SOMATOSENSORY EVOKED POTENTIALS IN SENSORY STROKES/Robinson et al
20. Rosenberg NL, Roller R: Computerized tomography and pure sensory stroke. Neurology (Ny) 31: 219-220, 1981
21. Landi G, Anzalone N, Vaccari U: CT scan evidence of posterolateral thalamic infarction in pure sensory stroke. J Neurol Neurosurg Psychiat 47: 570-571, 1984 (Letter)
22. Chiappa KH: Evoked potentials in clinical medicine. New York:
Raven Press, 1983
23. Chiappa KH, Choi S, Young RR: Short latency somatosensory
evoked potentials following median nerve stimulation in patients
with neurological lesions. Progr Clin Neurophysiol 7: 264-281,
1980

823

24. Goldie WD, Chiappa KH, Young RR, Brooks EB: Brainstem auditory and short-latency somatosensory evoked potentials in brain
death. Neurology (Ny) 31: 248-256, 1981
25. Chiappa KH, Ropper AH: Evoked potentials in clinical medicine
(part 2). New Engl J Med 306: 1205-1211, 1982
26. Celesia GG: Somatosensory evoked potentials recorded directly
from human thalamus and sml cortical area. Arch Neurol 36:
399-405, 1979
27. Mauguiere F, Desmedt JE, Courjon J: Neural generation of N18
and P14 farfield somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations. EEG
Clin Neurophysiol 56: 283-292, 1983

Amnestic Syndrome and Vertical Gaze Palsy: Early
Detection of Bilateral Thalamic Infarction
by CT and NMR
R. A. SWANSON, M . D . , AND J. W . SCHMIDLEY, M . D .
SUMMARY A 27 year old woman with mitral valve prolapse presented with somnolence, bilateral
Babinski signs, and grasp reflexes. As somnolence cleared, vertical gaze palsy and Korsakoffian memory
deficit were apparent. Initial CT scan was normal, but NMR scan 24 hours after the onset of symptoms
revealed prolonged T2 relaxation in medial thalami bilaterally, facilitating diagnosis of bithalamic infarction. Subsequent CT scans delineated infarction in the vascular territory of the paramedian thalamic
arteries. Previous clinical reports and the neuro- and vascular anatomy underlying this syndrome are
reviewed, including cases that suggest a relationship to the syndrome of transient global amnesia.
Stroke Vol 16, No 5, 1985
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IN 1978 MILLS AND SWANSON 1 described a patient with persistent vertical oculomotor apraxia, somnolence, and severe impairment of memory, presumably the result of bilateral medial thalamic infarction.
Two and one-half years after the acute event a CT scan
revealed a widened third ventricle, and small, approximately symmetric zones of low absorption in both dorsomedial thalami.
We have recently seen a patient with a nearly identical syndrome, and were able to use NMR imaging to
detect bithalamic lesions within 24 hours of admission.
High resolution CT scanning documented the evolution of bilateral dorsomedial thalamic infarctions over
a ten day period.

Case Report
A 27 year old woman awoke on the day of admission
complaining of headache, double vision, nausea and
unsteadiness. She returned to bed and two hours later
was barely arousable. She was taken to the emergency
room where she was lethargic and vomited several
times.
She did not use any medications, illicit drugs, or
cigarettes. Blood pressure was 110/70, heart rate 80,
From the Department of Neurology, University of California, San
Francisco, San Francisco, California.
Address correspondence to: R. A. Swanson, M.D., Department of
Neurology, M-794, University of California, San Francisco, San Francisco, California 94143.
Received August 9, 1984; revision #1 accepted February 21, 1985.

