NOTE
NEGATIVE EMOTIONS AND ANOSOGNOSIA
Oliver H. Turnbull, Cathryn E.Y. Evans and Vanessa Owen
(Centre for Cognitive Neuroscience, School of Psychology, University of Wales, Bangor, UK)

ABSTRACT
Patients with anosognosia fail to acknowledge, or feel distressed by, their disability. Given the recent suggestion that
right (frontal) systems are selectively involved in negative emotions, it might be claimed that anosognosia results from a
disruption in negative emotions. This is not consistent with the finding that some anosognosic patients exhibit substantial
fluctuations in emotion, including the experience of negative emotions such as sadness. The present study investigates a
patient (IW) with a right convexity lesion and anosognosia. He reported being frequently overcome by powerful emotions,
especially sadness. IW was assessed on a self-report emotion questionnaire, where his reports were typically of higher
levels of emotion than the control group. He was also assessed on the more indirect measure of Affective Story Recall.
Here his pattern of emotional experience was similar to that of two control groups, one of which consisted of nonanosognosic patients with hemiparesis. His performance on Story Recall was notable in that he directed his emotions to a
different ‘object’ to that of controls (other vs. self, respectively). These findings are not consistent with any claim that
anosognosia results from an absence of negative emotions.
Key words: Anosognosia, positive emotion, negative emotions, affect

INTRODUCTION
Denial of deficit (anosognosia) is a welldescribed disorder, encompassing a range of
unusual phenomena (see Bisiach and Geminiani,
1991; Feinberg, 1997; Gainotti, 1972; McGlynn
and Schacter, 1989, Prigatano and Schacter, 1991
for review). However, until recently, the disorder
was often regarded as little more than “an
enigmatic clinical curiosity” (Ramachandran, 1996,
p.124). In its extreme form the disorder presents as
a manifest denial of paralysis, despite clear
evidence to the contrary, where denial occurs even
after explicit demonstration of the deficit by the
examiner. In other circumstances, perhaps to be
regarded as milder forms (anosodiaphoria) the
patient may become aware of their hemiparesis, but
deny that it causes them any functional disability
(c.f. House and Hodges, 1988).
In some cases the denial of deficit is held with
such strong conviction that the false beliefs persist in
the face of all contradictory evidence and logical
argument, even if this results in strange beliefs or
perceptual experiences (Bisiach et al., 1986;
Halligan et al., 1995; Ramachandran and Blakeslee,
1998; Weinstein and Kahn, 1955). It is clear that
anosognosia can present in a number of ways
(Marcel et al., 2004), and this may be reflected in
the diversity of explanation for the phenomenon.
Some recent accounts stress the way in which
predicted or willed movement might be at variance
with the visual and somatosensory consequences of
the action itself (Blakemore et al., 2002; Daprati et
al., 2000; Frith et al., 2000; Heilman et al., 1998; see
also Fink et al., 1999; McGlynn and Schacter, 1989;
Sirigu et al., 1999). Accounts of this type almost
certainly have a role to play in explaining the nature
Cortex, (2005) 41, 67-75

of the disorder. However, there are several reasons
why such accounts are probably inadequate as a sole
explanation (Marcel et al., 2004). Thus, while
mismatches between intended actions and outcomes
“may be necessary for anosognosia they do not seem
to be sufficient” (Frith et al., 2000, p.1782).
Another potentially fruitful proposal focuses on
issues of motivation and emotion. There are some
theoretically-driven grounds for this idea – for
example the recent focus on the role of secondary
somato-sensory cortex, in the right-hemisphere, in
the higher aspects of homeostasis, somato-sensory
representation, and emotion regulation (Damasio,
1994 pp. 62-69; 1999 pp. 209-213; 1996). This
argument is supported by a well-established
literature suggesting a central role for the right
hemisphere in the perception and expression of
emotion (e.g. Borod, 2000). For example, there are
well-described effects of right-sided intra-carotid
amobarbital, which produces anosognosia in a high
proportion of cases (Brier et. al., 1995; Lu et al.,
1997, Meador et al., 2000), and has long been known
to differ from the more emotionally appropriate
outcomes that follow from left-sided amobarbital
(e.g. Gainotti, 1972, see Feinberg, 1997 for review).
There is also a long-standing clinical literature
on patients with right-sided brain lesions, showing
that patients with anosognosia often do not show
the negative emotional responses to their paresis
that one might expect. Most notably, they have
fewer so-called ‘catastrophic’ reactions (episodes of
tearfulness and emotional breakdown) that are
more frequently seen in patients with left
hemisphere lesions (e.g. Fedoroff et al., 1992;
House et al., 1990; Gainotti, 1972; 1997; Jorge and
Robinson, 2002). Also, anosognosics are often not
merely unaware of their deficits, but are sometimes

