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Conjugate eye deviation after acute hemispheric stroke Delayed recovery after previous contralateral frontal lobe damage.

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BRIEF COMMUNICATIONS
Conjugate Eye Deviation
after Acute Hemispheric
Stroke: Delayed Recovery
after Previous Contralateral
Frontal Lobe Damage
Israel Steiner, MD, and Eldad Melamed, MD
~~
In 42 patients with acute unilateral ischemic or hemorrhagic hemispheric stroke, conjugate eye deviation toward the lesioned side was usually of brief duration. It
subsided within 48 hours in 24 patients (57%) and lasted
no longer than 5 days in 38 patients (!No%Early
). disappearance of conjugate eye deviation was an isolated phenomenon and preceded any improvement in the other
focal neurological deficits, which persisted in their initial severity. In 6 additional patients with stroke, conjugate eye deviation was remarkably prolonged, lasting
from 13 to more than 43 days. In all 6 there was evidence
for preexisting damage to the contralateral frontal region. Our study suggests that early recovery of conjugate eye deviation in patients with acute hemispheric
stroke may be mediated by the contralateral unaffected
frontal eye field.
Steiner I, Melamed E Conjugate eye deviation
after acute hemispheric stroke: delayed recovery
after previous contralateral frontal lobe damage.
Ann Neurol 16:509-511, 1984
'\\
Conjugate eye deviation (CED) toward the side of the
lesion is one of the focal neurological manifestations
associated with acute completed hemispheric stroke.
Clinical experience indicates that, unlike other neurological signs, CED is usually of short duration and
subsides early after stroke onset r2, 31. Furthermore,
CED subsides despite frequent persistence of accompanying focal neurological deficits. The mechanism responsible for the relatively short duration of strokeinduced CED, particularly when there is no apparent
change in the location and size of the causative lesion,
is unknown. We have recently encountered 6 patients
with stroke in whom CED was unusually prolonged. In
all 6 there was evidence of previous damage to the
contralateral frontal lobe. The clinical features of these
From the Department of Neurology, Hadassah University Hospital
and Hebrew University-Hadassah Medical School, Jerusalem, ISrael.
Received Oct 10, 1983, and in revised form Feb 16, 1984. Accepted
for publication Feb 19, 1984.
Address reprint requests to Dr Melamed, Department of Neurology, Hadassah University Hospital, POB 12 000, Jerusalem 91 120,
Israel.
patients are described and compared with those observed in an additional 42 consecutive patients with
stroke who had CED as part of their neurological syndrome.
Patients and Methods
Records of all patients hospitalized with acute hemispheric
(ischemic or hemorrhagic) stroke from September 1981
through June 1983 were reviewed for the presence of CED
as part of the clinical syndrome. For the purpose of this study,
CED was defined as spontaneous and persistent extreme
turning of the eyes in the horizontal plane toward the
lesioned hemisphere. We determined the period elapsing
from stroke onset to disappearance of CED, defined as the
time when at rest, without visual or auditory stimuli, eyes
returned to midline position. Only patients who were followed and examined daily in the hospital long enough to
permit determination of the natural history of CED were
included. Patients with evidence for recurrent stroke or seizures during hospitalization were excluded.
Results
CED was present in 42 patients with acute hemispheric
stroke. These included 22 men and 20 women ranging
in age from 35 to 87 years (mean age, 69 years).
Twenty-eight patients had cerebral ischemia-infarction
(in 4 it was due to emboli of cardiac origin), and 14
suffered from intracerebral hematoma. Stroke involved
the right hemisphere in 23 patients (55%). Thirteen
patients (3 1%) died during hospitalization.
CED was transitory in all 42 patients and lasted several hours to 11 days. In 24 patients (57%) CED subsided within 48 hours, and in 38 (90%) it lasted no
longer than 5 days (Figure). All 42 patients had additional signs, such as aphasia, hemiplegia, and hemihypesthesia. The disappearance of CED was unrelated to
the outcome in the case of the other neurological manifestations. In 12 of 29 survivors there was mild to
marked improvement in the neurological deficits during hospitalization (ranging from 16 to 90 days), but
none showed complete recovery. In all 12 disappearance of CED preceded any improvement in the other
focal neurological signs. In 17 survivors there was no
neurological improvement throughout hospitalization
except for the disappearance of CED early after stroke
onset.
Alterations in consciousness were present on admission in 34 patients (23 patients were somnolent, 8 were
stuporous, and 3 were comatose). In 20 patients recovery of consciousness paralleled improvement in CED.