respiratory rate 18, and temperature 36°C. General
physical examination was unremarkable with the exception of a late systolic click with grade 3/6 apical
systolic murmur. Peripheral pulses were full throughout. There were no bruits or cutaneous lesions. Fundi
were normal.
The patient was stuporous but arousable with vigorous verbal or physical stimuli. When awakened she
was able to follow simple commands. She did not
speak spontaneously but was able to nod "yes" or
"no". Ocular axes were skewed in the vertical plane,
the left eye resting lower than the right, with full horizontal extraocular movements to doll's head maneuver. Pupils were 3 mm bilaterally and reactive. Corneal responses were brisk. Palate was midline, with brisk
elevation to gag. The limbs were paratonic. She moved
all limbs spontaneously, and withdrew from noxious
stimuli appropriately. The tendon reflexes were brisk;
bilateral extensor plantar responses and grasp reflexes
were present. There were no meningeal signs.
Twenty-four hours later the patient was much less
obtunded and was able to answer questions, although
still tending to sleep if not stimulated. She knew her
name, the year, her home address, and that she was in a
hospital. The skew deviation had resolved. Lateral
gaze was normal but she was unable to voluntarily
move her eyes up or down to command' or pursuit.
However, full ocular excursions in the vertical plane
were obtained with vertical doll's head maneuver.
Bell's phenomenon was present on attempted eye clo-

824

STROKE

sure and vertical optokinetic stimuli elicited nystagmus. There was mild ataxia of the right hand and leg
with normal strength and sensory functions.
Intravenous heparin anticoagulation was begun.
Over the next six days the ataxia and pathological
reflexes resolved and the patient became gradually less
somnolent. It became apparent that despite normal language, judgement, and arithmetic ability there was a
profound memory deficit. She could not remember the
names of test objects longer than two minutes. She was
unable to recall events of the day and frequently confabulated answers. Long term memory was affected in
an uneven fashion. Previous addresses, jobs, and acquaintances were recited accurately, but she was unable to give her phone number, and could not name
present or past California governors or U.S. presidents. Digit span, however, was excellent — seven
digits forward and five in reverse. Affect was characterized by indifference, facetiousness, and paucity of
spontaneous speech. The vertical gaze abnormality resolved by the 11th day after the ictus.
At one month her roommate described her as "taking
no interest in things" and as being deficient in personal
grooming. She "was easily upset by [trite] TV shows."
At three months she was felt by friends and family to
have entirely recovered, and on neurologic exam was
normal.

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Laboratory Studies
CBC, platelet count, sedimentation rate, urine homocysteine, serum protein electrophoresis, ANA titer,
and EKG were normal. 2D-echocardiogram revealed
mitral valve prolapse and mild aortic valve prolapse.
Anti-thrombin III activity was slightly low at 75%.
CSF obtained the day of admission and 9 days later
was entirely normal, including electrophoretic pattern
and IgG index. EEG (done on day 8) and visual evoked
responses were normal.
Radiographic Studies
A noncontrast CT scan with 5 mm images of the
posterior fossa (GE 8800 CT/T scanner) done on admission was normal. The following day a nuclear magnetric resonance (NMR) scan was done using a .35
Telsa cryogenic magnet (Diasonics MT/S imager) and
spin-echo imaging technique.2-3 Using parameters of
TE 2 sec, TR 28 and 56 msec, high signal intensity was
seen from both medial thalami (fig. 1). There was no
apparent abnormality in the midbrain although the 5
mm slices did not visualize the rostralmost area (red
nucleus). In addition to the thalamic lesions, high intensity was seen from a 5 x 5 mm area in the peripheral right cerebellar cortex and from a smaller region in
the anteromedial right cerebellum adjacent to the
fourth ventricle.
Four days later a second noncontrast CT scan revealed low density in the same thalamic areas described above, which became isodense after contrast.
At eight days contrast CT showed ring-like enhancement of the thalamic lesions (fig. 1). Using the fornices, third ventricle, trigone, pineal body and basis

