Case Report
Dementia 1995:6:294-300

Department of Neurology. University of
Erlangen-Nuremberg. Germany

A Case of Alzheimer's Disease
with Extensive Focal White
Matter Changes

KeyWords

Abstract

Alzheimer’s disease
Focal white matter changes

The case of a patient is reported who suffered from disturbed concentration
and memory' and constructive apraxia. She had only mild neuropsychological
deficits at the first examination. T2-weighted MRI presented extensive focal
white matter changes. A brain biopsy showed changes typical for Alzheimer’s
disease (AD). The extent of the white matter lesions was surprising compared
to the mild clinical signs she had. This case confirms that AD may result in
prominent white matter disease caused by incomplete infarction or demyelination.

Introduction

Case Report

The association of white matter changes (WMC) with
Alzheimer’s disease (AD) has been widely discussed re­
cently. There is disagreement whether there is any speci­
ficity in these changes or whether their severity correlates
with the severity of dementia. Many authors believe that
the lesions arc the result of subacute hypoperfusions for
which congophilic angiopathy is believed to be responsi­
ble [1].
Our patient was not diagnosed as having AD before
brain biopsy, since neuropsychological tests did not dis­
close marked dementia and MRT showed widespread
subcortical hyperintensities on T2-weighted images. The
distribution of these changes was uncommon, because
they were located not only pcriventricularly but reached
widely into the temporal lobes. Compared to other cases
with WMC they were very circumscribed on neuroimag­
ing. Because WMC are unspecific and similar in several
disorders on the basis of brain imaging only, a wide range
of disorders causing leukoaraiosis [2] had to be consid­
ered.

Accepted:
December 19.1994

At the age of 52 the patient first noticed an increasing disability to
concentrate and memorize things and a lack of orientation. At the
time of the first hospital examination these deficits were so minor
that her family had not noticed them. The patient had suffered from
some uncharacteristic symptoms such as occasional headache and
pain which according to her description might have been a symptom­
atic trigeminal neuralgia.
The patient had no history of hypertension or diabetes. In her
family, her father, uncle and an aunt on the father's side became
demented around the age of 60 years for unknown reasons.
In 1991. on the first neurological examination, she only showed
weakness of her left face, myocloni of both lids, slight pronation of
the right arm and myocloni of both arms, when she tried to stretch
them out simultaneously, and bradydiadochokincsia. There were no
release phenomena.
The routine laboratory parameters were normal except for mild
anemia. Serum arylsulfatase A and HIV tests were normal. CSF was
completely inconspicuous. No tumor or signs of an immunological
disease were found.
The clectrophvsiological assessment (electroencephalography,
electromyography, nerve conduction velocities, visual and sensory
evoked potentials) was normal, but central motor conducting veloci­
ty was delayed to the right side.

Dr. Birgit Zahner
Neurologische Universitätsklinik F.rlangen
Schwabachanlagc 6
D-91054 Frlangcn (Germany)

© 1995 S. Karger AG. Basel
1013-7424/95/0065-0294
$8.00/0

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B. Zahner
C.
J.G. Lang
A. Engelhardl
P. Thierauf
B. Neimdorfer

1

2

Fig. 1. CT scan showing an extensive hypodensity in the white matter of the right
temporal lobe and to a less severe extent on
the left side.
Fig. 2. Large white matter signal hyperin­
tensities seen on the T2-weighted MRI scan
of both temporal lobes, more marked on the
right side.

Fig. 3. "Tc-HMPAO-SPECT shows an
area of decreased HM PAO enrichment mea­
suring 5 x 4 cm in the right temporal lobe,
perfusion of the other areas is normal.

Premorbid intelligence estimate [3] was IQ = 92 (low normal range).
Drawing was severely defective. The patient was neither able to copy
a cube in perspective view nor to give the details o f a bicycle (fig. 4).
Angles were rendered distorted.
Despite unequivocal impairments (table I) the patient scored
above the cutoff level for dementia in the Mini-Mental State Exami­
nation [4] at the first testing. Nevertheless the patient was considered
mildly demented since the combination of global memory impair­
ment [5] and constructive deficits (drawing, visual reproduction)
agreed with the DSM-II1-R definition [6], Although not tested for­
mally. no language disorders were apparent. Altogether the neuropsy­
chological status was interpreted as indicating right hemisphere (tem­
poroparietal) involvement superimposed on a global memory im­
pairment.

