Archives of Gerontology and Geriatrics
33 (2001) 179– 190
www.elsevier.com/locate/archger

Dementia following posterior cortical
atrophy—a descriptive clinical case report
Nages Nagaratnam *, Kujan Nagaratnam, Daniel Jolley,
Allan Ting
Blacktown–Mount Druitt Health, Blacktown, NSW 2148, Australia
Received 5 December 2000; received in revised form 4 June 2001; accepted 6 June 2001

Abstract
Whether posterior cortical atrophy is a distinct entity or a variant of one of the other
degenerative processes continues to be debated. We describe five patients four of whom had
bilateral changes of posterior cortical atrophy on the CT scan. These four had a cluster of
symptoms consistent with parieto-occiptial dysfunction together with a spectrum of dementia. The fifth patient with unilateral changes had optic ataxia, apraxia of gait and dementia.
Three of the five patients were heavy drinkers of alcohol but any direct causal link between
alcohol and posterior cortical atrophy is tenuous but alcohol could be a consideration in
lowering the threshold for dementia in conjunction with other determinants. The study
revealed there is little or no difficulty in recognizing posterior cortical atrophy in the early
stages and the end stages are sufficiently uniform to reduce the diagnostic uncertainty.
© 2001 Elsevier Science Ireland Ltd. All rights reserved.
Keywords: Posterior cortical atrophy; Lobar atrophy; Optic ataxia; Apraxia of gaze; Asimultagnosia;
Gerstmann’s syndrome

1. Introduction
Cortical lobar atrophies are more common than is realized. Pick (1892) described
a man with dementia and aphasia, autopsy revealing changes primarily in the left
temporal lobe. Pick’s disease could be considered a form of localized cerebral
atrophy. Mesulam (1982) described a slowly progressive language disorder in which
* Corresponding author. Tel.: +61-2-9881-8000; fax: + 61-2-9881-8020.
0167-4943/01/$ - see front matter © 2001 Elsevier Science Ireland Ltd. All rights reserved.
PII: S 0 1 6 7 - 4 9 4 3 ( 0 1 ) 0 0 1 7 9 - 0

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radiological and histological changes were in the left perisylvian region. Predominant involvement of the frontal and temporal lobes give rise to fronto-temporal
degeneration (FTD) and often manifests as either overactivity and disinhibition, or
as apathy. Emphasis on one or the other has lead to two subtypes, a frontal variant
of FTD (Gregory et al., 1999) and a temporal variant (Edwards-Lee et al., 1997).
Lobar dysfunction attributable to posterior parietal and occipital regions have been
described. Benson et al. (1988) described a syndrome characterized by early ataxia,
anomia, agraphia, acalculia, visual agnosia, disorientation, disorders of ocular
fixation and transcortical sensory aphasia following lobar atrophy of the occipital
cortex.
There is as yet no clear statement as to whether posterior cortical atrophy (PCA)
is a specific entity. Nevertheless the concept that PCA is a definite entity is not
likely to disappear even though unresolved issues remain. This descriptive study of
five patients with PCA was undertaken towards emphasising the conceptual shifts
and new information that has guided our current view of PCA.

2. Materials and methods
This is a retrospective study of five patients admitted to the Blacktown– Mount
Druitt Health service over a period of 1 year. The inclusion criteria for the study
was the satisfaction of CT scan incidence of posterior cortical atrophy with or
without impairment of ocular fixation. Optic ataxia was defined as inability to point
accurately to a target under visual guidance. The patient was asked to touch a
number point on a picture, and to trace a line drawing. Apraxia of gaze was the
inability to gaze directly when desired and was tested by asking the patient to look
at an object held on the patient’s side and then to look at the examiner’s nose.
Simultagnosia refers to the inability of the patient to appreciate the significance of
a picture or scene as a whole although individual parts are recognised. The patient
was asked to pick the objects on a tray.
The presence of dementia was established on clinical grounds using a modified
form of the Cambridge Examination for Mental Disorders of the Elderly
(CAMDEX) (Roth et al., 1986). The CAMDEX composes a number of items,
namely medical and psychiatric history, physical examination, mental state examination, cognitive tests and an interview with a relative or carer. For the cognitive
part of the examination Folstein’s Mini-Mental State Examination (MMSE) (Folstein et al., 1975) was administered and supplemented by such items as the ability
to abstract, calculate and for perceptional abilities. Interview with the relative or
carer included such information as orientation, memory, behaviour and the ability
to maintain everyday activities. The diagnosis of dementia was based on DSM-III
criteria for primary degenerative dementia (American Psychiatric Association,
1987). The degree of language impairment was obtained from the MMSE after
Chui et al. (1985) adding the scores on selected items namely, naming of two
objects (2), repetition (1), 3-stage motor commands (3), written commands (1) and
writing a sentence (1) and defined as 0–8. The Barthel Index (Mahoney and