VOL 16, No

5, SEPTEMBER-OCTOBER

1985

pedunculi as landmarks, the lesions were seen to involve the central nuclei bilaterally and the inferior and
anterior portions of the median nuclei bilaterally, with
extension into the ventrolateral formation on the left
(classification of thalamic nuclei as by Van Buren and
Borke).4 Both lesions in the right cerebellum also enhanced. Ventricular size was unchanged.
Vertebrobasilar angiography was performed on day
6. The left vertebral artery was small and could not be
cannulated; the other posterior fossa vessels were considered uniformly narrow but not definitely abnormal.
Following angiography heparin was discontinued and
the patient was discharged on aspirin, 325 mg qd.
Four months later a contrast CT scan was performed
with sagittal and coronal reconstructions (fig. 2). Standard axial views showed a widened third ventricle with
nonenhancing lucencies in medial thalami bilaterally.
Reconstructions placed the lesions primarily in the regions of the central and median nuclei, as observed in
the earlier studies.
Discussion
This case illustrates a stroke syndrome with interesting clinico-anatomic implications with respect to eye
movement and memory, and which can be difficult to
diagnose at presentation. In our patient consideration
was given to posterior fossa subdural hematoma, acute
disseminated encephalomyelitis, brainstem or cerebellar hemorrhage, and ischemic stroke. The NMR scan
was useful in the early diagnosis of ischemic vascular
disease, at a time when the CT scan was unrevealing.
During the period of hospitalization the diagnosis of
bithalamic stroke was confirmed. The patient's clinical course was that of infarction, with improvement
over days and near complete recovery over weeks. CT
studies documented the evolution of low density regions followed by contrast enhancement characteristic
of infarction.5 Prolonged T2 relaxation on NMR imaging is also indicative of early infarct, signifying increased brain water.2-5-6 NMR has been shown to detect infarction within two hours of ischemia.7
The additional lesions seen in the cerebellum, combined with the history of diplopia and nausea as early
symptoms, suggested an initial basilar artery occlusion
which later fragmented and gave rise to distal emboli.
At age 27, our patient's only apparent risk factor for
stroke was mitral valve prolapse.
The clinical presentation and CT findings in our
patient are similar to other cases recently published.1 *~13 These reports share radiographic evidence
of bilateral medial thalamic infarction and a clinical
picture of initial somnolence, Korsakoffian memory
deficit, and vertical gaze palsy. The vascular supply to
this region has been well described, consisting of perforating vessels originating from the arterial segment
between the bifurcation of the basilar artery and the
junction of the posterior communicating arteries.14-15
This segment has been designated the "mesencephalic
artery" or, more recently, the "basilar communicating
artery."14 The perforating vessels, termed "thalamic
paramedian arteries" by Percheron,15 can arise from

AMNESTIC SYNDROME AND VERTICAL GAZE PALSY/Swanson & Schmidley

825

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C

D
FIGURE 1. (A) NMR scan 24 hours after ictus revealing increased signal intensity from both medial thalami. TR2.0 sec, TE28
msec. (B) Noncontrast CT scan at 4 days. Subtle medial thalamic lucencies are now apparent. After contrast these became
isodense with normal thalamus (not shown). (C) and (D) Contrast CT scan at 8 days.

STROKE

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C

VOL 16, No

5, SEPTEMBER-OCTOBER

1985

D
E
FIGURE 2. Contrast CT at 4 months. (A) Axial view showing widened third ventricle and bilateral thalamic lucencies. (B)
Coronal reconstruction. (C) Sagittal reconstruction 1cm right ofmidline, (D) approximately at midline, and (E) 2cm left of
midline. (Arrows indicate areas of infarction.)

