Original Paper
Eur Neurol 2002;47:156–160

Received: March 9, 2001
Accepted: November 5, 2001

Severe Personality Changes after
Unilateral Left Paramedian Thalamic
Infarct
Toshio Fukutake a Koichi Akada b Shoichi Ito a Tomoko Okuda b
Yoshihiro Ueki b
a Department of Neurology, Chiba University Graduate School of Medicine, and b Department of Psychiatry,

Tateyama Hospital, Chiba, Japan

Key Words
Personality change W Emotion W Frontal lobe function W
Thalamus W Magnetic resonance imaging W Wisconsin
Card-Sorting Test W Amnesia

Abstract
Personality changes are not uncommon after paramedian thalamic infarction, but usually bilateral or relatively
large lesions, often complicated by other neurological or
neuropsychological deficits, are present. ‘Pure’ cases of
unilateral lesions are extremely rare. We report that a
right-handed, 48-year-old man, who was hypertensive
and diabetic but had no prior psychiatric history, developed severe personality changes and a frontal-like syndrome after recovery from acute-onset impairment of
consciousness at the age of 43. Other neurological and
neuropsychological disturbances, especially verbal and
visual amnesia, were unremarkable. MRI showed a very
small infarct in the left paramedian area of the thalamus,
mainly involving the dorsomedial nucleus.
Copyright © 2002 S. Karger AG, Basel

Paramedian infarcts are rarely found as isolated, unilateral lesions, always being bilateral when there is only
one arterial pedicle [1]. Moreover, they may be overlooked because they produce no major focal neurological

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or neuropsychological findings and give rise to nonfocal
disturbances, such as impairment of consciousness, acute
confusional state or apathy [2]. In addition, bilateral paramedian infarcts characteristically produce severe amnesia
and, in the case of large lesions, typically dementia [3].
After recovery of consciousness, changes in personality, emotion or behavior are common when paramedian
infarcts mainly involve the dorsomedial nucleus (DM)
and are usually accompanied by apathy/abulia [2, 4–6].
Only rarely does a disinhibition syndrome with ‘frontallike’ disturbances, utilization behavior, bulimia or maniclike delirium develop [3–9]. Although such changes are
usually the result of bilateral lesions, some unilateral
(either right or left) cases have been described [1, 2, 10,
11].
We report a patient with a left paramedian thalamic
infarct, whose long-standing, main disturbance consisted
of severe personality changes and a frontal-like syndrome
unaccompanied by any significant memory disturbance.

Case Report
A right-handed, hypertensive, diabetic 48-year-old man was admitted to our hospital because of psychomotor excitation and
increased speech. He was a graduate, with low grade, of a junior high
school (9 years of education) and had been employed as a salesman in
a grocery store. Previously, he had been gentle, kind and helpful to
his colleagues and had no history of psychiatric illness or stroke. He

Dr. Toshio Fukutake
Department of Neurology, Chiba University Graduate School of Medicine
1-8-1 Inohana, Chuo-ku, Chiba 260-8670 (Japan)
Tel. +81 43 226 2129, Fax +81 43 226 2160
E-Mail fukutake@med.m.chiba-u.ac.jp or f1040@eb.mbn.or.jp

Fig. 1. Axial (a), coronal (b) and parasagittal
(c) T2-weighted MRI showing a discrete left

paramedian thalamic infarction that mainly
involves the DM.

had not been exposed to toxins nor did he drink alcohol in excess. His
family’s medical histories were unremarkable for neurological or psychiatric disorders. At the age of 43, he developed acute-onset impairment of consciousness and was admitted to a local neurosurgical hospital after diagnosis of a nonhemorrhagic infarct in the left medial
thalamus. Within 6 weeks of hospitalization, his arousal and alertness were gradually improving, but he became egocentric and stubborn, his emotional and behavioral status fluctuating between an irritative, insomniac state and a hypoactive, apathetic one. On becoming overly irritated, he carried on in a loud voice, littered his room
and threatened violence to the members of his family. Three times
over the next 5 years, he was forcibly admitted to a local psychiatric
hospital with the diagnosis of schizophrenia-like disorder, because of
excessive talkativeness, disinhibited behavior and stubborn adherence to his own opinions. At the age of 45, he was fired from his job
and divorced by his wife. No memory or intellectual disturbance was
detected by family or company members, but he could not handle
money well. During the past 2 years he had not taken any antipsychotic drugs.
On admission he was very agitated, incoherent and used inflammatory and arrogant speech. Blood pressure was 146/100 mm Hg
with a regular cardiac rhythm (84/min). Cranial nerve functions were
normal, except for downbeat nystagmus with both lateral gazes. The