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Cranial computed tomography (CT) (fig. I) showed temporopa­
rietal white matter hypodensities bilaterally, more pronounced on
the right side. Magnetic resonance imaging (MRI) (fig. 2) also clearly
disclosed white matter changes (WMC) more prominent in the right
than the left temporal lobe. Therefore degenerative, tumorous,
inflammatory or vascular disease was suspected.
‘wTc-HMPAO-SPECT examination showed an area of decreased
enrichment in the right temporal lobe measuring 4 x 4 cm: perfusion
of other areas was normal (fig. 3).
In the neuropsychological evaluation dementia scales, tests for
handedness, verbal and nonverbal memory, attention and a behav­
ioral rating were given.
The patient was strongly right-handed (90%. Edinburgh Handed­
ness Inventory) also preferring the right eye and leg, respectively.

Fig. 4. The patient tried to draw a bicy­
cle. two intersecting pentagons, to copy a
cube (right upper comer), all severely defec­
tive.

Fig. 5. Brain biopsy. Bodian silver im­
pregnation. 2 5 1 x 200. Senile plaques in the
cortex.

296

Six months later no significant change o f the neurological status,
the neuroimagingor the patient’s self-report was noted. The results of
the neuropsychological assessment not only did not deteriorate (ta­
ble I), they even showed a mild (insignificant) trend towards im­
provement. Once again performance was poorest in those tests which
required visuomotor processing or memory. Since on second exami­
nation there was no cleareut global memory deficit, the diagnosis of
dementia was questioned because there was mild improvement in
some of the subtests within 6 months and according to the MiniMental status the patient still did not score as 'demented'. Compared
to a sample of clinically diagnosed Alzheimer patients our patient fell
within ± I SD of their scores in only one of five subtexts of the Mattis
Dementia Rating Scale [7] at each lest session.
2 '/i years later the patient was examined again because of increas­
ing apathy and depression plus sudden uncontrolled aggressive cpi-

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Relatives' rating of behavioral symptoms disclosed marked de­
pression (55/70 points) and decreased motivation (10/20) with pre­
served or only mildly disturbed emotional stability, level of activa­
tion. self-care and social behavior. Attention and concentration,
communicative abilities and insight were also rated as normal,
whereas intellectual abilities and orientation were considered mildly,
memory' markedly abnormal. There were no psychotic signs or symp­
toms.
The brain biopsy from the right temporal lobe, where the MRI
lesions were most marked, showed many plaques and congophilic
angiopathy as well as mild cortical and subcortical astrogliosis
(fig. 5). The pathologists diagnosed AD. Because of the neuropsycho­
logical lest results that ranged above the score ‘demented' the patient
was asked for a new neuropsychological and neurological evaluation
after 6 months.

Table 1. Neuropsychological assessment of the patient's mental impairment
Test

Maximum Normal
score
range

Mini Mental Status Examination
(severity ordem entia)1
30
[4]

January 22, 1991
first examination

July I2, 1991
second examination

March 3. 1994
third examination

raw
interpretation
score

raw
interpretation
score

raw
interpretation
score

24-30
25
(not demented)

not demented

29

not demented

22

demented

144

134-144

120

impaired

30

mildly impaired

91

37
37
6
39
25

35-37
34-37
6
35-37
23-25

35
24
6
39
16

normal
impaired
normal
normal
impaired

36
31
3
39
21

normal
mildly impaired
impaired
normal
mildly impaired

32
16
I
28
14

severely
impaired
subnormal
subnormal
impaired
mildly impaired
impaired

Multiple Choice Vocabulary' Test
37
(verbal intelligence) [8]

17-32

20
IQ = 89
(low normal range)

16
IQ = 83
(subnormal)

IQ = 88
19
(low normal range)

Dementia Rating Scale
(severity o f dementia)
[7]
Attention
Initiation and perseveration
Construction
Conceptual thinking
Memory

Raven’s Standard
Progressive Matrices
(nonverbal intelligence) [9]

60

(18-40)

8
IQ = 63.6
(floor effect; distinctly
impaired)

13
IQ = 63.6
(floor effect; distinctly
impaired)

8
IQ = 63.6
(floor effect, distinctly
impaired)

93

50-70

32.5

32.5

6
5
4-8
5-13
8-12
6-12
11-19

4
4
3
4.5
7
2.5
7.5

5
5
5
5
8
3
II

MQ = 86
(low normal)
subnormal
normal
normal
normal
normal
subnormal
normal

32.5

6
5
9
23
15
14
21

MQ = 72.5
(subnormal)
subnormal
subnormal
subnormal
subnormal
subnormal
subnormal
subnormal

