Original Paper
Eur Neurol 2000;44:216–218

Received: February 18, 2000
Accepted: April 13, 2000

Total Recovery after Bilateral
Paramedian Thalamic Infarct
Pierre Krolak-Salmon a Bernard Croisile b Claire Houzard c Alice Setiey d
Philippe Girard-Madoux d Alain Vighetto a
Departments of a Neurology, b Neuropsychology and c Nuclear Medecine, P. Wertheimer Neurological Hospital,
Lyon, and d Department of Neurology, CHR Villefranche S/S, Villefranche, France

Key Words
Paramedian thalamic infarct W Neuropsychological
recovery W MRI W Cerebral blood flow

Abstract
Bilateral paramedian thalamic infarcts are characterised
initially by the association of acute vigilance disorders
and vertical gaze palsy, followed by persisting dementia
with severe mnemic disturbance, global aspontaneity
and apathy. We describe a patient with a dramatic neuropsychological recovery, confirmed by testing examination and completed by a cerebral metabolism study.
The pathophysiology of this type of cognitive deficit is
discussed.
Copyright © 2000 S. Karger AG, Basel

Introduction

When the paramedian thalamopeduncular arteries
arise from a common trunk [1], arterial occlusion may
result in the rare bilateral paramedian thalamomesencephalic infarcts (BPTI), which give rise to vigilance disorders, cognitive deficit and vertical gaze palsy [2–8]. The
onset is acute, with deep stupor or coma, evolving into a

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lethargic state with hypersomnia. Follow-up of these patients is characterised by a persistent apathy, motor and
verbal aspontaneity, anterograde and retrograde amnesia
[2, 3, 8]. Vertical voluntary saccades, smooth pursuit and
vestibulo-ocular movements are often impaired. We
present a case of BPTI characterised by a particularly
favourable outcome.
Case Report
A 53-yearl-old right-handed tradesman treated with coumadin
for a severe atherosclerotic disease with lower limb arteriopathy suddenly lost consciousness. On admission to the emergency department, he was only reacting to painful stimuli. He emerged 2 days
later in a somnolent state that gradually improved, but he tended to
sleep if not stimulated. He did not speak spontaneously, but was able
to answer simple questions. A total vertical gaze palsy was observed.
Neurological examination was otherwise negative. Brain MRI demonstrated a bilateral paramedian thalamic and mesencephalic infarction, extending from the ventral part of the dorsal nucleus to the rostral medial midbrain (fig. 1). The left lesion appeared to be somewhat
larger than the right one.
For the next 3 months, he still remained drowsy and tended to
sleep up to 18 h per day. Attention was poor and ideation was slow.
There was a reduction of verbal and motor spontaneity, but no perseverations. He was disoriented to time and place, and had a marked
memory loss for recent and past events with no confabulations. He
could not report basic biographical data nor recall 3 words after
5 min. His language comprehension and expression were normal.

P. Krolak-Salmon
Service de Neuro-ophtalmologie, Hopital Neurologique et Neuro-chirurgical P. Wertheimer
59 Boulevard Pinel, F–69394 Lyon Cedex 03 (France)
Tel. +33 4 72 31 80 71, Fax +33 4 72 35 73 51
E-Mail pkrolak@club-internet.fr

b

a

Fig. 1. a Axial post-contrast T1-weighted MRI showing the bithalamic paramedian ischaemic lesions. b Coronal post-contrast T1-

weighted MRI showing the thalamic and the paramedian mesencephalic ischaemic lesions.

