Neuroradiologv

Neuroradiology (1985) 27:414-419

© Springer-Verlag 1985

Presentation of bilateral thalamic infarction on CT, MRI and PET
H. Bewermeyer, H.A. Dreesbach, A. Rackl, M. Neveling, and W.-D. Heiss
Max-Planck-Institutftir neurologischeForschungund NeurologischeKlinikdes KrankenhausesKrln-Merheim,Krln, FRG

Summary. Paramedian thalamic structures and part
of the upper midbrain are frequently supplied by
posterior thalamoperforating arteries originating
from one common trunk. Local impairment of flow
entails a bilateral more or less symmetric thalamic infarction with varying involvement of the midbrain.
Diagnosis usually can neither be firmly established
on clinical grounds nor by angiography alone. In the
present series of four patients the two cases observed
before the CT era were diagnosed correctly only at
autopsy. Only one patient presented the classical
syndrome of hypersomnia, thalamic dementia, and
oculomotor nerve paralysis, while in the others clinical signs were probably masked by serious impairment of consciousness. In two cases X-ray computed
tomography and magnetic resonance tomography
(one case) afforded precise definition of infarct localization and size. Infarction in the described terminal vascular supply territory may be detected more
often by these modern diagnostic techniques than
anticipated from previous clinico-pathological experience as the underlying cause of coma in the elderly
- a group of patients at particular risk for low-flow
states. Positron emission tomography repeat studies
with 18F-2-fluorodeoxyglucose (one case) revealed
complex disturbances of brain energy metabolism;
correlative analysis of clinical function and metabolic patterns during the course of the disease may not
only advance individual prognostication but also
contribute to the understanding and localization of
brain function.
Keywords: Bilateral thalamic infarction - cerebrovascular pathology - computerized tomographic
imaging - brain glucose metabolism

Acute bilateral thalamic infarction used to be an elusive diagnosis as long as clinicans had to rely on neurological examinations and angiographic studies as
their main source of information. Accordingly, exact
topographic diagnosis in general was established at

autopsy only [13] as shown in two of the following
cases observed before the advent of X-ray computed
tomography (CT). The latter method and other modem computerized tomographic imaging techniques,
such as magnetic resonance imaging (MRI) and positron emission tomography (PET), have greatly advanced diagnostic accuracy as demonstrated by two
other cases.

Report of cases
Case I

A 66-year-old female with a history of hypertension
suddenly fell into a semicomatose state with dilated
unreactive pupils and plantar extensor reflexes.
ECG showed tachyarrhythmia with atrial fibrillation. Right retrograde brachial angiography revealed
no major abnormalities. There was progressive general slowing of the EEG during repeat studies. A few
days after onset of symptoms as the level of consciousness improved voluntary movements were
strong with only a mild left spastic hemiparesis present. However, the patient remained unable to open
or move her eyes and pupillary unresponsiveness
persisted. After developing pneumonia she died on
the twelfth day.
Postmortem examination disclosed ulcerating
mitral valve stenosis, an old cortical infarct of the
right temporal lobe, atherosclerotic plaque formation of the basilar artery close to the origin of the
posterior cerebral artery, and right and left posterior
communicating arteries of very small calibre. There
was a butterfly-shaped infarction of the medial parts
of both thalami (Fig. 1) and of the tegmentum.
Case 2

A 50-year-old male on getting up complained of
blurred vision and unsteadiness of gait. On admission he was found semicomatose with ocular diver-

415

Fig. 1. Case 1. Twelve-day-old bilateral symmetric medial thalamic infarction
Fig.2. Case 2. Seven-week-••d

bi•atera• butter•y-shaped infarct inv••ving media• tha•amic nuc•ei and midbrain tegmentum

Fig.3 a and b. Case3. a Bilateral inhomogeneous low-density lesions of medial and lateral thalamic structures extending to the internal capsule, b internal hydrocephalus and multiple small infarcted areas in both cerebral hemispheres

answer simple questions; bilateral complete ophthalmoplegia persisted, while movements of extremities
were not obviously impaired. Several days later right
hemiplegia evolved; he developed dysarthria, dysphagia, and frequent yawning; finally there was continuous deterioration of consciousness. Seven weeks
after onset of the disease the patient died from pneumonia.
At autopsy a bilateral symmetric infarct was
found involving the medial parts of both thalami and
extending to the tegmentum of the midbrain from
the aqueduct to both cerebral peduncles (Fig. 2).
Case 3