In 11 patients improvement in consciousness preceded
changes in CED, and in 3 patients who were fully alert
at stroke onset, stupor developed after disappearance
of CED.
Computed tomographic (CT) scanning was performed on 33 of the 42 patients. In 26 it showed cerebral infarctions (14 patients) or hemorrhages (12 pa-
509
15
-
10
-
The clinical and CT features of the 6 patients who
had uncommonly prolonged CED are summarized in
the Table.
m
Discussion
1 2 3 1 S 6 7 8 9 1 0 1 1
CEO Duration ( d a y s I
Duration of conjugate eye deviation (CED) in 42 patients with
acute unilateral hemi.rphericstroke.
tients) of various sizes involving the frontal lobes. In 3
patients stroke (hemorrhagic in 2) was located in the
thalamus or internal capsule. In 4 patients no lesion was
seen on the CT scan. Five patients had repeat CT scans.
In all 5 the first study showed acute damage to the
frontal region. The second CT scan, performed 1 to 3
months later, demonstrated atrophic lesions in the
same area. In all, however, CED disappeared within 5
days of stroke onset. In only 3 patients was there CT
evidence of old infarctions in the hemisphere contralateral to the acute stroke. These were located in the
occipital (2 patients) and parietal (1 patient) areas but
not in the frontal region.
In most patients with unilateral ischemic or hemorrhagic cerebral stroke, CED is of brief duration and
usually (9096 of cases) lasts no longer than 5 days.
More important, CED subsides when the other focal
neurological signs, such as hemiplegia and aphasia, persist in their initial severity. CED in such patients with
stroke is probably due to involvement of the frontal
eye field and its connections by the acute vascular lesion. This region is involved in the control of eye
movements to the contralateral side in the horizontal
plane {I, 4 , 61. Although it has been suggested that
CED can accompany damage to almost any area of the
cerebral hemisphere [ 2 , 71, it seems to be associated
mainly with frontal lesions [S, 101. In most of our patients the C T scan showed an infarct or hemorrhage
located in the frontal lobe.
Early improvement in CED is most likely not a result
of recovery of the damaged frontal eye field, because
both other focal neurological deficits and CT findings
usually remain unaltered. The present study suggests
that the frontal eye field in the contralateral intact
hemisphere takes over the function of the affected
frontal eye field. In 6 patients with acute unilateral
hemispheric stroke in whom there was evidence of previous damage to the contralateral frontal eye field (usually by another stroke), the duration of CED was markedly prolonged. Latto and Cowey [S] have produced
similar findings in monkeys with frontal eye field le-
Clinical Features in Patients with Acute Stroke and Marked Prolonged Conjugate Eye Deviation
Patient
No.
Age (yr),
Sex
Type and Location
of Acute Vascular
Lesion
Previous Contralateral
Hemispheric Lesion
Neurological Deficit
1
72, F
R frontal infarction
L frontal old infarction
2
85, F
R frontal infarction
L frontal old infarction
3
62, F
R frontoparietal
L frontal old infarction
4"
81, M
hematoma
L hemispheric stroke
R hemispheric stroke
5
80, F
L frontal infarction
R frontal old infarction
6
80, M
R basal ganglia hematoma with intraventricular extension and
frontoparietal edema
L frontal old infarction
"Computed tomographic scan not obtained.
F = female; M
=
male; R
=
right; L = left; CED = conjugate eye deviation.
510 Annals of Neurology Vol 16 No 4
October 1984
Onset
Outcome
Somnolence; L
hemiplegia
Somnolence; L
hemiplegia
Stupor; quadriplegia
Mild dementia;
L hemiplegia
L hemiparesis
Stupor, asphasia; R
hemiplegia
Somnolence, aphasia;
R hemiplegia
Coma; L hemiplegia
Dementia;
quadriplegia
Death
Dysphasia; L
hemiparesis
Dementia; L
hemiplegia
Duration
of CED
(days)
25
41
31
43
17
13
sions. Unilateral damage produced a brief, transient
shift of the eyes to the ipsilateral side. On recovery,
removal of the second frontal eye field resulted in a
longer-lasting deviation of the eyes to the newly
lesioned hemisphere. There is evidence that each frontal eye field may be involved in conjugate, horizontal
eye movements, not only in the contralateral, but also
in the ipsilateral direction. Electrical stimulation of the
frontal eye field in the alert monkey produces mainly
contralateral but also ipsilateral eye movements [9].
There are focal increases in regional cerebral blood
flow in the frontal eye field during contralateral as well
as ipsilateral horizontal eye movements in human subjects, indicating neuronal activation of this region [b].