a

Oculocephalic eye movements improved in upward then in downward gaze, but pursuit and saccadic movements were absent. One
month after onset, the Wechsler Adult Intelligence Scale [9] yielded a
verbal IQ of 84 and a performance IQ of 73. The global IQ score was
77. The Signoret Memory Scale [10] showed an equal impairment on
verbal and visual memory. The verbal subscore was 13/72 (mean
controls 55.7, SD 5.9). The visual subscore was 19/72 (mean controls
53.2, SD 6.7).
On follow-up examination 1 year after onset, there was a dramatic improvement in his behaviour and cognitive functions. His level of
consciousness was normal. The patient was oriented to time and
space, well-informed on current events, and his domestical abilities
were similar to his premorbid ones. There was no marked change in
his personality. He only complained of blurring downward vision.
His evaluated sleeping time was about 12–14 h per day, which was
more than the premorbid need (around 6–8 h per day). Spontaneous
speech and comprehension were normal. Clearly, he had no dementia according to the criteria of the DSM-IV [11]. Verbal and performance IQ were both 100, and the score of the Signoret Memory Scale
was 110.5 out of 144 (verbal subscore 50, visual subscore 60.5). The
Grober-Buschke Memory Scale [12] was normal. The most meaningful performance in this test, i.e. the delayed free recall score (at first
trial) was 14 (mean controls 12.2, SD 2.7). The total delayed recall
(free and cued) was 16 (mean controls 15.7, SD 0.8). The Wisconsin
Card Sorting Test (WCST) [13] was normal: the patient completed 6
categories and made no perseverative errors. Forward and backward
digit spans were normal.
Single photon emission tomography (SPECT)-hexamethyl propylen amine oxime 99 metastable technetium (HMPAO 99m-Tc)
studies were performed 6 and 12 months after the stroke. The first
examination showed a relative hypoperfusion in the frontal lobes
(parietal/frontal ratio = 1.14). Right parietal lobe perfusion was
somewhat higher than the left one. The relative frontal hypoperfusion was confirmed by a 133 Xenon regional cerebral blood flow
(CBF) measurement (left frontal lobe CBF value 37 ml/min/100 g;
left hemisphere CBF 42 ml/min/100 g; mean controls 44.7 ml/min/
100 g, SD 4.5). On the second SPECT examination, no significant
change was observed in the frontal lobes compared to the first examination, but increased perfusion was seen in the parietal lobes, especially in the right one (+ 11.3%, fig. 2).

Total Recovery after BPTI

b

Fig. 2. SPECT-HMPAO 99m-Tc performed 6 months after the
stroke showing a relative hypoperfusion in the frontal lobes (a) and
12 months after the stroke showing increased perfusion in the parietal lobes compared to the first examination (b).

Discussion

The outcome of BPTI is bad, mostly characterised by
persistent hypersomnia, akinetic mutism and global impairment of intellectual performances. Patients are apathetic, presenting poor insight and slowness of thought [3,
4]. Perseverations and confabulations have been reported
[3, 6, 14, 15]. Persistent impaired IQ and a low memory
quotient are always observed. Our case appears to be
exceptional because of the clinical cognitive recovery confirmed by the psychometric testing. One year after the
stroke, memory and language examinations did not reveal
any abnormality; neither did tests evaluating mental flexibility like the WCST. The only clinical abnormalities were
represented by a relative hypersomnia of 10–12 h per day
and the ocular-motor deficit.

Eur Neurol 2000;44:216–218

217

The pathophysiology of memory disorders after thalamomesencephalic lesions has often been debated. Firstly,
the initial attentional deficit due to the interruption of
ascending noradrenergic pathways in the mesencephalic
reticular formation and intralaminar nuclei do not allow
good consolidating and retrieving processes that lead to
formation and activation of memory traces [4, 6, 16]. Secondly, the mamillothalamic tracts, that connect mamillary bodies with the anterior nuclei of the thalamus, can be
interrupted bilaterallyl [2, 4, 6, 16]. Lastly, lesions of the
inferior part of the internal medullary lamina or the dorsomedian nucleus itself must interrupt the amygdalothalamic projections. Akinetic mutism and lethargic state are
quite similar to those seen in lesions of the internal frontal
lobe and the anterior cingulate cortex. This aspect of frontal lobe syndrome has been related to lesions of the intralaminar and median nuclei, and their connections with
the prefrontal, orbitofrontal and anterior cingulate cortex
[12, 14, 15]. The involvement of these connections in the
origin of the ‘frontal symptomatology’ may be confirmed
by the study of functional neuroimagery.
A pre-eminent bifrontal reduction of regional CBF is
not usually observed in BPTI [7, 14, 17]. There is rather a

diffuse hypoperfusion of the cortex, which is matched to a
similar hypometabolism on position emission tomography, as the perfusion-metabolism coupling is preserved
[17, 18]. In our case, the dramatic neuropsychological
improvement is not correlated to frontal CBF evolution.
The relationship between the clinical outcome and the
increase in parietal CBF is not clear. Firstly, we can suppose that some connections between the thalamic nuclei
respected by the infarction and the parietal cortex may
have been restored after a period of oedema and neurotransmission impairment. Secondly, the smaller right infarct on MRI and the better cortical perfusion with greater
improvement in the right parietal lobe suggest that some
connections may have been preserved on the right side.
Lastly, the role of the dorsomedian nucleus in thalamic
amnesia, which is the principal structure involved in this
case, has been debated [4, 16]. Von Cramon et al. [16]
emphasised that its role was minor, they reported 1 case
of pure BPTI without amnesia, whereas large parts of the
dorsomedian nucleus were involved. Our case presenting
a lesion of both dorsomedian nuclei supports this opinion.

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Krolak-Salmon/Croisile/Houzard/Setiey/
Girard-Madoux/Vighetto

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