strength, muscle tone and tendon reflexes of the extremities were
symmetrical and normal. Plantar responses were flexor. There was
no forced grasping or utilization behavior. Sensations to pinprick and
vibration were normal. Coordination in all four extremities was normal as was his gait. A general examination and routine laboratory
blood and urine tests detected no abnormalities, except for mild
hyperglycemia.
Brain MRI on admission showed an old small infarct adjacent to
the third ventricle on the left in the most medial aspect of the thalamus (fig. 1). Axial, coronal and sagittal slices suggested involvement
of the heart of the paramedian territory (a typical ‘rabbit ear’ sign on
the coronal images), the ventroposteromedial part of the DM, as well
as the midline nuclei and parafascicular nucleus [12, 13]. EEG 1
week after admission showed a poor 10-Hz alpha wave and a prominent dysrhythmic 15- to 25-Hz beta wave with moderate bradyrhythmia over the anterior region, predominantly on the left. He was diagnosed as having a simple exacerbation of a frontal pseudomanic syndrome.
One to two months after admission, when he had become a little
less agitated owing to the administration of neuroleptics (30 mg zotepine, 4 mg timiperone and 2 mg trihexyphenidyl three times daily;
50 mg chlorpromazine, 25 mg promethazine, 80 mg phenobarbital,
6 mg timiperone, 200 mg carbamazepine and 2 mg flunitrazepam

Unilateral Left Paramedian Infarct

Eur Neurol 2002;47:156–160

157

nightly), the following neuropsychological observations and tests
were made (some tests, including SPECT, could not be completed
due to his rejection or impatience). His language was normal. He
showed no apraxic errors in our routine praxis tests. Based on clinical
observations in the ward, his psychiatric symptoms were categorized
as: (1) emotional unstableness, explosiveness or lability (he made
many demands to go to the toilet, take a meal, leave the hospital and
so on and would not wait for permission from the medical staff nor
control outbursts of rage and sometimes of crying); (2) poor ability in
the time domain to (carefully) organize behavioral acts (he bought
more cake than necessary in the hospital shop; could not clean up his
bedside by the regular procedure; prepared inappropriate things for
taking a bath and bathed in an untraditional manner); (3) distractability or poor concentration (subjects of his conversations often
changed; he could not make a complete count of the number of cars
in the parking area), and (4) poverty of flexible thinking and tact (he
would stubbornly stick to his demands and sometimes repeated the
same information over and over, e.g. his body’s weight control or
renewal of his driver’s license, and could not complete the form for
renewal of his driver’s license because he became stuck as to details).
His intelligence quotient fluctuated with his state of mood or attention; once, he scored 29 out of 30 on the Mini-Mental State Test,
Japanese version (missing only 1 point on the orientation question
for the part of country in which he lived). He was relatively cooperative when taking the Revised Wechsler Adult Intelligence Scale test,
Japanese version, and had an overall IQ of 70, a low average for his
education and type of job, a verbal IQ of 78 and performance IQ of
67: (1) verbal scale subsets: information 6, comprehension 10, arithmetic 7, similarities 5, digit span 5 and vocabulary 6; (2) performance
scale subsets: digit symbol 6, picture completion 7, block design 6,
picture arrangement 4 and object assembly 3. In the Modified Wisconsin Card-Sorting Test, Keio version [14], he established only 1 of
6 categories, color (normal controls 5.3 categories), and made a large
number of total errors (42/48) and perseverative errors of the Nelson
type [15] (27/42/48; normal controls 1.6/48). He could recall 4 of 5
objects immediately and had no problem in the delayed recall of 3
words after a 3-min distraction or in spontaneous recall (within 60 s)
of 10 vegetable names. In the Benton Visual Retention Test [16],
Japanese version, he had a correct score of 5 and an error score of 7,
normal for his IQ and age. Eight months after admission, he had
become less agitated, even though the dose of neuroleptics had been
reduced to approximately one third, and was discharged to a nursing
home.

Discussion

The transient impairment of consciousness in this
patient, who showed no significant neurological signs, was
followed by severe personality changes and a frontal-like
(dysexecutive) syndrome. No other neuropsychological
disturbances, in particular memory disturbances, were
significant. In many ways, he seemed very much like a
patient with extensive medical prefrontal damage, e.g.
like the famous Phineas Gage [17] or a patient with an
antisocial personality disorder reported by Blair and Cipolotti [18]. Imaging studies detected a left thalamic

