Eur Arch Psychiatry Clin Ncurosci (1991) 241 : 91-97

0oeoo Psychiatry
Clinical
Neuroscience
Archives of

and

9 Springer-Verlag1991

Evaluation of Dementia in Subcortical Arteriosclerotic Encephalopathy
(Binswanger's Disease)
Andrzej Bogucki 1, Ellbieta Janczewska 1, Iwona Koszewska 2, Micha Chmielowski 3, and R6~a Szymafiska I
Departments of 1Neurology, 2Psychiatry (2nd) and 3Diagnostic Imaging, Medical Academy, Kopcifiskiego22, 90-153 Ldd~, Poland

Received November 11, 1990

Summary. Sixteen patients with a clinical diagnosis of
subcortical arteriosclerotic encephalopathy (Binswanger's
disease) were studied. Mild or moderate dementia was
found in 14 cases, with characteristic disturbances of
concentration, and psychic retardation with apathy.
Neuropsychological studies revealed that signs of diffuse
lesions in the frontal lobes dominated. Impairment of
memory was significant in all cases. Although intellectual impairment in subcortical arteriosclerotic encephalopathy resembled subcortical dementia, some significant differences were found.

Key words: Subcortical arteriosclerotic encephalopathy
- Dementia - Subcortical dementia - Neuropsychological evaluation

Introduction
Subcortical arteriosclerotic encephalopathy (SAE), or
Binswanger's disease, is a clinicopathological entity with
quite well defined neuropathological features. Its pathogenesis remains unclear [14] and the diagnostic clinical
criteria are still not clearly established [6, 14].
The neuropathology of SAE consists of symmetrical
areas of demyelination in cerebral white matter (with
subcortical U fibres spared), loss of oligodendroglia and
astrocytic gliosis. Lacunar infarcts are usually present (in
subcortical grey matter as well) and cortical infarcts frequently co-exist. Thickened subcortical arteries and arterioles show lipohyalinosis and fibrosis [7, 12, 16, 21,
22]. Arteriosclerosis is considered to be the cause of ischaemia and hypoxia, which are responsible for incomplete infarctions in the white matter. However, the exact
pathomechanism of SAE remains unclear [6, 14].
In the past, the diagnosis of SAE was based on neuropathological data, and the disease appeared to be uncommon. When in the late 1970s computed tomography
(CT) became widely available, the clinical diagnosis of
Offprint requests to: A. Bogucki

SAE became possible. CT in SAE shows diffuse areas of
white matter low attenuation (lucency) [16, 19-21, 23].
Both CT and magnetic imaging (MRI) studies have revealed that white matter pathology is relatively common
among the elderly [19, 24, 25, 27]. Radiological features
of white matter pathology have been found also in patients without dementia or other signs of SAE [24, 25].
The morphological basis of these changes and their relation to SAE remains unknown. On the other hand, during the last 10 years, there have been several case reports
[4, 16, 19, 21, 27] in which clinical, radiological and neuropathological correlations were established. Analysis of
these reports shows that the clinical diagnosis of SAE is
possible after careful evaluation of clinical and radiological data [21].
Dementia is the most prominent clinical feature of
SAE [6]. Abulia and mental slowing are well pronounced.
There have been few reports describing the pattern of
the dementia. According to Loizou et al. [20] "no specific
features could be ascertained, the dementia being global
and affecting verbal, visual and cognitive functions".
Kinkel et al. [19] stated that "the dementia associated
with SAE is predominantly of the subcortical type". A
similar opinion was expressed by Gupta et al. [17]. The
neuropsychological studies of Derix et al. [13] showed
the resemblance of intellectual impairment in SAE to
the dementia of subcortical type.
The term "subcortical dementia" was proposed in
1974 by Albert et al. [11 to denote the picture of intellectual impairment in patients with progressive supranuclear palsy. The characteristic features of subcortical dementia were forgetfulness, slowness of thought process
or bradyphrenia, disturbance of mood and personality,
reduced ability to manipulate acquired knowledge [1].
The same symptoms were subsequently attributed to
other disorders associated with predominantly subcortical pathology, such as Parkinson's disease and Huntington's disease [5, 9, 10, 15].
Views on the nature of subcortical dementia are still
debated after more than 10 years of study and discussion. While some authors, e.g. Cummings [9], consider
that there exist sufficient data to sustain the concept that