3
3
5
1.5
8
6.5
8

MQ = 67
(subnormal)
subnormal
subnormal
normal
subnormal
normal
subnormal
subnormal

40

(25-40)
(reproduction)

20

(subnormal)

21

(subnormal)

19

(subnormal)

Recurring Figures Test
(visual memory) [12]

56

17-36

-1
T = 25
(severely impaired)

3
T = 28
(severely impaired)

Continuous Figure Recognition
(visual memory) [ 13]

66

(26-64)

34

normal range

39

normal range

16

subnormal

9

mild deficit

8

questionable or
very mild deficit

18

severely
impaired

Wechsler Memory Scale
(global memory)
[10.11]
Information
Orientation
Mental control
Semantic memory'
Digit span
Visual reproduction
Verbal paired associated
learning
Selective Reminding Test
(verbal memory)
[3.11]

Syndrome Short Test
(memory and attention)
[14]

0-4
0
(maximum
score of 27
= maximum
deficit)

3
T = 28
(severely impaired)

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1 Comments in parentheses indicate functions assessed.

Discussion

Differential Diagnosis
According to the results of serial neuropsychological
examinations and the brain biopsy we diagnosed AD. The
extensive WMC in MRI and the reduction of perfusion
raised some possibilities of other differential diagnoses.
Progressive multifocal leukencephalopathy was excluded
because tumor search was negative and the course too
benign, encephalitis was not likely because CSF was nor­
mal. Metachromatic leukodystrophia was an unlikely
diagnosis since serum arylsulfatase A was normal. Binswanger’s disease was not probable, because the patient
did not suffer from diabetes or hypertension. In the
absence of risk factors there was not much reason to sup­
pose she might have a severe atherosclerosis or arteriolosclerosis as an underlying disease, although this cannot be
excluded from the performed imaging devices. The histopathological results also showed no signs of arteriolosclerosis.
Although the changes were much more pronounced on
the right side, there were also signal alterations on the left
side, which made tumor a very unlikely diagnosis.
Occurrence o f WMC
Recently many authors have described WMC in pa­
tients with AD [2, 15, 16. 18-25]. There is still consider­
able disagreement about the nature and significance of
these changes in healthy persons, persons with cardiovas­
cular risk factors, AD patients with early onset and AD
patients with late onset.
Some authors think that WMC are unspecific occur­
ring in all kinds of diseases such as senile dementia of Alz­
heimer type. Binswanger’s disease [16] and even in clini­
cally healthy persons [26].
Beyond a certain age, periventricular changes were
found in almost 80% of patients older than 50 years with a

298

history of cerebrovascular risk factors [27], subcortical
lesions being a very frequent incidental finding in elderly
patients without having clinical significance. Therefore,
some studies assume that WMC are not more frequent or
relevant in AD patients than in healthy controls [25, 28],
whereas others report differences in the frequency of
WMC between AD patients and normal elderly [29].
However, the appearance of WMC in Alzheimer pa­
tients is usually different. Their distribution is more dif­
fuse and they are not as hypodense as incidental findings.
Clinical Relevance o f WMC for the Course o f AD
There is also disagreement about the clinical relevance
of WMC for the course of AD and their relation to the
severity of dementia. White matter lucencics, also termed
leukoaraiosis, might represent a marker for early demen­
tia [31], They also may predict the development of clini­
cally significant cerebrovascular disease [32], Because
WMC may only be found in some cases of AD, many
authors [24,25, 30] assume a high correlation between the
age of disease onset and the presence of WMC. WMC arc
supposed [24, 30] to be more frequent and severe in the
late-onset form of AD (age at onset beyond 66 years). One
of these studies [30] might be questioned, because pa­
tients with vascular risk factors were not excluded. In con­
trast, some studies [20] suggest an association of the pres­
ence of white matter low attenuation not only with higher
age but with a more severe degree of dementia and
increased CSF/serum albumin ratio. Others could not
establish a correlation of MRI white matter and periven­
tricular hyperintensities with Mini Mental State Exami­
nation scores [25], Another investigator assumes [16] that
WMC are neither related to the severity nor to the region­
al appearance and accentuation of the cortical Alzheimer
process. We believe that, as reported by Besson et al. [15]
and Almkvist et al. [33], specific regional WMC and local
perfusion deficits may result in specific focal neuropsy­
chological impairment measurable by psychometric tests
relating to certain brain areas. Our case does not support
the notion of a correlation between severity of WMC and
dementia but rather the existence of a relationship be­
tween localization of WMC and neuropsychological defi­
cits. In spite of extensive changes on MRI our patient was
not severely demented at the time the extensive focal
WMC were noticed first and she had a normal CSF/serum
albumin ratio. Thus, the case of our patient, who was 52
years old at onset and presented WMC, cannot support
the notion of early onset being associated with less fre­
quent or severe WMC.

