J Neurol (1999) 246 : 764–769
© Steinkopff Verlag 1999

S. Madureira
M. Guerreiro
J. M. Ferro

Received: 20 October 1998
Received in revised form:
30 December 1998
Accepted: 11 February 1999

S. Madureira (쾷) · M. Guerreiro ·
J. M. Ferro
Department of Neurology,
Santa Maria Hospital,
1600 Lisbon, Portugal
e-mail: jferro@mail.telepac.pt,
Tel.: +351-1-7974956,
Fax: +351-1-7957474

O R I G I N A L C O M M U N I C AT I O N

A follow-up study
of cognitive impairment due
to inferior capsular genu infarction

Abstract Abulia, memory loss,
other cognitive deficits, and behavioral changes consistent with dementia can follow an inferior capsular
genu infarction, but only little is
known about the time course of these
disturbances. The present study describes the long-term outcome of
cognitive defects in four patients
with inferior capsular genu infarction
who underwent a neuropsychological
examination within 3 and 12 months
of onset. Three patients had infarcts
in the inferior genu of the left internal capsule and had similar symptoms in the acute phase: disorientation, memory loss, language impairment, and behavioral changes. The
patient with right-side infarct showed
memory impairment and behavioral

Introduction
“Focal forms” of vascular dementia were first described
by Delay and Brion [14]. Several clinical studies have confirmed the relationship between ischemic damage to specific cortical areas such as the angular gyrus, inferomesial
temporal lobe, and medial frontal lobe [26] and dementia.
Subcortical infarcts such as those involving the thalamus
[9, 18], caudate nucleus [10, 11] and internal capsule
[1, 23, 24, 25] are also reported as producing a frontallobe syndrome with abulia, hypokinesia, amnesia, and inattention. Tatemichi et al. [30] identified the genu of the internal capsule as a relevant site for dementia. They described six patients who, following acute capsular genu
infarction, showed fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation within

changes. Three patients had deficits
in one or more cognitive domains on
the first assessment, but none was
demented. By the second evaluation
all subjects had improved. In two patients there were a moderate memory
defect persisted and a language disturbance. Improvement in these disturbances during long-time follow-up
demonstrates that there are alternative pathways that reestablish the
functional connections damaged by
the strategically located capsular
genu infarct. Inferior capsular genu
infarction is not a cause of persisting
“strategic infarct dementia.”
Key words Subcortical infarction ·
Cognition · Dementia · Stroke
outcome

6–12 weeks of onset. Four of the five patients with leftsided lesions still displayed severe memory impairment and
other cognitive deficits consistent with dementia 10 weeks–
10 months after the capsular genu infarction. There are no
other reported series investigating the time course of behavioral and cognitive deficits associated with inferior
capsular genu infarcts.

Patients and methods
The patient population in this study included stroke patients admitted to the Santa Maria Hospital Stroke Unit or evaluated at the
Stroke Outpatient Clinic between November 1995 and November
1997 and participating in a prospective study of dementia and cognitive impairment after first ischemic or hemorrhagic stroke. From
these we retrieved the patient data on those who showed either language, cognitive, or behavioral changes associated with an infarct of
the inferior part of the internal capsule. Patients with infarcts on

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Table 1 Neuropsychological evaluations
Cognitive domains

Tests

Global mental state
evaluation
Verbal and visual memory
Orientation

Mini-Mental State Examination

Attention
Language
Visual neglect and visuoconstructional abilities
Executive functions
Motor control
Praxis
Functional Activities
Depression