A 67-year-old woman fell ill with pneumococcal
meningitis and gradually lost consciousness. Cranial
CT only gave evidence of multiple old small infarcts.
Although CSF count and protein content decreased
significantly during standard antibiotic treatment
and CSF cultures became negative, the patient remained comatose. Two weeks following initial symptoms bilateral thalamic infarction was documented
by a repeat CT scan (Figs. 3 a, b). The patient eventually succumbed to pneumonia. No autopsy was performed.
Fig. 4. Case 4. 39-year-old patient 15 months after onset of symptoms. Bilateral ptosis, lids are passively retracted to demonstrate
ocular divergence and mydriatic pupils

Case 4

gence, unequal mydriatic fixed pupils and bilateral
positive pyramidal signs. Right and left retrograde
brachial angiography showed occlusion of the right
vertebral artery with good filling of the basilar artery
territory from the left vertebral artery. EEG recordings documented diffuse slow-wave activity of varying degree. On the fourth day the patient regained
consciousness and though disoriented was able to

A 38-year-old woman without known risk factors for
ischemic stroke suffered sudden loss of consciousness; pupils were dilated and fixed, there was bilateral ptosis and ocular divergence. Following a long period of extreme, only gradually subsiding hypersomnia and accordingly slow mobilization, 7 months after onset of symptoms the still quite lethargic patient
presented a moderate to severe organic brain syndrome characterized primarily by partial loss of

416

Fig. 5 a and b. Case 4. Retrograde left brachial angiogram with laminar filling of the basilar artery supplying both posterior cerebral arteries (lower contrast of right PCA); no definite visualization of thalamoperforating arteries; no obvious atherosclerotic changes
Fig. 6 a-d. Case 4. CT scans, 2 days after onset of symptoms, with bilateral-right larger than left-low density areas in the paramedian
thalami and midbrain predominantly involving the medial nuclei, quadrigeminal plate, pretectal area, pe6aqueductal region, and the posterior commissure

Fig.7 a-c. Case4. CT scans with
coronal and parasagittal reconstrutions, 15 months after onset of symptoms, showing bilateral-right larger
than left-cystic defects of the paramedian thalami

memory functions and severe affective disturbances;
dysarthria and unsteadiness of gait had remained
largely unchanged for several months. Fifteen
months after onset of symptoms bilateral complete
ophthalmoplegia (Fig.4) and dysarthria appeared
unimproved. Intellectual functions were obviously
reduced compared with the patient's premorbid state
as inferred from biographical data; on subtests of the

Wechsler Adult Intelligence Scale she functioned
within t h e mentally defective range. Persistent
though fluctuating hypersomnia, organic brain syndrome - in particular impairment of short-term
memory, naivety and emotional instability with occasional agressive outbursts - as well as marked clumsiness of all motor activities called for constant
charge.

417

Fig.8 a-c. Case4. Magnetic resonance tomograms, 15 months after
onset of symptoms, demonstrating
bilateral cystic defects of the paramedian thalami (diameter of right lesion = 8 mm, left lesion ~ 5 mm)
without ventricular enlargement
(b: transaxial plane, inversion recovery mode; a and c: parasagittal
planes, spin-echo mode)

Fig. 9 a-d. Case 4. 18F-2-Fluorodeoxyglucose PET, 18 days after onset of symptoms, showing generalized depression of glucose metabolism by approx. 40% of normal, within thalamic lesion (right: 18 ~tmol/100 g/min, left: 20 ~tmol/100 g/min) reduction of glucose metabolism by approx. 45%
Fig. 10 a-d. Case 4. 18F-2-Fluorodeoxyglucose PET, 10 weeks after onset of symptoms, showing generalized increase in glucose metabolism, with normalization of cerebellar glucose utilization; basal ganglia, temporoparietal-occipital cortex and white matter still 20%, and
frontal cortex 30% below normal