this segment in several ways. Frequently both arise
from a single common stem originating from one or the
other basilar communicating artery such that occlusion
of this stem can result in bilateral infarctions.
The territory supplied generally begins immediately
superior to the red nucleus and extends superiorly and
anteriorly into the thalamus to include the nuclei parafascicularis, mamillothalamic tracts, central nuclei,
and the inferior portion of the median (dorsomedial)
nuclei. In cases with pathologic confirmation, areas of
infarct match the described vascular distribution. "• 16~"
Such lesions affect structures believed necessary for
normal vertical eye movements as well as for memory
function.
The terms "vertical gaze palsy," or "paralysis," are
used by Buttner-Ennever and others20 to describe an
inability to voluntarily produce fast conjugate vertical
eye movement. Mills and Swanson1 employ the term
"vertical gaze apraxia" to emphasize preservation of
vertical eye movements with oculocephalic reflex or
Bell's maneuver. Christoff,21 however, in a clinicopathologic study, notes that there is not a consistent
relationship between site or size of lesions and preservation of reflex vertical eye movements. Vertical gaze
palsy has resulted from bilateral lesions of the rostral
interstitial nucleus of the media longitudinal fasciculus

(dorsomedial to the anterior pole of the red nucleus) or
unilateral lesions of the posterior commissure. "• M - n - n
The vascular supply to these areas is derived from the
same vessels as those supplying the medial thalamus,
i.e., the thalamic paramedian arteries.13
Victor et al24 has defined the amnestic syndrome
(Korsakoff s psychosis) as (1) impaired ability to retrieve information acquired before the onset of the
illness, invariably coupled with an inability to learn
(i.e., to form new memories); (2) a relatively minor
impairment of perceptual and conceptual functions;
and (3) a diminution of initiative and spontaneity.
Confabulation is a common but inconstant and often
transient feature. The memory and affective disorder
seen in the present case is well characterized by this
description.
Pathologic study of patients with amnestic syndrome associated with alcohol abuse revealed invariable and extensive involvement of the median (dorsomedial) thalamic nuclei and suggested this as the lesion
responsible for memory loss.24 Other evidence points
to a role for the hippocampus, mammillary bodies,
and/or temporal stem and their connections to the
thalamus.23 In the present case the median thalamic
nuclei appear less severely affected than the central
nuclei and the mammillothalamic tracts. In clinically

AMNESTIC SYNDROME AND VERTICAL GAZE PALSY/Swanson & Schmidley

similar cases this distribution of infarction has been
confirmed pathologically."1l6~19 Of note is that these
lesions interrupt input to the median nuclei from limbic
structures, perhaps resulting in a functional deficit of
the median nuclei similar to that produced by destruction of the median nuclei per se.12
The occurrence of amnesia as a result of bithalamic
stroke in this syndrome raises the possibility that transient memory loss may result from transient ischema in
this region. Transient global amnesia (TGA) is a well
recognized clinical entity of unknown etiology; both
seizure and bitemporal ischemia have been suggested.26- 27 Bithalamic stroke usually presents as amnestic
syndrome plus vertical gaze palsy and an initial period
of somnolence — the latter two features not generally
associated with TGA. However, three cases of TGA
with concomitant vertical gaze palsy have been reported.28 Variations in the stroke syndrome are also seen;
in some cases vertical gaze palsy is absent or subclinical12- '3 and in one case amnestic syndrome was the sole
abnormality at onset.8 CT abnormalities in these patients appear to spare the inferior thalamic and subthalamic regions. These clinical variations presumably
reflect the variable vascular anatomy of the region.
Thus transient occlusion or near-occlusion of the paramedian thalamic arteries at a common stem might, on
occasion, produce transient global amnesia.
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Although concurrence of the amnestic syndrome
and vertical gaze palsy is an unusual and almost pathognomonic entity, its recognition may be difficult
when somnolence or coma dominate the clinical picture acutely. In the present case early diagnosis was
facilitated by NMR scanning, and CT later localized
bithalamic infarction with sufficient resolution to permit correlation of the clinical findings to the recently
detailed vascular and neuro-anatomy of this region. In
conjunction with reports of similar cases, commonality with transient global amnesia is apparent, and a
possible etiology for that syndrome is suggested.
Acknowledgments
The authors thank Dr. Kenneth Nudleman, University of California
Irvine, for follow-up data, and Dr. Jack DeGroot, of the Departments of
Anatomy and Radiology, UCSF, and Drs. Robert O. Messing and Faith
Allen of the Department of Neurology, UCSF, for their assistance.

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