92
s u b c o r t i c a l d e m e n t i a is d i f f e r e n t f r o m c o r t i c a l d e m e n t i a ,
o t h e r s , e.g. W h i t e h o u s e [26] a n d B r o w n a n d M a r s d e n
[5], c o n s i d e r t h a t t h e c o n c e p t is n o t well f o u n d e d . F r e e m a n a n d A l b e r t [15] p o i n t e d o u t t h e significance o f anatomical and functional connections between subcortical
structures and the cortex of the frontal lobes and prop o s e d t h e t e r m s " f r o n t o - t e m p o r a l o r f r o n t a l s y s t e m dem e n t i a " , since " t h e y m o r e a c c u r a t e l y r e f l e c t t h e c o n c e p t
previously labelled subcortical dementia". The aim of
this s t u d y was t h e e v a l u a t i o n of d e m e n t i a in S A E a n d
t h e analysis of its r e l a t i o n to s u b c o r t i c a l d e m e n t i a .

Patients and Methods

Patient Selection
The group studied consisted of patients who, after referral from
several neurological departments and outpatient clinics, underwent CT examination in the Department of Diagnostic Imaging.
Patients with diffuse white matter low attenuation on CT scans
were selected. Subjects with multiple sclerosis, brain tumour, previous brain radiotherapy and/or chemotherapy (methotrexate), or
a history of severe head trauma, were excluded, If other clinical
data obtained from the referring unit suggested the clinical diagnosis of SAE, the patient was admitted to the Department of Neurology, Medical Academy of L6d~, for at least 2 weeks. Informed
consent of the patient and his/her family was obtained.

Clinical Diagnostic Criteria for SAE
The following criteria for diagnosis of SAE were used:
1. Presence of white matter low attenuation on CT scans (obligatory criterion)
At least three of the following:
2. Hypertension
3. History of stroke (or transient ischaemic attack)
4. Focal neurological signs
5. Dementia or marked impairment of intellectual function which
did not achieve the level of dementia.

Clinical Evaluation
Clinical evoluation included medical history using available records and interview of a close informant, detailed general and neu-

rological examination. The clinical laboratory tests included: erythrocyte sedimentation rate, red and white blood counts, haemoglobin, serum electrolytes, serum glucose, proteins, lipids and lipoproteins, kidney, liver and thyroid tests, VDRL. Chest radiography,
electrocardiography (ECG) and electroencephalography (EEG)
were performed.

Analysis of CT Scans
A Siemens DR2 scanner was used. Intensity of white matter low
attenuation, cortical atrophy, ventricular dilatation (expressed as
Evan's ratio) and subcortical and cortical focal ischaemic lesions
were evaluated on CT scans.
The intensity of white matter lucency was expressed as the difference (in Hounsfield Units (HU) between densities of grey and
white matter (according to Zeumer et al. [27] with modifications):
I, 8-9 HU; II, 10-12 HU; III, difference > 13HU.
The following grading of cortical atrophy was used (according
to Zeumer et al. [27]): I, prominent Sylvian fissure and slightly visible cortical sulci; II, Sylvian fissure dilated and cortical sulci
< 3 mm in width; III, numerous cortical sulci > 3 ram.

Diagnosis and Evaluation of Dementia
All patients underwent detailed psychiatric and neuropsychological examination. Dementia was diagnosed according to DSM III-R
[2]. The diagnosis was based on clinical examination and information obtained from a person well acquainted with the patient. The
severity of dementia was evaluated as mild (9 patients) or moderate (5 patients) according to DSM III-R [2]. There were no cases
of severe dementia in the group. In 2 patients intellectual impairment did not achieve the level of dementia. In all cases the Wechsler-Bellevue Intelligence Scale, Benton Visual Retention Test and
Luria's tests for detection of neuropsychological deficits [8] were
performed.

