Copyright 0 Micnksgaard 1997

Acra Neurol S c a d 1997: 96.732-336
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ACTA NEUROLOGICA
SCANDINAVICA
ISSN 0001-6314

Case report

Selective vertical saccadic palsy from
unilateral medial thalamic infarction:
clinical, neurophysiologic and MRI
correlates
Deleu D. Selective vertical saccadic palsy from unilateral medial thalamic
infarction: clinical, neurophysiologic and MRI correlates.
Acta Neurol Scand 1997: 96: 332-336. 0 Munksgaard 1997.

D. Deleu
Department of Clinical Neuropharmacology and
Neurology. College of Medicine, PO Box 35.
Sultan Qaboos University, Al-Khod. Muscat-123.
Sultanate of Oman

Background - Impairment o f vertical gaze has been attributed to lesions
involving the neural structures at the mesodiencephalic level. Objective Eye movements were studied in a patient with a unilateral paramedian
thalamic infarction documented by MRI. Case description - A 63-year-old
man presented 3 days after sudden onset vertical diplopia and hypersomnia.
Eye movements were studied with electro-oculography and revealed
impairment of vertical saccades with sparing of the vertical vestibulo-ocular

reflex, vertical pursuit, Bell’s phenomenon and vertical optokinetic
nystagmus. MRI scan revealed a circular zone of altered signal intensity,
suggesting infarction, in the paramedian ventral part of the right thalamus.
Conclusions - This case demonstrates that a unilateral lesion mainly
affecting the dorsomedial nucleus of the thalamus can result in selective
impairment of vertical saccades and suggests that the corticofugal fibers
mediating vertical saccades traverse in the medial thalamus en route to the
I rostral midbrain.

Abnormalities of vertical gaze in addition to hypersomnia and amnesia are the cardinal features of
paramedian thalamic infarction (1-4). In these
reports, the vertical gaze palsy was, however,
almost invariably due to coexisting lesions at the
mesodiencephalic junction, in which the neural
structures for vertical gaze (rostral interstitial
nucleus of the medial longitudinal fasciculus
(riMLF), the interstitial nucleus of Cajal, the
nucleus of Darkschewitsch, and the posterior
commissure and its nuclei) are located (5, 6).
Sixteen cases of vertical gaze palsy from pure
medial thalamic infarction have been reported (1,
7-15). However, none of these patients presented
with selective impairment of vertical saccades due
to unilateral paramedian infarction.
Eye movements were studied in a patient with a
discrete unilateral infarction in the paramedian
part of the right thalamus. Correlations of defective
vertical saccades with magnetic resonance imaging

332

Key words: eye abnormalities; ocular motility
disorders; thalamus; magnetic resonance imaging;
ophthalmoplegia: saccades
Dirk Deleu, M.D.. Ph.D.. College of Medicine,
PO. Box 35, Sultan Qaboos University, Al-Khod.
Muscat-123, Sultanate of Oman
Accepted for publication July 15, 1997

(MRI) findings indicate the role of the thalamus in
the mediation of vertical saccades in humans. To
our knowledge,,this pattern of abnormal eye movements has not been reported in association with a
unilateral infarction at this location.
Case report

A 63-year-old rnan presented 3 days after an acute
onset vertical diplopia and hypersomnia. There was
no history of cerebral infarctions or other neurological diseases and the patient had no risk factors
for stroke. Neurological examination on admission
showed an alert patient with normal speech ability
and cognitive functions. In particular, there was no
anterograde or retrograde amnesia, confabulations
or perseverations.
Neuro-ophthalmologic examination revealed
normal visual acuity, fields and fundi. The pupils
were equal, and normally reactive to light and near

Vertical saccadic palsy
stimuli. There was no ptosis. There was no eye
deviation in primary position. Vertical voluntary saccades were reduced above and below the midposition, with sparing of the vertical vestibulo-ocular
reflex (VOR) and vertical pursuit (Fig. 1). Bell's
phenomenon, vertical optokinetic nystagmus ( O W )
and all types of horizontal eye movements were
preserved.
The other cranial nerves were unaffected. There
were no sensory and motor deficits, all tendon
reflexes were normal and plantar responses were
flexor.
Blood pressure was 160/80 mmHg. Cardiopulmonary examination was normal. There were
no cervical bruits. The remainder of the general
examination was also normal.
All serum laboratory values were within the
normal range. Digital subtraction angiography of
carotid and vertebral arteries was normal. MRI
scans were obtained 4 days after the onset of
symptoms. MRI images (5.00mm thick slices in the
axial and coronal planes and 3.00 mm slices in the
sagittal plane) revealed a circular zone of altered
signal intensity, suggesting infarction, in the right
paramedian ventral part of the thalamus (Fig. 2).
There were no supratentorial, cerebellar or other
brainstem lesions. The mesodiencephalic region
was well visualized in all dimensions and appeared
to be unaffected.
Two months after the onset of the vertical
diplopia the patient recovered completely, except
for slightly restricted downward saccades.

1

t

C

v

A

1s

Fig. 1. Vertical eye movement recordings from the right eye.
(A) Vertical visually guided saccades. The upward deflection
indicates the upward movement of the target and the downward deflection the downward movement of the target. A 20"
upward saccade is slow and hypometric. A backdrift towards
the primary position was occasionally observed. The downward
saccade back to the midposition is very slow. A 20" downward
saccade was also very slow and hypometric. (B) Vertical smooth
pursuit was normal. (C) Optokinetic nystagmus (V:downward,
A:upward) was normal in both directions.