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181

Barthel, 1965) commonly used as a rating scale of physical dependency was scored
on a shortened form. The overall disability was based on the Rankin Grades for
accessory functional disability (Rankin, 1957) and relied on information obtained
from caregivers. Severity of the dementia was graded based on the Clinical
Dementia Rating (CDR) of Hughes et al. (1982). All the patients underwent
physical examination together with a meticulous neurological examination. Routine
laboratory investigations and special investigations were not done on some of the
patients for reasons of cost.

3. Results

3.1. Case 1
GW, a 59-year-old engine driver, was retrenched 2 years earlier for redundancy.
He was escorted by his wife, who was the informant. There was a history of
fracture of the skull in early childhood. He had been a smoker and heavy drinker
over several years, but more recently had reduced his intake. It was alleged he was
forgetful. He was described by his wife as having a placid disposition, but had of
late become unstable at times, argumentative and ‘cranky’. His functional capacity
was assessed by the wife’s report. He was capable of basic self care, but had
difficulty with dressing (often confusing front and back). There was no history of
mental illness, nor has he had any symptoms of disordered perception, depression
or cerebro-vascular accident.
Physical examination revealed normal vital signs. He was normotensive and there
were no past abnormalities in the respiratory or cardiovascular systems. Neurological examination revealed normal muscle strength and bulk, and there was no
detectable rigidity. Visual fields were normal, although he had impaired ocular
fixation — when confronted with objects it took a long time for him to recognise
and name the object. He had no difficulty in naming colour. Finger movements
were not possible under visual guidance. The gait was normal. He was alert and
somewhat cooperative. He was poorly oriented for year, month and date, but not
to city. He could not spell the word ‘world’. He had impaired memory, remembering only one of three objects after 5 min. Remote memory for personal and
historical details was poor. He could not name the present Prime Minister or any
former prime ministers. Serial 7s were not possible. He could only make general
statements regarding current events. Interpretation of similarities and proverbs were
poor. He could not draw the face of the clock and indicate any specific time, nor
could he copy 2 or 3 dimensional geometric designs. He could not trace an
approximation of the map of Australia, and there was poor coordination of the eye
and hand. He had difficulty in reading but could pick all the objects placed in front
of him. He could sign his name with difficulty. The CT scan demonstrated
enlargement of the posterior horns of both lateral ventricles, with patchy widening
of the sulci over the posterior aspect of the brain (Fig. 1(a)). GW had evidence of
parieto-occipital involvement manifesting as dressing apraxia, memory deficits,

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abnormalities of ocular fixation and required considerable time to locate target
visually and could not use his hands to guide visual search together with alexia and
agraphia.

3.2. Case 2
DC, a 74-year-old right-handed retired farmer of Italian extraction, was seen
with a history of progressive deterioration in his ability to converse over 4–5 years.
He was escorted by his wife. Apart from this his previous health was of no clinical
significance. He hardly drank and did not smoke. He was born in Italy and
migrated to Australia at 55. Direct enquiry into mood, capacity of pleasure,
thoughts about the future, loss of appetite, weight and sleep, did not reveal any
symptoms of significant depression. There was no history of suspiciousness, para-

Fig. 1. (a) Case 1 CT scan showing dilatation of the posterior horns of the lateral ventricles and
prominence of the sulci in the parieto-occipital regions bilaterally. (b) Case 2 showing dilatation of the
posterior horns of the lateral ventricles and cortical atrophy.

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183

noia or behavioural problems. His mood was described as neutral. Frequently he
mistakes his wife for someone else. He had poor hearing. According to his wife
he was independent for most activities of basic self-care.
General physical examination was unremarkable. Neurological examination
found him to be alert and cooperative. The ‘head turning sign’ was positive. He
scored poorly in the MMSE. He was poorly orientated. He could not name the
current year, nor the year of his birth or street where he lived. Remote memory
was poor for personal and historical details. He could not recall the name of
Italy’s leader during the second World War, Mussolini, even given the name. He
was unable to perform verbal or written calculations, or simple instructions
mobilising single digits. Spontaneous speech was markedly reduced and had
significant slurring of the words. Comprehension of complex phrases and multistage commands was impaired. He could not read or write. He could not draw
the face of a clock or copy two and three dimensional geometric designs. He
pointed erratically to objects, lacked eye and arm coordination, and was unable
to trace a hand drawing. When about to sit on the chair he nearly missed the
seat. He picked seven of the ten objects presented in front of him, and could
name objects and colour. The CNS was grossly intact. Muscle strength and bulk
was normal. There was no detectable rigidity. The gait was normal. The CT
scan of the brain showed dilatation of the posterior horns of the lateral ventricles bilaterally (Fig. 1(b)). DL had impaired visuospatial skills, Balint’s syndrome, agraphia, alexia, acalculia, environmental agnosia, language and cognitive
impairment.