Laboratory results including CSF were unremarkable; CW-Doppler studies, real-time B-Scan of
the extracranial cerebral arteries, and radionuclide
angiography revealed no abnormalities. Likewise no
pathology was detected by retrograde left brachial
angiography - the small arteries supplying the mesencephalic and thalamic regions not being visualized
(Fig. 5). However, infarcts of the medial parts of the
thalamic regions, extending to the midbrain and involving oculomotor and trochlear nerve nuclei as
well as supranuclear tracts, were repeatedly demonstrated by CT and MRI scans (Figs.6-8). Eighteen
days after onset of symptoms positron emission tomography with 18F-2-fluorodeoxyglucose (Fig.9,
Table 1) disclosed severe reduction of glucose metabolism in the infarcted areas as well as metabolic depression in nearly all gray matter structures in comparison to normal controls. A control study approximately 8 weeks later showed slight metabolic improvement (Fig. 10); some 9 months later another

PET examination corroborated the trend of receding
metabolic depression. Frequent EEG recordings
demonstrated irregular alpha activity not blocked by
external stimuli, furthermore there was no change in
frequency following i.v. injection of thiopental. Cortical somatosensory evoked potentials were normal.
Discussion

Bilateral thalamic low-densitiy lesions are quite a
rare CT finding [20]. Acute ischemia is the leading
cause of anterior and dorsal paramedian thalamic
pathology; in a few cases a degenerative disorder has
been thought to be the underlying mechanism [12,
19, 24]. The simultaneous appearance of bilateral
more or less symmetric thalamic infarctions may be
explained by the peculiarities of the vascular topography of this area [8, 16, 28]; the posterior thalamoperforating arteries that arise from the posterior cerebral artery between the basilar bifurcation and the

418
Table 1. Regional cerebral metabolic rates for glucose (CMRG1) in normal volunteers [18] and in a patient with bilateral mesencephalicthalamic infarction. Reason of metabolic depression in most deactivated structures after clinical improvement
Region

Cerebellar cortex
Dentate nucleus
Vermis
Pons
Midbrain
Thalamus
Lentiform nucleus
Caudate nucleus
Frontal white matter
Temporal white matter
Oval center
Cingulate gyrus
Hippocamp. structures
Frontomesial cortex
Frontolateral cortex
Insular cortex
Temporal cortex
Parietal cortex
Occipital cortex
Visual cortex

CMRG1 in normals
(~tmol/100 g/min)

Bilateral thalamic infarction
11

29

82

01

L

R

L

28.9
28.5
28.8
26.7
22.3
20.7
39.7
35.2
17.6
15.9
18.6
34.4
28.7
28.3
31.0
29.7
29.3
32.0
29.6
36.8

28.1
25.2

R

L

R

28.0+3.88
29.3 _ 4.71

28.2+4.15
29.1 ___3.35

18.3
17.9
25.3
22.4
18.8
19.3
19.0
18.9
13.2
18.4
19.8
33.1
31.0
26.2
25.5
15.8
16.6
15.5
16.6
14.0
15.2
25.4
25.4
23.4
22.4
25.8
23.8
25.0
25.0
26.8
26.9
24.0
23.4
25.4
24.8
22.6
21.9
29.4
27.3

27.6 + 2.02
22.8 _ 4.67
26.0 _ 6.78
37.0 _+7.90
41.8 + 7.68
41.9 _ 6.65
19.0 ___3.71
17.8 _+4.11
17.5 ___2.65
40.8 ___5.21
30.1 _+5.28
39.3 _ 5.40
41.6 _+5.95
39.1 ___5.61
35.0__- 5.67
37.7 __+_4.05
33.5 _ 5.59
41.0 ___5.94