Results

Patients
T h e g r o u p s t u d i e d c o n s i s t e d of 11 m a l e a n d 5 f e m a l e p a tients. T h e i r age r a n g e d f r o m 56 to 85 y e a r s ( m e a n 67).
T h e d u r a t i o n of illness v a r i e d f r o m 6 to 24 m o n t h s in
m o s t cases, b e i n g n o t a b l y l o n g e r in 4 cases. T h r e e p a tients d i e d a n d in 2 cases a u t o p s y was p e r f o r m e d . N e u r o p a t h o l o g i c a l e x a m i n a t i o n c o n f i r m e d t h e clinical diag-

Fig. l a , b. Case 6. CT scan: moderately
diminished attenuation of white matter,
moderate cortical atrophy, dilated ventricles

93

Figs.2-5. 2 Case 2. CT scan: moderate
hypodensities of white matter adjacent to
horns of lateral ventricles, cortical infarct in
left occipital lobe, subcortical lesion in the
right frontal lobe, moderate cortical atrophy and ventricular dilatation. 3 Case 16.
CT scan: moderate to severe white matter
low attenuation, severe cortical atrophy,
dilated ventricles. 4 Case 3. CT scan:
moderate white matter low attenuation,
severe cortical atrophy, dilated lateral
ventricles. 5 Case 8. CT scan: mild periventricular white matter low attenuation,
bilateral subcortical focal ischaemic lesions,
severe cortical atrophy and ventricular
dilatation

Table 1. Characteristics of patients
Patient
no.

Sex

Age
Dura(years) tionof
illness

Blood
pressure
(mmHg)

1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16

f
m
m
m
f
m
f
m
m
m
m
m
m
f
m
f

56
62
61
62
72
73
79
64
70
60
67
64
62
85
74
63

140/80
185/115
170/115
180/110
170/110
130/90
120/80
210/140
170/110
200/105
160/120
200/130
190/120
170/110
125/90
170/100

4
12
1.5
0.5
1.5
1.5
0.5
1.5
1.5
1
5
2
12
2
1.5
13

Diabetes

Numberof
strokes

Focalsigns
(side)

Pseudobulbar palsy

Pattern
of the
disease

+

2
8

Right
Bilateral

+
+
Slight dysarthria

1 (TIA) a
1

Right
Right
Left
Bilateral
Left
Bilateral
Right
Bilateral
Bilateral
Right
Right
Left
Bilateral

S, P, I
S, P
S, P
S, P
S, P, I
S, P, I
S, P
S, P, I
S, P, I
S, P, I
S, P, I
S, P, I
S, P, I
S, P, I
S, P
S, P, I

+
+
+
+

1
1
1
4
2
2

1

Dysarthria
+
Dysarthria
+
+

S, Periods of stepwise deterioration; P, plateau periods; I, periods of improvement
a Transient ischaemic attack

Incon- Severity of
tinence dementia
(DSM III-R)
+

+

+
+
+

Moderate
Moderate
Mild
Non-demented
Non-demented
Moderate
Moderate
Mild
Mild
Mild
Mild
Mild
Mild
Mild
Mild
Moderate

94
Table 2. Computed tomography findings
Patient
1
2
3
4
5
6
7
8
9
10
11
12
13
14
15
16

White matter low attenuation
intensity
localization

Cortical
atrophy

Focal lesions
subcortical

cortical

III
III
II
II
II
II
I
I
II/III
II
II
II/III
III
II
III
II/III

I
II
III
II
II
II
III
III
III
II/III
II
II
III
III
III
III

1F, rF
1F
1T
1F, rF, 1P, rP
1P, rP
1P, rP, rF
1T, 1P
1P
rF, rP-O
IT, 10, rT, rP
-

1T
rO
1T
1P, 10, rF
IT, rO
1P
1P
-

F, P
F, P
P, F
P
F, P
F, P
P
P
F, P
F, P
P> F
F, P
F, P
F, P
P> F
F, P, O

Evan's ratio
0.29
0.35
0.31
0.27
0.33
0.36
0.31
0.34
0.35
0.33
0.31
0.35
0.33
0.35
0.31
0.37

F, Frontal lobe; O, occipital lobe; P, parietal lobe; T, temporal lobe; 1, left; r, right. For other explanations see text
nosis. In 1 of the autopsied cases, cerebral amyloid angiopathy was partly responsible for the development of
SAE [4]. The patients' data are summarized in Table 1.
A detailed description of 3 cases is presented below.