Wechsler Memory Scale
Temporal, Spatial, and Personal
Orientation Test
Letter Cancellation
Token Test
Draw by Copy, Wechsler Adult Intelligence Scale Block Design Subtest, Raven Progressive Matrices
Verbal Initiative, Luria’s Graphomotor Sequences
Motor Alternate Sequences
Performance of Learned Movements
by Verbal Instruction (Ideomotor and
Buccofacial Praxis)
Blessed Dementia Scale
Hamilton Depression Scale

domains assessed were memory, orientation, attention, language,
spatial attention and visuospatial ability, executive functions, motor control, calculation, and praxis. All tests had previously been
validated in the Portuguese population [16, 21]. MMSE normative
values took account of educational levels: severe impairment was
considered when scores were below 16 in subjects who had never
attended to school; below 23 in patients who had had at least 1 year
of schooling; and below 28 in those with more than 11 years of
schooling. In the complementary neuropsychological battery, patients were classified as having mild cognitive impairment in a particular test when they scored 2 SD below the mean (for their age,
gender, and educational level), moderate impairment when they
scored below 3 SD, and severe impairment when they scored 4 SD
or more below the mean. The Hamilton Depression Scale (HDS) [22]
was used to assess depressive symptoms. Depression was diagnosed
when the HDS score was 13 or higher [2]. We used the Blessed
Dementia Scale (BDS) [4] to evaluate the impact of cognitive impairment on daily life activities; functional impairment was considered when patients scored higher than 4. Dementia was defined according to the NINDS-AIREN criteria for vascular dementia [26].

Results
other locations or multiple lacunae were excluded. Whenever possible subjects underwent a neuropsyhological evaluation 3 and
12 months after the stroke.
Neuropsychological examination included the Mini-Mental State
Examination (MMSE) [15] for global assessment of the mental state
and a complementary battery as described in Table 1. Cognitive

Case description

Table 2 Patient characteristics

Gender
Age
Years of schooling
Side of lesion

We found seven cases with infarcts on the inferior part of
the internal capsular genu. Three were excluded because
they had other hemispheric lesions. The four patients’ characteristics and scores on neuropsychological tests are summarized in Tables 2 and 3.

Patient 1

Patient 2

Patient 3

Patient 4

Male
64
7
Left

Male
70
11
Left

Female
59
4
Left

Female
64
0
Right

Patient 1 was a 64-year-old retired insurance broker with
a history of hypertension, previous smoking, and a transient ischemic attack 3 years before. He reported a sudden
onset of drowsiness and incoherent speech after an emotional upset. On examination he had diminished initiative,
disturbed memory for recent events, difficulty in organiz-

Table 3 Neuropsychological test scores at 3 and
12 months

a Mild impairment
b Moderate impairment
c Severe impairment

Patient 1

MMSE
Memory with Interference
Logical Memory
Visual Memory
Orientation
Letter Cancellation
Token Test (mod)
Draw by Copy
Wechsler Adult Intelligenc Scale Cubes
Raven Progressive Matrices
Verbal Initiative
Graphomotor Initiative
Ideomotor and Buccofacial Praxis
Blessed Dementia Scale
Hamilton Depression Scale

Patient 2

3M

12 M 3 M

30
13
10
4a
15
8
13b
11
36
10
6c
2
12
2
3

30
11
9
5
15
6.9
13b
14
29
10
8b
2
12
0.5
5

24b
7c
4c
5
12c
5.7
17
13
28
11
10
2
12
3
9

Patient 3

Patient 4

12 M 3 M

12 M 3 M

12 M

28
10
2.5b
5
14
6.5
17
13
28
10
12
2
12
3
8

28
13
3
6
15
6
17
11
24
8
11
2
12
1
2

23
13
7
2
11
2.1
17
12
14
6
12
2
12
2.5
2.5

27
11
4.5
6
15
2.7
17
11
24
8
13
2
12
0.5
0

22
10
3a
2
10b
3.2
17
12
14
6
15
2
12
5a
7

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Fig. 1 Patient 1: CT obtained 48 h after the stroke onset, showing
an infarct on the left capsular genu