origin of the posterior communicating artery or directly from the basilar artery supplying paramedian
thalamic and mesencephalic regions [14] not infrequently originate from a common trunk [22, 26]. Angiography hardly ever is diagnostic since - due to
their very small calibre - these arteries are rarely visualized [1].
Sudden onset of clinical symptoms is suggestive
either of cardiogenic embolism or of emboli originating from thromboses formed in the proximal basilar
or a vertebral artery. However, occlusion of these latter, larger arteries more often accounts for low-flow
hemodynamic infarcts in their terminal supply territory; thrombotic occlusion of the distal basilar artery
does not give rise to a clinically apparent thalamic
syndrome, since it usually is fatal [1, 6, 7, 30].
As with ischemic strokes of other localization
thalamic infarction in general occurs in the elderly
with atherosclerosis of the vertebral and basilar arteries. Very rarely bilateral symmetric thalamic infarction has been reported in young women on oral
contraceptives, with no other known risk factors [21,
23]. Thalamic infarction following a basilar meningitis was described by Graff-Radford et al. [15] and
was observed in our Case 3.
Bilateral paramedian thalamic infarction often
leads to a fatal outcome after only a short period of
time; however, many of the younger patients survive.
After subsidence of the severe initial impairment of
consciousness, the latter present the well known clinical syndrome of persisting hypersomnia and thalamic dementia with behavioral abnormalities and
amnesia.

21.3 + 4.45
25.9 ___5.28
36.7 _+7.93
39.8 + 7.44
39.9 + 7.79
18.8 _+3.03
17.8 + 2.41
17.4 + 2.29
41.1 + 6.03
29.7 __+5.74
39.5 + 5.24
40.6 _ 5.31
39.8 + 5.67
33.9 + 4.72
36,6 + 3.77
32.6 + 5.88
39.2 + 6.18

21

83

25.9
22.8
20.6
32.4
33.1
18.7
14.2
20.6
30.7
27.2
29.6
28.7
31.4
27.9
28.8
28.5
32.5

As documented by anatomical and CT studies
corresponding with the critical vascular supply the
mesial thalamic structures (medial nucleus, centromedian nucleus, parafascicular nucleus, intralaminar nucleus, mamillothalamic tract) are the predilection sites for ischemic injury with varying involvement of adjoining areas (thalamic nuclei, red nucleus, hypothalamus, midbrain) [2, 8, 10, 11, 13, 21, 23,
281.
In patients with larger lesions extending to the
upper midbrain impairment of ocular motility due to
combined nuclear and supranuclear involvement
may be found [4, 5, 25].
As in three of our patients, corresponding with
the level of consciousness, diffuse slowing of the
EEG is frequently observed during the initial stage
of the disease, later on electrophysiological activity
may return to normal - a so-called alpha-coma being
a rare exception [9, 13, 16, 27, 29].
In accord with the literature, in two of our patients CT and MRI, respectively, afforded good topographical definition of the lesion.
In the last patient repeat PET studies revealed
complex disturbances of brain energy metabolism.
Aside from the morphological lesion pronounced
generalized depression of glucose utilization was observed during the initial stage of the disease. This
uniform pattern of functional deactivation is in contrast with the usual finding of secondary reductions
of glucose metabolism due to deafferentation of a
comparatively small number of dependent structures
in supratentorial infarctions of other localization [3,
17].

419

In view of the severe hypersomnolence and the
EEG changes bearing some resemblance to an alpha-coma, general functional depression of glucose
metabolism may be interpreted as due to severe involvement of the ascending activitating system. This
tentative explanation may be further corroborated
by the conspicuous coincidence of clinical improvement, especially as to the level of consciousness and
vigilance, and the receding cerebral metabolic depression documented on follow-up studies.
Furthermore, the differential changes in regional
glucose consumption appear noteworthy: Comparatively rapid normalization of cerebellar metabolism
is suggestive of an initial deactivation due only to a
tertiary mechanisms, since thalamo-cerebellar projections are largely lacking. Persisting relatively
marked depression of the frontal cortex may be interpreted as deafferentation due to disruption of the
numerous well-known thalamo-frontal projections,
which may also be considered the pathophysiologic
correlate of the personality disorder.
In this view PET demonstrated its potential to
elucidate complex interactions of brain functional
units and to contribute to individual prognosis.
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Received: 22 September 1984

Dr. H. Bewermeyer
Neurologische Klinik des Krankenhauses
KOln-Merheim
Ostmerheimer StraBe 200
D-5000 K61n 91
FRG