Method

Oculographic study

On the 4th day after the onset of the symptoms,
eye movements were recorded, and assessed qualitatively, while the patient was cooperative and
attentive. He was not taking any other medication
than acetylsalicylic acid and dipyridamole. Direct
current electro-oculography was used for each eye
separately, in darkness, with the head immobilized
(16). The following movements were studied: (a)
horizontal and vertical visually guided saccades,
performed by instructing the patient to look as fast
as possible at a suddenly appearing 10" or 20"
lateral or vertical target; (b) horizontal and vertical
smooth pursuit induced by instructing the patient
to follow a target moving sinusoidally with an
amplitude of k20 at 25 or 40"d.The saccades and
smooth pursuit were elicited in a dimmed room.
Horizontal (or vertical) OKN was elicited with a
whole-field stimulus consisting of vertical (or horizontal) black and white stripes moving horizontally
(or vertically) at 10, 20 and 3OO.s-l across a screen

covering 60" of the visual fields. Horizontal VOR
were studied in complete darkness on a vestibular
chair rotating at 0.40 Hz with an amplitude of 20"
on each side of the midline. Vertical vestibular eye
movements were induced by active vertical head
shaking with the head erected (active vestibuloocular and otolith-ocular reflexes). Bell's phenomenon was tested by manually resisting the patient's
attempts at forced eye closure.
Discussion

This patient presented with loss of vertical saccades
with preserved vertical pursuit and VOR from a
right paramedian thalamic infarction. There was no
clinical evidence of midbrain involvement, particularly of the posterior commissure and/or riMLF,
which would typically result in loss of both saccadic
and pursuit vertical eye movements (17). Furthermore, MRI did not reveal any ischemic lesions
at the mesodiencephalic level, midbrain or lower
333

Deleu

(C)

Fig. 2. (A) Magnification of T,-weighted axial brain MRI scan at the level of the pulvinar, dorsomedial, ventral posteromedial
and ventral posterolateral nucleus of the thalamus. The lesion is compatible with an infarction (arrow) and affects mainly the right
dorsomedial nucleus. (B) Magnification of TI-weighted coronal brain MRI image showing the lesion (arrow) affecting mainly the
right dorsomedial and centromedian nuclei without extension to the rostra1 midbrain. (C) Parasagittal T,-weighted MRI image of
the brainstem depicting the localization of the lesion (arrow) in the thalamus.

334

Vertical saccadic palsy

brainstem. Topographically,the infarct was localized
with the use of corresponding anatomical sections
as described by Tatemichi et al. (4) and by MRI
neuroanatomy (18). According to these methods, a
section through the pulvinar, dorsomedial, ventral
posteromedial and ventral posterolateral nuclei of
the thalamus corresponded to the level of the infarction, with the core of the ischemic lesion affecting
the right dorsomedial nucleus of the thalamus.
Vertical gaze palsy has previously been reported
in infarctions limited to the paramedian thalamus
(1, 7-15). In only 6 of these patients vertical gaze
palsy was characterized by selective impairment of
vertical saccades (1, 9-13) and, unlike in our
patient, the lesions were all bilateral. However, all
of these cases except for 1 (12), were documented
by CT scan, making precise anatomoclinical correlations difficult. The patient reported by Swanson
& Schmidley (12) presented with selective vertical
saccadic palsy and paramedian infarction on MRI.
However, the lesion was also bilateral and the
rostral midbrain was not visualized properly due to
the limited quality of the images.
The cerebral cortical commands for saccades are
delivered to the brainstem via two parallel corticofugal projections (19). An anterior pathway
projects from the human homologue of the frontal
eye fields directly, and indirectly to the riMLF (19).
This pathway primarily generates intentional saccades. The posterior pathway is responsible for
reflexive saccades and projects from the parietal
cortex to the superior colliculus and subsequently
to the riMLF (19). In our patient, impairment of
vertical saccades was therefore attributed to the
thalamic lesion per se by interruption of the corticofugal fibers as they traverse the medial thalamus
en passage to the rostral midbrain structures subserving vertical saccades. The precise arrangements
of these converging pathways in the thalamus
remain, however, uncertain. In accordance with the
prevailing concept, that supranuclear vertical gaze
palsy spares the VOR, our patient had preserved
VOR in all directions (20). These data also indicate
that, at least at the thalamic level, the pathways for
vertical smooth pursuit project separately from the
pathways for vertical saccades. Moreover, it seems
that unilateral disruption of corticofugal projections mediating vertical saccades can result in
vertical saccadic palsy.
In addition to vertical gaze palsies, unilateral
paramedian infarction can also cause hypersomnolence, amnesia and “frontal syndrome” (13). The
anatomical structures involved in hypersomnia are
the midline thalamic nuclei in particular the medial
anterior part of the centromedian nucleus and
inferior region of the dorsomedial nucleus, which
form part of the rostral extension of the midbrain

reticular activating system (13). The incomplete
expression of the syndrome in our patient might
probably be related to the discreteness of the
thalamic lesion.
The medial part of the thalamus is supplied by
perforating branches that arise from the arterial
segment between the bifurcation of the top of the
basilar artery (basilar communicating artery) and
the posterior communicating and posterior cerebral arteries (2). The paramedian thalamic arteries
arise from the basilar communicating artery. Occasionally, both paramedian thalamic arteries arise
from a single common stem originating from one
or the other basilar communicating artery. This
variation in vascular anatomy of the region probably accounts for the variable clinical presentation
(2). In addition, sparing of the midbrain is probably
explained by the fact that the superior and inferior
paramedian mesencephalic arteries arise separately
from each other from the basilar communicating
arteries.
In conclusion, more sophisticated methods than
the one used for investigation of this patient’s
vertical eye movements might have revealed additional subtle abnormalities. However, this would
not substantially jeopardize our conclusion that a
unilateral lesion mainly affecting the dorsomedial
nucleus of the thalamus can result in selective
impairment of vertical saccades.
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