3.3. Case 3
LS, a 72-year-old right handed woman was seen for poor vision and forgetfulness. The exact duration of the illness was unclear but according to the daughter
who accompanied her it could be several years. She lives with her husband and
was independent for all activities of daily living. There was no history of strokes,
alcoholism, mental illness, nor was she on any medication. She was eating
poorly and has lost weight, but there were no symptoms of depression.
Physical examination revealed a blood pressure of 120/80 mmHg. There was
no evidence of cardiac decompensation. The CNS was grossly intact apart from
the oculomotor signs. There was no detectable rigidity. She was alert but poorly
orientated in time and place. She could not name the street and number of her
house, the current year and month, nor could she recall the year of her birth.
Her ability to calculate was impaired, as was her ability to abstract. She recalled
one of three objects at three minutes. She could not draw the face of a clock to
indicate the time. Copying of 2–3-dimensional geometric designs was poor. She
could not read or write, and scored 14/30 on the MMSE. She had difficulty in
ocular fixation. Object naming was variable, for instance she took a long time to
name the pen shown and knew its use, but when shown the glasses she could
not name it nor could she recognise even with palpation. When told it was a

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Fig. 2. (a) Case 3 CT scan showing dilatation of the posterior horns of the lateral ventricles bilaterally,
cortical atrophy and widened Sylvian fissures. (b) Case 4 dilatation of the posterior horns.

pair of glasses she could not describe its use. She had poor arm/eye coordination
and could not trace the outline of a map. She however picked all the objects on the
tray. She was able to recognise colour. Visual fields were difficult to test. The CT
scan of the brain showed significant dilation of the posterior horns of the lateral
ventricles suggestive of bilateral posterior cerebral atrophy (Fig. 2(a)). LS exhibited
components of Balint’s syndrome (Balint, 1909), higher visual dysfunction, acalculia, agraphia with cognitive and memory impairment.

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185

3.4. Case 4
RS, a 78-year-old man, presented with fluctuating confusion following a fall. He
had tripped when feeding his dogs and fell backwards hitting the back of his head.
He had lost consciousness momentarily. He had been living with a friend of his,
although no clear history of his pre-morbid cognitive status was available. He is
said to have had problems with his vision and had shortly prior to the event had
complained of blurring of vision and disturbance of colour perception. His family
members with whom he had not kept close contact, said that he over several
months he had been telephoning them repeatedly over trivial matters.
The vital signs were unremarkable. There were significant findings in the cardiovascular or respiratory systems. Neurological examination revealed his visual fields
to be intact. The pupils were equal and reacted to light and near response. He had
difficulty in comprehending what was said. He remained confused and when seen 2
weeks later he was alert but with worsened attention span. He was unable to gaze
directly when requested. A further 2 weeks later he could not coordinate hand and
eye movements and pointed erratically to objects. He could not touch the finger of
the examiner. He could not name ordinary objects, their use or colour. His speech
output was markedly reduced and he had difficulty with comprehension. He could
neither read nor write. No formal memory or cognitive tests were possible. On
neurological examination muscle strength and bulk were normal, but he could
neither stand nor walk. The post-stroke period was complicated by acute renal
failure resulting from dehydration. He was discharged to a nursing home facility.
The CT scan done soon after the initial event showed a small right occipital
intracerebral haemorrhage with extension into the posterior horn of the right lateral
ventricle. The left posterior horn was dilated. A repeat CT scan done 2 weeks later
showed dilatation of both posterior horns (Fig. 2(b)) RS showed components of
Balint’s syndrome, acalculia, agraphia and visual agnosia for objects.