Fig. 2 Patient 2: CT obtained 3 months after stroke onset, showing
an infarct on the inferior part of the genu of the left internal capsule

ing long runs of speech, and a right emotional facial palsy.
Computed tomography showed an infarct on the inferior
part of the left internal capsule genu (Fig. 1). Duplex examination and electrocardiography were normal. Three months
later he had returned to his social activities and complained only of decreased enthusiasm. On neuropsychology evaluation he showed mild memory impairment, moderate deficit in verbal fluency, and a language comprehension defect. Twelve months after the stroke, on the second
neuropsychology evaluation, he scored low on the Token
test but had no other deficit or impairment. He mentioned
occasional sadness but did not fulfill depression criteria.
Patient 2 was a 70-year-old hypertensive, former smoker,
and retired army officer who had a sudden onset of mild
right upper limb weakness, dysarthria, and trouble in word
finding. CT showed an infarct on the inferior part of the
left internal capsule genu (Fig. 2). Doppler showed a less
than 50% ipsilateral carotid stenosis. Electrocardiography
and echocardiography were normal. He recovered from his
motor deficit, but anomia persisted, and his family reported
apathy and decreased initiative to start conversations. He
also complained of decreased initiative and enthusiasm. On
neuropsychological evaluation he had a low score on the
MMSE (24 points) because he had temporal disorientation

and failed in the memory items. In the complementary
battery he showed a moderate defect in all memory tests
but had no deficits in other cognitive domains. On the second neuropsychology evaluation 12 months upon the stroke
his MMSE score improved (28 points). His memory impairment persisted, and he still complained of some irritability and decreased enthusiasm.
Patient 3 was a 59-year-old hypertensive housewife. Her
close relatives reported a subacute onset of word finding
troubles and difficulty in recalling recent events. On examination she produced occasional semantic paraphasias
and could not recall any of the three names 1 min later.
CT and magnetic resonance imaging (MRI) showed an infarct on the genu of the left internal capsule, probably not
involving the head of the caudate nucleus (Fig. 3). Carotid
duplex examination was normal. Ten months after the
stroke she underwent a neuropsychological examination
and showed neither cognitive nor functional deficits. Meanwhile she had returned to her previous household activity.
Eighteen months after stroke she had no cognitive, emotional, or functional deficits or complaints.
Patient 4 was a 64-year-old hypertensive, hypercholestreolemic housewife who reported having a sudden onset of forgetfulness and apathy perceived as diminished

767

Fig. 3 Patient 3: MRI obtained 10 months after stroke, showing
an isolated infarct circumscribed to the inferior part of left capsular genu

spontaneous speech and decreased willingness to start her
daily routines, although she remained independent in the
activities of daily life. CT showed an infarct on the inferior part of the genu of the right internal capsule (Fig. 4).
On the first evaluation she rated high on the dementia
scale (5 points), but neuropsychological tests showed only
a moderate impairment in memory and temporal orientation. She complained of irritability and memory defects affecting some of her household activities such as cooking
and shopping. On the second evaluation 12 months after the
stroke she had improved on her functional activities and
showed no cognitive impairment or emotional complaints.
In summary (Tables 2, 3), three of these four patients
had infarcts on the inferior genu of the left internal capsule and suffered similar disturbances in the acute phase,
consisting of disorientation, language and memory impairment, and behavioral changes. The patient with an infarct on the right internal capsule genu showed behavioral
changes and memory impairment. Although three patients
had deficits in one or more cognitive domains on the first
neuropsychology assessment, none was demented. All patients had improved on the second examination performed
at least 12 months after the stroke. A moderate memory

Fig. 4 Patient 4: CT obtained in 48 h, showing an infarct on inferior part of the right internal capsular genu

impairment prevailed in two cases (patient 2), along with
a moderate verbal comprehension deficit (patient 1).