CT Scans
Mild low attenuation of the white matter was found in 2
cases and moderate and/or severe in the other patients.
The white matter of the frontal and parietal lobes was affected predominantly. Cortical atrophy and enlargement
of the lateral ventricles were present in almost all cases.
In 3 cases single and in 7 cases numerous subcortical infarcts were present. In 5 patients they were bilateral.
Cortical infarcts were found in 7 cases and they were
mostly single. Details of CT findings are presented in
Table 2.

Neurological status
Weakness of limbs and gait disturbances were not severe
enough to reduce significantly patients' ability to move
around and undertake self-care. Patients with pseudobulbar palsy were able to swallow food (except patient 1
in the terminal stage). Dysarthria occurred often as an
isolated symptom and, if it co-existed with dysphagia,
the latter was less pronounced.

Psychiatric and Neuropsychological Evaluation
M e m o r y disturbance was the most prominent feature in
non-demented and mildly demented patients with SAE.
Recognition of the intellectual decline was preserved for
a relatively long period of time. This is consistent with
the opinion that preserved insight concerning mental deficiency is a differentiating feature between vascular dementia and the dementia of Alzheimer type.

Moderately demented patients showed marked apathy,
withdrawal from former activities and loss of interest.
The loss of spontaneity was remarkable, but under stimulation they were able to perform basic activities connected with self-care or even more complicated tasks,
such as simple car repair. Families often complained that
the patient became lazy and would not do things he or
she was capable of doing. The patients' mood was that of
indifference; recognition of illness was not accompanied
by the adequate emotional reaction. The loss of activity
and emotional blunting were the features which were responsible for the change of personality of the patient.
Thus, the report of "well-preserved personality" in vascular dementia [18] did not apply to our patients with
SAE.
One of the patients (no. 6), besides being moderately
demented, showed marked character changes. H e had
frequent outbursts of temper; occasionally he refused
steadfastly to cooperate during psychological examination. Early in the course of his illness temporal lobe epilepsy developed.
The comparison of the behaviour of demented SAE
patients and patients with Alzheimer's disease during
their stay in the hospital showed a remarkable difference. While the latter often wandered around losing
their way to bed, the former tended to spend the whole
time in their room, mostly in bed.
Difficulties in solving both concrete and abstract problems were found in mildly and, more pronounced, in
moderately demented patients. The ability to shift from
one strategy to another was impaired. The patients perserverated in their mistakes; their thinking was stereotyped. They were often unable to overcome an established response set. Speed of responding was low or fluctuating. Verbal behaviour of the patients was related to
their disturbances of thought processes: impoverishment
of vocabulary, incoherent statements, perseverations,

95

Table 3. The results of neuropsychological evaluation
Patient

1

2

3

4

5

6

7

8

9

10

11

12

13

14

15

16

Verbal IQ
Performance IQ

-

91
92

113
112

96
103

90
97

-

-

100
97

-

102
82

120
110

106
94

98
93

74
89

75
89

89
89

Attention and concentration
Memory
Speech
Reading
Writing
Arithmetic
Praxis
Visuoconstruction
Visuoperception
Thinking

+
+

+
+

+
+

+
+
+

+
+
+

+
0
0
0
0
0
+
0
0

+
+
+
+
+
+
+
+

+
+
+

+'
+
+

+
+
+

+
+
+

+
+

+
+

+
+

+
+

+
+

+
+
+
+

+
+
+
+
+
+
+
+

+
+

+

+

+

+

+

+

+

+
+

+
+
+

+

+

+
+

+
+
+

+

+

+
+
+

+

+
+
+
+

+

+, Impaired function; 0, patient refused to cooperate
bizarre speech were noted. The observed visuoconstructional deficits were mainly the result of impaired concentration. Mental and m o t o r retardation were most prominent in all cases. Besides the disturbances of mental
functions, apractic disturbances were also observed.
This particularly concerned alternating m o v e m e n t s and
repetitive actions (Table 3).

