEG abnormality. In our
review of the literature, we found only 4 reported cases of
tumor in the central nervous system with infantile spasm
syndrome [l-41. Of these, only one patient became seizure free and continued to develop at a normal rate after total
removal of a choroid plexus papilloma [l]. Charlton [2) reported a patient in whom postmortem examination disclosed
a left hemispheric glioma. A patient with ganglioglioma who
died postoperatively was reported by Gabriel [ 3 ] . Gastaut
and colleagues [ 4 ] studied cranial computed tomographic
Pretreatment electroencephalogram .Ibowing modijed bypjurrhythmic pattern consisting of high-amplitude disorganized
background activity and superimposed niult$)cal spikes.
scans in 37 infants and children with infantile spasm syndrome and found one calcified tumor of the basal ganglia.
In our patient, a single neoplasm in the temporal lobc
produced multifocal epileptiform discharges with disorganized background activities on EEG. The patient’s course
illustrates the importance of a thorough diagnostic evaluation
of infantile spasms.
Department of Pedtatrto
Osaka Unzoevsity Medical School
FukuJhima 1-1-50. Fukujhima-Ku
Osaka,Japan 553
References
1. Branch CE, Dyken PR: Choroid plexus papilloma and intitntilc
spasms. Ann Neurol 5:302-104, 1979
2. Charlton MH: Infantile spasms. In Myoclonic Seizures. Arnsterdam, Excerpta Medica, 1975, p 116
3. Gabriel YH: Unilateral hemispheric ganglioglioma with intantiltr
spasms. A n n Neurol 7:287-288, 1980
4. Gasraut H, Gastaut JL, Regins H, et a1 Computerized tomog.
raphy of West’s syndrome. Dev Med Child Ncurol 20.21-27,
1978
Aneurysms and Third
Nerve-Palsies
James R. Keane, M D
Two aphorisms regarding the relationship between oculomotor nerve palsies and aneurysms have guided clinicians:
(1) an isolated fixed pupil is (almost) never the result of aneu-
696 Annals of Neurology Vol 14 N o 6 December 1983
rysmal compression and (2) a third nerve palsy with complete
pupillary sparing rarely is caused by an aneurysm. The recent
report by Kissel and colleagues { 11 that pupillary sparing may
be present in as many as 14% of oculomotor palsies caused
by posterior communicating artery aneurysms prompted me
to review my own experience.
Of 34 patients I examined personally who had third nerve
paresis and an appropriate angiogram-proved carotidposterior communicating artery aneurysm, none had complete pupillary sparing. The pupil was fixed in all 16 patients
with complete external (muscles supplied by the third nerve)
ophthalmoplegia. Of 18 patients with partial external
ophthalmoplegia, the pupil was fixed in 2 and partially involved in 16. Six of 7 patients with unruptured aneurysms
had complete ophthalmoplegia, whereas only 10 of 27 patients had complete palsies when first seen following subarachnoid hemorrhage.
My experience with third nerve palsies caused by aneurysms agrees with the following findings of Kissel and
colleagues El): (1) third nerve palsies are frequently incomplete initially, (2) partial pupillary involvement often accompanies partial external ophthalmoplegia, and ( 3 ) complete pupillary sparing does not occur in patients with total
external ophthalmoplegia.
That none of our patients with partial external ophthalmoplegia had complete pupillary sparing contrasts with the experience of Kissel and colleagues. It is likely that our patients
delayed longer before corning to the hospital. Indeed, since
about one-third (11 of 34 patients) were first examined five
or more days after the onset of ptosis or diplopia, some, like
4 patients of Kissel and colleagues, could have developed
pupillary involvement in this interval. In addition, because
the study of l s s e l and colleagues was based on a retrospective chart review, some patients with subtle pupillary
involvement may have been categorized as having pupillary
sparing.
The risk of selective arterial catheter angiography in patients with pupil-sparing third nerve palsies, a group likely to
have widespread vascular disease, might well be higher than
mentioned by Kissel and colleagues [l], althe 1 to
though refinements in digital subtraction arterial angiography
may eventually provide sufficiently high resolution with
fewer complications.
In our population, patients having oculomotor nerve palsies with complete pupillary sparing and, possibly, those with
complete external ophthalmoplegia and partial pupillary involvement are unlikely to harbor causative aneurysms. The
suggestion of Kissel and colleagues that patients be observed
closely for pupillary involvement during the first week is
eminently sensible. At our hospital, however, the risk of
angiography for patients with isolated pupil-sparing third
nerve palsies appears likely to exceed any benefits.
Department of Neurology
Los Angeles County-University of Southern Calzfornia
Medical Center
Los Angeles, C A 90033
Reference
1. Kissel JT, Burde RM, Klingele TG, Zeiger HE: Pupil-sparing
oculomotor palsies with internal carotid-posterior communicating artery aneurysms. Ann Neurol 13:149-154, 1983
Pupil Sparing in
Oculomotor Palsy and
Claude Bernard Horner
Syndrome
Michel Serdaru, MD, Monique Schaison, MD,
and Fransois Lhermitte, M D
Pupil sparing in oculomotor palsy has usually allowed the
physician to rule out a compressive origin and avoid arteriography. Kissel and colleagues [2) found normal pupils in 14%
of their patients with aneurysm-related third nerve palsy.
Among their criteria for normal pupils, they included equal
size and equal reaction of both pupils on clinical examination.
Nadeau and Trobe [3] correctly point out the possibility of
real pupillary sparing related to the insidious growth of a
compressive lesion and to the relative resistance to pressure
of smaller pupillomotor fibers. The simultaneous occurrence
of parasympathetic and sympathetic paresis leading to “apparent pupil sparing” is often considered only in cavernous sinus
lesions. This antagonistic situation can be observed also in
internal carotid-posterior communicating artery aneurysms,
as in the following report.
A 65-year-old mildly hypertensive woman was admitted to
the hospital with a three-month history of progressive right
oculomotor nerve palsy. Examination confirmed severe and
isolated external dysfunction with apparent pupil sparing. At
rest, the patient had equal pupils 2 mm wide, which reacted
normally and equally to direct light and to near stimulus. In
very dim light, however, a relative myosis could be observed
on the right side. Pharmacological testing with pilocarpine
produced a bilateral decrease of 1 mm in pupil size; cocaine
4% and atropine did not cause mydriasis on the right side,
but the left pupil reacted normally with extreme mydriasis. A
right-sided arteriogram revealed an internal carotidposterior communicating artery junction aneurysm 1 mm in
size. We suggest that in the assessment of normal pupils
in external oculomotor palsies, dim light examination and
pharmacological tesrs including cocaine should always be
used.
There is little to add to the comprehensive review of
Nadeau and Trobe. Among the scarce examples of intraaxial
lesions of the third nerve related to stroke, we would like to
add the early clinical pathological report of Achard and Levi
111, describing a complete oculomotor nerve palsy due to
lacunar infarction of the mesencephalon.
Department of Neurology and Neuropsychology
Htpital de la Salpitri6re
47 Blvd de PH@ital
75634 Paris Cedex 13, France
References
1. Achard C , Levi L Paralysie totale et isolee du moteur oculaire
commun par foyer de ramolissement pedonculaire. Rev Neurol
646-648, 1901
2. Qssel JT, Burde RM, Klingele TG, Zeiger HE: Pupil-sparing
oculomotor palsies with internal carotid-posterior communicating artery aneurysms. Ann Neurol 13:149-154, 1983
Notes and Letters 697
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