3.5. Case 5
AC, a 60-year-old man, was seen with a history of having suffered a seizure
secondary to non-compliance with medication. He was on phenytoin and carbamazepine. There was a strong history of heavy drinking over several years. He was
alert with near normal attention span. He performed poorly in the MMSE. Speech
output was reduced with poor comprehension for complex phrases. He had
difficulty naming objects and their use, but could identify colours. Neurologically
there were no focal localising signs. There was no detectable rigidity and could not
coordinate eye and hand. The gait was abnormal broad-based and sway. Tandem
stance and tandem walk were not possible.
Routine investigations, including B12, iron studies, folate and TSH were all
normal, while TPPA was negative. CT scan of the brain showed marked dilatation
of the posterior horn of the left lateral ventricle with prominent sulci over the
occipital and parietal regions (Fig. 3). AC had only optic ataxia, ataxic gait and
moderate cognitive and memory impairment and the scan showed only unilateral
changes.

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186

Fig. 3. Case 5 CT scan shows unilateral dilatation of the posterior horn of the left lateral ventricle with
prominent sulci over the left parieto-occipital regions.

Tables 1 and 2 summarize the individual characteristics, neurological and neurobehavioural changes.

4. Discussion
We have described five patients with a cluster of symptoms associated with
posterior cortical atrophy. Four had bilateral changes on the CT scan. Their ages
ranged from 59 to 78 years with a mean of 71 years and the symptomatology dating
back to several years before their presentation. The four patients had visual
complaints, forgetfulness and difficulties in communication. All four had features
(complete or partial) consistent with Balint’s syndrome (optic ataxia, apraxia of
Table 1
The patients characteristics and radiological findings
Case

Age/sex

Symptom/
duration
(years)

Symptom
presentation

Other
relevant
history

CT scan

Severity of
dementia
(CDR)

1

59/M

Several

Head injury/
alcoholism

74/M
72/F
74/M

4-5
Several
Years

Dilatation of
posterior horns
As above
As above
As above

2

2
3
4
5

60/M

2

Reduced speech/
forgetfulness
Inability to converse
Poor vision
Inability to name
or recognise objects
Poor memory

Alcoholism
Alcoholism/
epilepsy

Dilatation of
L-posterior
horn atrophy
parieto-occipital
regions

2
1
3
2–3

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187

Table 2
The neurological and neurobehavioral changes
Case Balint’s

Higher visual Languageb Cognitivec
dysfunctiona

Gerstmann’s

Optic Apraxia Simultagataxia of gaze nosia
+
+
+
+
+

1
2
3
4
5
a
b
c

Acalculia Agraphia l-r
Finger
discrimination agnosia
+
+
+
+
+

+
+
+
+
−

+
+
−
+
−

+
+
+
+
+

ND
ND
ND
−
ND

ND
ND
ND
−
ND

+
+
+
+
−

+
−
+
+
+

1
2
4
2
2

Severe
Severe
Moderate
Moderate
Moderate

Alexia and visual agnosia.
Language based on MMSE scores 0–8.
MMSEB9, severe; 10–20, moderate; \21, mild.

gaze and asimultagnosia) and components of Gerstmann’s syndrome (agraphia,
acalculia, finger agnosia and right /left discrimination) and a spectrum of dementia.
Case 5 had unilateral changes in the left parieto-occipital regions on the CT scan
and differed from the others in that he had no oculomotor abnormalities but for
optic ataxia. He had an ataxic gait and significant cognitive and memory impairment. Three of the five patients had a history of heavy drinking over several years.
Benson et al. (1988) described five patients with progressive dementia who at the
onset had higher visual dysfunction and subsequently developing alexia, agraphia,
visual agnosia, components of Balint’s and Gerstmann’s syndromes and transcortical sensory aphasia. The memory and cognition were spared until late in the course
of the illness. Since then there had been other reports (Kiyosawa et al., 1989; Hof
et al., 1990, 1993; Berthier et al., 1991; Levine et al., 1993; Victoroff et al., 1994;
Wakai et al., 1994; Ardila et al., 1997).
Balint’s syndrome is characterized by optic ataxia, apraxia of gaze and asimultagnosia All four patients had at least two or three components of Balint’s syndrome.
Many of the patients with this syndrome had bilateral parieto-occipital lesions and
the possibility of a selective involvement of the dorsal occipito-parietal pathways. It
has been suggested that Balint’s syndrome results from disconnection rather than to
focal posterior damage (Hausser et al., 1980). Case 5 with unilateral changes had
only optic ataxia which could follow unilateral damage in the parieto-occipital
region (Haaxma and Kuypers, 1975; Nagaratnam et al., 1998) or further forwards
due to disruption of its occipito-frontal connections (Nagaratnam et al., 1998). A
lesion in the left occipito-temporal junction gives rise to another group referred to
as ventral simultagnosia and associated with agnosia, prosoagnosia and alexia and
attributed to the ventral occipito-fugal pathways and the occurrence of Gerstmann’s syndrome (Gerstmann, 1940) to involvement of the adjacent inferior
parietal lobes.
Posterior cortical dysfunction may have a variety of causes such as progressive
degenerative cortical disease, vascular, tumour or metabolic causes. Three of the