Case Reports
Case 8
A n industry m a n a g e r came to medical attention aged 55
years because of severe hypertension (210/140mmHg).
H e retired at the age of 60 years. Discrete gait disturbances were noticed by his wife 2 years later. H e began
to have difficulty in recognizing characters from T V serials. At age 63 chest pains developed. The antihypertensive treatment was modified and nitrates were administered. It is probable that he took an overdose of the
latter. Three days later, he gradually became apathetic
and confused. Blood pressure was found to be 120/80
m m H g . Slight left hemiparesis was present. After the
next 3 days he improved; apathy and lack of spontaneity
were striking, however. Slowing of p e r f o r m a n c e and
m e m o r y was prominent. H e was afraid to go out of the
house. A few episodes of incontinence occurred.
One year after the stroke the patient was admitted to
hospitals. The blood pressure was 150/105 m m Hg. There
was bilateral palatal weakness, m o r e pronounced on the
left side. H e was dysarthric but had no difficulty swallowing. P a l m o m e n t a l reflexes were present bilaterally.
Mild weakness of both lower limbs with exaggerated left
knee and ankle reflexes were found. The left plantar response was extensor. The E E G showed bilateral slight
theta activity.
A p a t h y and p s y c h o m o t o r retardation were marked.
H e spoke with a soft voice. Speed of p e r f o r m a n c e during
examination fluctuated. Verbal and visual m e m o r y were
markedly impaired, he perseverated with his errors frequently during m e m o r y testing, There was slight dys-

praxia and difficulty in word-finding occurred occasionally. His I Q was 20% reduced when c o m p a r e d with his
premorbid intelligence.

Case 10
A 59-year-old engineer was admitted to the regional hospital because of sudden development of mild aphasia
and confusion. H e was unable to recognize his wife,
daughter and attending physician. H e was disorientated
in time and place. H e could not feed and dress himself.
Slight right limb weakness with hyper-reflexia was found.
Blood pressure was 200/105 m m Hg. H e improved gradually after some days, but, as his wife stated, he was a
completely different man. H e was very inert. The speed
of response was low and there was a lack of facial expression. A t h o m e he spent time in bed or staring at the TV.
H e was afraid to go out of the house without his wife.
CT 3 weeks later showed white matter low attenuation around the bodies, anterior and posterior horns of
the lateral ventricles and in the centrum semiovale. There
was a small infarct in the white matter of the right frontal
lobe and a larger one in the cortex of the left occipital
lobe. There was m a r k e d cortical atrophy and m o d e r a t e
ventricular dilatation.
Eight weeks from the onset of his illness the patient
was admitted to the D e p a r t m e n t of Neurology, Medical
A c a d e m y of Ldd~. H e gave his name, date of birth, but
not his age. H e was orientated in place but not in time.
H e could find his way to the toilet and T V room; however, he seldom left his r o o m spontaneously. H e was
able to wash, shave and dress himself, but he had to be
reminded about it m a n y times.
Partial right h o m o n o m o u s hemianopia limited to the
periphery of the visual fields, bilateral palmomental reflex and extensor right plantar response were present.
H e was not incontinent. His blood pressure was 150/100
mmHg.
H e was very apathetic but cooperative during neuropsychological examination. The speed of responses fluctuated markedly when observed on subsequent days. His
ability to sustain attention was significantly reduced.

96
Visual and verbal memory was impaired. His conversational speech was reduced to short, adequate answers;
occasionally there was word-finding difficulty. He had
mild dyslexia and dysgraphia. On visuoperceptual tasks
he performed well in contrast to his performance on visuoconstructional tasks. His level of intellectual performance was reduced (14%) when compared with the estimated premorbid level.
EEG showed symmetrical theta activity. Digital subtration angiography (DSA) did not show any abnormality in the cerebral arteries.
During the next 3 years dementia progressed, although
transitory priods of improvement were observed. Neurological status was stable and no strokes were noted. Prominent apathy and lack of initiative were interpreted by
the psychiatrist as signs of depression, and mianserin was
administered without any beneficial effect.