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sodes. The neurological status did not show any change. CT scan
revealed the defect caused by a brain biopsy and the same findings as
before, SPECT also gave the same result as in the previous examina­
tion.
The relatives of the patient now reported severe memory deficits.
The neuropsychological examination showed a deterioration of most
subtests performed: constructive-apractic disturbances were most
severe. The result o f the Mini-Mental status was within the demented
range for the first time, the memory quotient of the Wechsler Memo­
ry' Scale was obviously subnormal. The results of the Syndrome Short
Test and the Dementia Rating Scale according to Matlis also dis­
closed impressive deterioration (table I). The diagnosis of AD could
not be questioned any more.

The large MRI alterations were located prominently in
the right hemisphere and the patient’s constructive and
spatial orientation deficits also pointed to the right hemi­
sphere, whereas her other deficits were only mild and not
very typical of AD at the early stage. Therefore the estab­
lishment of this diagnosis was difficult. It was only after
follow-up that dementia became more evident.

circumscribed as in our patient seems to be very rare.
Anyway, the SPECT examination in this patient also
showed that hypoperfused regions may give a hint as to
the area responsible for the cognitive deficits.

Etiology and Morphology o f WMC
The etiology of leukoencephalopathy in the elderly
consists mainly of arteriolosclerosis and atherosclerosis
[ 1]. Surprisingly, Ferrer [ 1] found the same morphology of
lesions in Binswanger’s disease, multi-infarct encephalop­
athy and AD and suggested that this might be the result of
subacute hyperperfusion or hypoxic damage caused by
different etiologies in different diseases. The cause of
hypoperfusion in AD may be congophilic angiopathy of
the meningeal and cortical vessels with moderate arterio­
lar hyalinosis in the white matter, leading to incomplete
infarction. In contrast to this, Besson [15] believes that
WMC in AD are caused by a higher free-to-bound water
ratio compared to healthy persons. Either way findings
may be explained by alteration of myelin structures, or by
fluid increase in glial cells or in the extracellular compart­
ment following loss of nerve fibers.
Selective incomplete white matter infarctions were
found [17, 18] in areas where a reduction of gangliosides
and changes in the ganglioside pattern reflected the histo­
logical degree of severity of the infarctions.
These studies confirm the theory of WMC being a sub­
total infarction of myelin and axon. The brain biopsy of
our patient showed senile plaques and a congophil angio­
pathy with intramural storing of amyloid and cortical and
subcortical astrogliosis. Thus, we conclude that some
cases of AD may also belong to the vascular diseases [34],
although there are probably many interfering pathomechanisms involved. As considered by some investigators
[35], AD might be a heterogenous disease.

This case of AD is very' interesting due to various
aspects. First, many authors have described WMC in AD
patients before, whereas signal alterations as extensive as
those in our case, which are not widely distributed but
rather focused in the temporal lobes, are rare [38], Brain
biopsy was taken directly from the area most severely
involved and showed the changes typical of AD. Second,
for the first 3 years the course of the disease was benign
although the focal WMC were already extensive. This
supports the notion that the correlation between severity
of MRI changes and severity of dementia is rather low.
Summing up we may say that the diagnostic relevance
of WMC in AD is not yet fully understood, but it may
pathogenetically resemble other diseases that cause WMC
by the mechanism they cause incomplete infarctions,
which might either lead to signs and symptoms or remain
asymptomatic.
In our opinion brain biopsy is only warranted if the
diagnosis is doubtful and some benefit for the patient may
be anticipated. Nevertheless, larger series of biopsies will
be required in order to clarify the etiology and diagnostic
significance of white matter changes in patients with AD.

Conclusions

Perfusion Deficits and W MC

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In the HMPAO-SPECT examination our patient had a
large perfusion deficit in the right temporal lobe in an area
where WMC on MRI scan were most distinct. The histol­
ogy of the brain biopsy from this area showed senile
plaques and congophilic angiopathy. In our case the
angiopathy may have led to incomplete infarction as an
underlying cause of the WMC. SPECT m ight be helpful to
establish the diagnosis AD, but careful interpretation of
the results is necessary, because changes are frequent but
may not be specific for AD [36, 37], A perfusion deficit as

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References