158

Eur Neurol 2002;47:156–160

infarct in the territory of the paramedian artery, which
mainly involved the ventroposteromedial part of the
DM.
Unilateral infarcts that are limited to the paramedian
thalamus are uncommon. Moreover, reports of prominent psychiatric symptoms are extremely rare. As for left
unilateral medial thalamic lesions, Castaigne et al. [1]
reported autopsy findings for a 64-year-old man who had
become aggressive and violent in the acute stage and who
later showed agitation, incoherence, confusion and disorientation as to time and place, as well as extensor plantar
responses, impaired position sense in the toes, grasping
and rooting reflexes on the right and fluctuation of consciousness. Their anatomical study detected an infarct
lesion in the medial thalamus, which predominantly involved the DM, parafascicular and central nuclei and
which extended to the internal and external ventrocaudal
nuclei and the pulvinar. The site of that lesion was slightly
lateral to that of our patient. The cases of lesions confined
to the left DM with no significant memory dysfunction,
reported by von Cramon et al. [19] and Kritchevsky et al.
[20], included no description of personality or behavioral
disturbances. Three other reports described patients with
CT/MRI-verified infarcts in the anterior medial thalamus
served by the polar artery. In the first, the mental symptoms were confusion and slow mentation in the early
stage, and limited memory impairment in the chronic
stage [11]. In the second, there was a subacute change of
personality in the form of depression and a feeling of
inadequency as well as memory impairment [10]. In the
last, there was impairment of complex executive behavior, anomia and verbal memory deficits in the early stage
[21]. The patient reported by Bogousslavsky et al. [22] had
a relatively large lesion (verified on autopsy) in the paramedian thalamus and showed manifest ophthalmic, sensory, aphasic and amnesic symptoms and signs, apathy
being a minor sign in the acute stage. Recently, Ikeda et al.
[23] have reported a patient with bilateral but predominantly left paramedian infarcts (verified by MRI) who
became childish and euphoric in the acute stage and who
showed emotional lability, disinhibition and decreased
spontaneity in the chronic stage. These symptoms and the
location of the left-side lesion resemble those of our
patient.
As for right unilateral medial thalamic lesions, Castaigne et al. [1] reported autopsy findings for a 72-year-old
man who had gradually become apathetic and disinterested after sudden-onset left hemiparesis and who later
showed psychomotor retardation. An anatomical study
found infarct lesions in the medial thalamus, similar to

Fukutake/Akada/Ito/Okuda/Ueki

those in the previously mentioned left-side case, as well as
long-standing bilateral posterior cerebral infarcts. Bogousslavsky et al. [2] reported a CT-verified case in which
there were manic delirium and a frontal-like syndrome,
the lesion seeming to be in a region similar to that of the
right-sided case of Castaigne et al. [1]. A case of a right
unilateral-most medial lesion that resembles ours (disregarding side/laterality) has been described, in which the
patient presented with impaired visuoconstructive abilities, low average verbal IQ, borderline performance IQ, a
normal score in the Wisconsin Card-Sorting Test and normal memory [19]. A case of bilateral, but predominantly
right medial infarcts (verified by CT) has also been
reported, in which the patient presented with inappropriate behavior and amnesia [11].
The DM is the thalamic relay nucleus for association
areas in the frontal lobe, receiving input from the amygdala, nucleus accumbens, olfactory region, hypothalamus
and basal ganglia. It projects to the nucleus basalis of
Mynert, frontal eye field, prefrontal cortex and cingulate
gyrus [24, 25]. The DM relays limbic system information
to the prefrontal and cingulate cortexes and has importance in such limbic and paralimbic functions as emotions, cognition learning and memory [24, 25]. Results of
a recent functional neuroanatomy study suggest three primary frontal circuits: dorsolateral, orbitofrontal and anterior cingulate, all connected to the DM [26]. The dorsolateral circuit is postulated to facilitate organization, planning and attention. Patients with damage to these socalled executive functions show concrete thinking, perseveration, impaired set shifting or inability to change tasks,
inability to filter or ignore, environmental distractions
and inability to organize or plan [26–28]. The orbitofrontal circuit is thought to mediate socially appropriate
behavior and empathy. Lesions produce such marked personality changes as impulsiveness, explosiveness, tactlessness, lability and lack of interpersonal sensitivity [26–28].

The anterior circuit produces motivation by balancing the
inhibitory input of the supplemental motor area with its
own stimulus that supports wakefulness and arousal. Patients with bilateral lesions in this circuit show akinetic
mutism, profound apathy, lack of motivation and immobility [26–28]. A similar, transient disability may occur in
patients with unilateral lesions [26]. Our patient’s clinical
features are very compatible with these descriptions,
indicative that his DM damage produced dysfunction in
all three frontal lobe circuits. Moreover, the parafascicular nucleus, as well as other intralaminar nuclei, has a
strong association with the ascending reticular activating
pathways and a putative role in the control of arousal and
attention [24]. Fibers from the midline nuclei project diffusely, their targets including the amygdala and anterior
cingulate gyrus. The midline nuclei provide an indirect
link from the brainstem to these limbic structures and
function in the regulation of forebrain excitability [24]. In
our patient, the lesions in these areas may have been
responsible for the impairment of consciousness in the
acute stage and fluctuation of personality or attention in
the chronic stage. In their comprehensive review of the
literature, Van der Werf et al. [29] indicated that damage
to the DM, midline nuclei or intralaminar nuclei, or a
combined lesion involving these structures, may be responsible for a frontal-like syndrome, especially executive
dysfunction.
In our patient’s case, his personality changes and frontal-like (dysexecutive) syndrome seem to be associated
because both were caused simultaneously by a very small
lesion. A recent detailed report of 2 other cases showed,
however, that the two conditions may be dissociated
[18].
In summary, our findings show that severe personality
changes and a frontal-like syndrome unaccompanied by
significant amnesia may be caused by lesions confined to
the left medial thalamus.

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