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five patients in this study were heavy drinkers. In several disorders there is a
predilection for certain parts of the brain to be affected, for example in Alzheimer’s
disease the hippocampus has an increased vulnerability and occurs early and
Alzheimer’s disease has been characterised as ‘a hippocampal dementia’ (Ball et al.,
1985). Focal damage to the corpus callosum a hallmark of Marchiafava-Bignani
disease is a rare complication of chronic severe alcoholism and in the late stage of
the disease the MRI shows diffuse atrophy and focal necrosis of the corpus
callosum (Chang et al., 1992) and the signs are that of interhemispheric disconnection. The frontal hypometabolism that had been demonstrated in chronic alcoholism did not correlate with the degree of frontal atrophy in the frontal lobes on
the MRI which showed a global cortical atrophy. (Boller et al., 1995). Although a
causal link between alcohol and PCA seems remote yet alcohol could be a factor
interacting with any other factors to reduce the threshold for the progression to
dementia.
The question is whether the syndrome of posterior cortical atrophy is a distinct
entity or a variant of one of the well known tissue processes and had been seen not
only with Alzheimer’s disease (Berthier et al., 1991; Victoroff et al., 1994), Pick’s
disease, Creutzfeld-Jakob Disease and progressive subcortical gliosis. Although
there is a common pattern in its presentation in early Alzheimer’s Disease there is
a heterogeniety (Mayeux et al., 1985) and had led to the identification of subtypes
(Chui et al., 1985). The visuomotor visuospatial, components of Balint’s syndrome
and reading disorders the hallmark of posterior dysfunction occurs in AD. Of the
30 patients with one or more visual deficits due to probable AD 6 had Balint’s
syndrome (Mendez et al., 1990). Hof et al. (1990) compared eight patients with AD
and Balint’s syndrome early in the course of the illness with AD patients without
Balint’s syndrome found there was a greater histological changes of AD in the
occipital regions of the former. Other investigators however had shown that in AD
patients with visual symptoms there was no such dominance (Levine et al., 1993;
Victoroff et al., 1994). Although posterior dysfunction does not represent a single
pathology due to an intrinsic disease according to Victoroff et al. (1994) it may not
be the pathology but the neurobiological change most relevant to the clinical
features.
Whether PCA is a specific entity or not depends on: (1) one’s starting point of
view; and (2) the need to look beyond what might be expected from the atrophy
(Ardila et al., 1997). There are pathological, clinical and radiological evidence for
and against PCA being a discrete disease.
In support of a definite disease:
1. It is clinically homogenous (Benson et al., 1988; Victoroff et al., 1994).
2. There is little difficulty in recognizing PCA in the early stage of the disorder on
clinical evidence.
3. Although it does not represent a single pathology (Alzheimer’s disease; subcortical gliosis; prion diseases), it is the neurobiological changes and not the
pathology that are more relevant to the clinical features (Victoroff et al., 1994).
4. The focal cerebral atrophy giving rise to a variety of symptom clusters reflects
the distribution of the lesion rather than the pathology.

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189

5. Although there is great difficulty in recognising clinically PCA in the late stages
however the end stages of PCA are sufficiently uniform to reduce the diagnostic
uncertainty (present study).
Against a definite disease:
1. Multiple factors may play a role in its causation and pathogenesis.
2. Dementia presenting with visual abnormalities and focal posterior cerebral
atrophy may be due to several other dementing illness (Cogan, 1985; Nissen et
al., 1985; Feher et al., 1989).
3. Focal symptoms for instance apraxia or agnosia though unusual does occur in
the early stages of Alzheimer’s disease and predominantly focal variant is a
common occurrence.
4. Focal attenuation as part of a generalised degenerative disease could give rise to
progressive focal neurological deficit (Crystal et al., 1982).
5. Precise pathology cannot be predicted clinically.
6. The pathological changes are not specifically associated with PCA (Benson et
al., 1988; Victoroff et al., 1994) and the underlying heterogeneity may represent
atypical variant of AD, Picks or other distinct entities.
None of the above is satisfactory on its own and it may be difficult to synthesize
them with a single description without oversimplification. There remains unresolved
issues and PCA has its critics because of the considerable overlap in the clinical and
pathological findings which argue for a simple explanation. For the clinician there
is much to be attained by simplification and accepting that PCA is an entity.

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