Eye movements recover even after unilateral hemispherectomy [lo], and CED does not occur with
slowly progressive destructive or degenerative lesions
of the frontal area. Taken together, the data suggest
that disappearance of CED after acute stroke involving
the frontal lobes and their connections depends on the
integrity of the contralateral frontal eye field in patients
with acute hemispheric stroke.
References
1. Daroff RB, Troost BT: Supranuclear disorders of eye movements. In Glaser JS (ed): Neuro-ophthalmology. Hagerstown,
MD, Harper & Row, 1978, pp 201-218
2. De Renzi E, Colombo A, Faglioni P, Gibertoni M: Conjugate
gaze paresis in stroke patients with unilateral damage: an unexpected instance of hemispheric asymmetry. Arch Neurol
39~482-486, 1982
3. Gay A, Newman N, Keltnerj, Stroud M: Eye Movement Disorders. St Louis, Mosby, 1974, p 20
4. Hoyt WF, Frisen L Supranuclear ocular motor control: some
clinical considerations- 1974. In Lennerstrand G, Bach-Y-Rita
P (eds):Basic Mechanisms of Ocular Motility and Their Clinical
Implications. Wennergren International Symposium Series, Vol
24. Oxford, England, Pergamon, 1975, pp 379-392
5. Latto R, Cowey A: Fivation changes after frontal eye field lesions
in monkeys. Brain Res 30:25-36, 1971
6. Melamed E, h s e n B: Cortical activation pattern during saccadic
eye movements in humans: localization by focal cerebral blood
flow increases. Ann Neurol 5:79-88, 1979
7. Pasik P, Pasik T: Oculomotor functions in monkeys with lesions
of the cerebrum and the superior colliculi. In Bender MB (ed):
The Oculomotor System. New York, Harper & Row, 1978, pp
201-218
8. Pedersen RA, Troost BT: Abnormalities of gaze in cerebrovascular disease. Stroke 12:251-254, 1981
9. Robinson DA, Fuchs AE: Eye movements evoked by stimulation of frontal eye fields. J Neurophysiol 32:637-648, 1969
10. Troost BT, Weber RB, Daroff RB: Hemispheric control of eye
movements. I. Quantitative analysis of refixation saccades in a
hemispherectomized patient. Arch Neurol 27:44 1-448, 1972
Supported in part by a grant donated by the Blaustein family for
cerebrovascular research.
~
~
NOTES AND LETTERS
Genetic Testing
in Huntington’s Disease
William C. Koller, MD, PhD,
and Joyce Davenport, MSW
The presymptomatic detection of gene carriers of Huntington’s disease has not been previously possible 151.The recent
discovery of a genetic marker linked to the Huntington gene
has made it likely that a reliable predictive test or even gene
identification itself will soon be available {4]. Controversy
exists regarding the value and ethics of such testing, however
{2,3, 111. To assess the views of persons at risk, we surveyed
7 5 individuals with an affected parent, asking whether they
would take a test to identify the presence of the Huntington’s gene. O n the questionnaire they could respond yes, no,
or undecided, and state the reason for their choice. Of the 75,
61 (81%) indicated a desire to take the test when it became
available. Reasons for their willingness included elimination
of uncertainty about the future and the ability to plan for it
intelligently, to decide whether to have children, and to know
if they could have passed the gene o n to their children. Nine
(12%) indicated that they would not take the test, stating that
they did not want to know a future that they perceived as
hopeless. Five (7%) were undecided. In another survey of an
American population, 77% (307 of 339) indicated willingness to take a predictive test 181. In the United Kingdom
80% (80 of 100) and in Wales 56% (51 of 91) of individuals
surveyed wished to take such a test El, 12). In an Australian
study, 84% of at-risk subjects were found to have a positive
attitude toward a predictive test [lo].
The results of a reliable genetic test would produce two
groups: those who have escaped the disease and those who
possess the gene. It has been suggested that the latter group
will be deprived of all hope and be prone to despondency and
possible suicide {9]. Several authors have stated, therefore,
that predictive testing should not be offered to anyone until
effective treatment or a cure becomes available [b, 91. This
view is centered o n the presumed need to protect individuals
from the knowledge that they will develop an incurable disease. H o p e is, however, far from totally lost. Symptoms may
not occur for many years, and useful lives are possible for
some time even after the onset of symptoms. T h e opportunity to cope, prepare, and plan appears for many individuals
more desirable than the burden of uncertainty. Treatment
(neuroleptics) already exists for control of some symptoms.
Laypersons also express the realistic hope that future research
advances will lead to suppression of the illness within their
lifetimes. Currently there are no data that indicate any poten-
511
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