Case 16
A female schoolteacher came to medical attention at the
age of 41 years when she suffered an acute episode of left
limb weakness from which she fully recovered. She retired prematurely at the age of 51 years because of her
reduced efficiency. In the same year she was admitted to
a psychiatric hospital because of depression. She was
treated with a tricyclic antidepressant with some initial
effect only. Mild dementia was diagnosed. She was followed up by a psychiatrist as an outpatient. Her mood
was often depressed, but she never improved significantly on antidepressants. The intellectual deterioration
progressed gradually over the course of the next 12 years.
At the age of 63 she was housebound. She was unable
to feed, wash or dress herself, but she was continent.
Transitory episodes of disorientation in time and place
were observed. Slight dysphasia and gait disturbances
developed. CT showed severe symmetrical white matter
hypodensities in the frontal, parietal and occipital lobes,
moderate cortical atrophy and ventrical dilatation but no
focal ischaemic changes.
During her stay in the Department of Neurology, she
left her room sporadically. Her appearance was untidy.
Blood pressure was 170/100 mm Hg. Palmomental reflexes
were present bilaterally. Tendon reflexes in upper and
lower limbs were exaggerated symmetrically and equivocal piramidal signs on both sides were observed. The gait
was apractic.
The EEG showed widespread bilateral theta and delta
slowing. DSA revealed occlusion of the left internal carotid artery.
She cooperated poorly during neuropsychological testing. She was euphoric and she dissimulated occasionally.
Difficulty in sustaining attention was prominent. Her
conversational speech was restricted and perseverations
were observed. Verbal and visual memory was seriously
impaired; the Benton test could not be reliably assessed
because of perseverations of errors. Dyspraxia, dysphasia
and dysgraphia were present. She was unable to calculate above the threshold of 10. Her IQ could not be reliably assessed.

Discussion
The clinical diagnosis of SAE in the studied group was
based on the CT findings, the presence of intellectual
impairment and focal neurological signs and other data
suggesting a vascular aetiology. Such diagnostic criteria
make the diagnosis of SAE highly probable [21].
Intellectual deterioration was present in each patient
and in 14 cases it was advanced to the point of dementia.
Disturbances of concentration, and psychic retardation
with apathy were characteristic of the patients with mild
and moderate dementia. These were responsible for the
results of psychological tests being better than expected
from the low level of patients' daily activities and capabilities.
The results of neuropsychological studies showed that
symptoms of diffuse damage of frontal lobes dominated,
although it should be noted that Luria's tests do not
allow for quantitative evaluation of neuropsychological
deficits. Frequent abnormalities of gait (10 patients) and
urinary incontinence (5 patients) could also be interpreted as symptoms of frontal lobe disorder [11]. However, in most cases signs of lesions in other cortical areas,
more or less pronounced, were present. This could be
expected from the cortical infarcts visible on CT scans.
The pattern of intellectual impairment in the group
studied in some ways resembled that of subcortical dementia. The slowed speed of cognition, apathetic personality and depressed mood were present in most cases.
The memory disturbances, however, were severe and do
not correspond to the "forgetfulness" of subcortical dementia. One of the reasons for the only partial similarity
of dementia in this group to subcortical dementia might
be the presence of cortical infarcts. Cerebral infarcts are
relatively common among SAE patients: they were observed in about 30% of cases diagnosed at autopsy [3].
On the other hand, it cannot be excluded that in some
cases the degenerative process of Alzheimer type coexisted and was co-responsible for the dementia. At present, it is not possible to differentiate, using clinical data
only, between pure vascular dementia and the mixed
forms of dementia.
The dementia in SAE seems to have features different from dementia of Alzheimer type. It can be presumed that SAE patients require different rehabilitation
techniques, which could improve their self-sufficiency.

Acknowledgement. This study was supported by MZ V R-30.
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