Discussion
All four patients with inferior internal capsular genu infarction displayed either memory loss, language deficits,
apathy, or other behavioral changes on the first examination, but none fulfilled the dementia criteria. Twelve
months after the stroke only two showed persisting moderate focal deficits in language comprehension and memory while two recovered. Our investigation was handicapped by two factors: (a) Although we used a comprehensive neuropsychological battery, complex tests assessing executive functions such as the Stroop [28] and Wisconsin Card Sorting Test [19] could not be used because
normative data on the Portuguese population are lacking.
(b) Although patients with multiple lesions on CT were excluded, and infarcts on CT had a similar location to that in
cases of inferior capsular genu infarct as previously reported [30], MRI was performed in only one of our patients.
The capsular genu is supplied by perforating arteries
that arise from the apex of the internal carotid or by ante-

768

rior cerebral artery branches [17]. The lower part is also
supplied by anterior choroidal artery branches [30]. Various clinical features may result, depending on the upper
or lower involvement of the capsular genu [7]. Infarcts of
the inferior part of the internal capsular genu can disturb
memory and executive functions, in particular initiative,
and if located on the dominant hemisphere they produce
language disturbances [1, 23, 24, 30], as confirmed in the
present series. These clinical features have some similarity to those found following frontal lobe dysfunction and
anterior or dorsomedial thalamic infarct, indicating that
these anatomical structures are included in the same functional networks. A strategic infarct in the region of the inferior genu causes interruption of the inferior and anterior
thalamic peduncles, thus determining a clinical profile similar to those caused by thalamic infarct. Memory impairment, language disturbances, and defects in executing functions associated with anterior and dorsomedial thalamic
infarcts have been well described [8, 9, 18]. Damage to
the anterior thalamic peduncle that connects the dorsomedial thalamic nuclei with the anteromedial frontal cortex
is the most probable anatomical basis for diminished initiative and abulia. Fibers projecting from the anterior thalamic nucleus to the cingulum and to the subiculum must
pass through the internal capsule and corona radiata [31].
The mediodorsal thalamic nucleus, subcallosal area, and
amygdala are interconnected via the inferior thalamic peduncle, ventral amygdalofugal pathway, and bandeletta
diagonalis. Amnesia may therefore result from basolateral
limbic system disconnection [24, 27]. Language is subserved by multiple interconnected cortical subcortical
neural networks including a prefrontal cortex–striatum–
ventral anterior thalamus network for articulation and language production, a pulvinar-temporoparietal cortex-caudate nucleus network for auditory comprehension and a
cingulum-supplementary motor area–striatum–ventral anterior thalamus network for speech production [12]. Left

inferior internal capsular infarct can damage the reciprocal connection between the prefrontal cortex, striatum,
and ventral anterior part of the thalamus as well as between the temporoparietal cortex and the caudate nucleus.
Cognitive and behavioral disturbances produced by a
single lesion confined to the inferior capsular genu can be
due to several mechanisms, such as cortical hypoperfusion
related to the internal carotid or middle cerebral artery occlusion, remote cortical metabolic depression or functional interruption. None of our patients had carotid occlusion or severe stenosis. Metter et al. [25] studied a patient
with multiple subcortical infarcts, including one located
in the left internal capsule genu. Tatemichi et al. [30] used
single photon emission computed tomography in three patients and described hypoperfusion in superomedial and
infrolateral frontal regions in one patient who had a small
infarct in the left capsular genu area.
While unilateral polar or tuberothalamic infarcts may
cause abulia, apathy, and amnesia clearing usually in the
chronic phase, bilateral paramedian thalamic infarcts may
lead to a dementia syndrome [5, 6, 20, 29]. In our four patients the acute mental and behavioral changes improved
within 3–12 months, confirming that these disconnection
or cortical inactivation mechanisms are not permanent.
Gradual recovery of initial hypometabolism upon unilateral thalamic infarcts has been reported by several authors
[3, 13]. The mechanism underlying this improvement may
indicate recovery of cortical metabolic activity, contralateral compensation, or establishment of ipsilateral alternative pathways.
The series of patients presented here points out the importance of considering time from onset in vascular dementia diagnosis. Current criteria establish a 3-month interval between stroke and the assessment of cognitive impairment. However, serial evaluation is crucial for establishing a reliable long-term prognosis.

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