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unnecessarily optimistic about their medical
condition (i.e. ‘euphoric-maniacal’, Gainotti, 1997),
and may also over-emphasize their abilities with
the paretic limb (e.g. Ramachandran and Blakslee,
1998, pp.138-139).
The absence of a negative attitude towards
impairment in patients with right-sided lesions,
together with reports of low mood after left-sided
lesions (Fedoroff et al., 1992; Gainotti, 1972; Jorge
and Robinson, 2002) has led to Davidson et al.’s
(e.g. Davidson, 2001; Davidson and Irwin, 1999)
suggestion of a right frontal system involved in
negative (withdrawal-related) emotional states, with
left frontal regions associated with positive
(approach-related) emotion1. Thus, Davidson et al.
have suggested that depression might result from
disruption of a (left-sided) positive emotion system
(e.g. Davidson and Irwin, 1999, p. 13). On this
argument anosognosia would result from a
disruption of negative emotion systems, leaving the
patient with only a (left-sided) positive emotion
system.
However, there are several reasons to doubt this
possible link between an absence of negative
emotions and anosognosia. For example, a
disruption of negative emotions would explain only
the absence of emotion in relation to paresis, not
why the patient might actively deny their paresis
and explicit evidence thereof (Marcel et al., 2004).
It has also been pointed out (see Gainotti, 1997 for
review) that the low mood seen in patients with
left-sided lesions is likely to result from an
emotionally-appropriate response to their
substantial levels of disability – which typically
involves hemiparesis and non-fluent aphasia. A
further line of argument is that there are some
circumstances when right-sided lesions produce an
increase, rather than a disruption, in negative
emotion. For example, the occasional finding of
explicit dislike or obsessional hatred of the paretic
limb (‘misoplegia’, Critchley, 1974) seen after
right-sided lesions, which is discordant with a lossof-negative-emotions account. Finally, there have
been reports of frank depression after right
convexity lesions in patients who were also
anosognosic (e.g. Kaplan-Solms and Solms, 2000;
Starkstein et al., 1990; see also Turnbull et al.,
2002). Thus, many hold the position that the data

1The question of exactly how to define a ‘negative’ emotion is a complex
one. Some authors (e.g. Davidson) classify all experiences that appear to be
aversive in a unitary ‘negative’ category. However, recent work separating
independent emotions suggest that there may be several distinct classes of
negative emotion, with fear, anger and sadness (and perhaps others) as
likely candidates (e.g. Calder et al., 2001; Damasio et al., 2000; Le Doux,
1996; Panksepp, 1998). All such states appear to result from ‘aversive’
events or potential events: for example, anger with frustration of goaldirected action; fear with risk to bodily harm; and sadness with separation
and loss (e.g. Panksepp, 1998, p.52). A second line of evidence that
supports the claim that these emotions have a negative valence is that the
core anatomy of the purported anger, fear and sadness systems (such as the
amygdala, hypothalamus, and dorsal peri-aqueductal gray matter) appear to
have their substrate in regions that produce aversive responses when
electrically stimulated (Bandler and Shipley, 1994; Depaulis and Bandler,
1991; Panksepp, 1998).

are more consistent with “a general dominance of
the right hemisphere for emotional behavior than
with the alternative hypothesis assuming a different
specialization of the right and left hemispheres for
opposite aspects of… mood” (Gainotti, 1997, p.
692).
One class of evidence which bears on this
question, but is little cited, are the fluctuations in
emotion, and awareness of deficit, seen in some
anosognosic patients. For example, transient
recovery of awareness after caloric irrigation has
been reported by various authors (Cappa et al.,
1987; Ramachandran, 1994; 1996; Rode et al.,
1998; Vallar et al., 1990). It is of interest that, at
least in some of these cases, such patients often
had a selective failure to recall their, earlier
acknowledged, paresis when they had returned to
their anosognosic state. A further type of
fluctuation was noted by Moss and Turnbull
(1996), who described a patient who shifted
between a state of anosognosic denial and
misoplegia (i.e. from unawareness to obsessive
hatred). Finally, Kaplan-Solms and Solms (2000,
see also Turnbull et al., 2002) reported patients
who experienced transient awareness of their
deficit, including “sudden moments of tearfulness
and pre-tearfulness” (p. 166) which appeared to be
preceded by themes of ‘loss’ – even if the cause of
such loss was apparently unrelated to the
hemiparesis. Similar examples have been reported
by Ross and Rush (1981), and Starkstein et al.
(1988). This suggests that negative emotions may
be intact in at least some instances of anosognosia.
However, we note also that awareness of
hemiplegia may appear to vary, depending on the
nature of the question asked of the patient (see
Marcel et al., 2004), so that it is important to base
examples of fluctuations in emotion on the same
class of question asked at different times.
The fluctuations in emotion seen in these
patients suggests that they might show the full
range of emotional experience appropriate to their
neurological deficits, including anger and sadness.
This runs contrary to any claim (e.g. Davidson,
2001) for a right hemisphere system specialized for
negative emotions, and a role for loss of negative
emotions in anosognosia. The present study
investigates an anosognosic patient (IW) on direct
and indirect measures of emotion, especially
focusing on three classes of negative emotion.
CASE REPORT
IW was a 70-year-old, right-handed, man, who
had long been regarded as an upstanding member
of the community, and had spent his life in various
forms of public service (Royal Air Force, Police
Service, and political office). He was married, with
several children. In his younger years he had also
been an enthusiastic sportsman.

Negative emotions and anosognosia

69

may be the exact nature of the question asked of
him (see Marcel et al., 2004).
NEUROPSYCHOLOGICAL ASSESSMENT
Visuo-Spatial Ability

Fig. 1 – Lesion site in IW: a large right middle cerebral
artery infarction.

At age 68 he suffered a right fronto-parietal
cerebro-vascular accident (see Figure 1). Cortically,
this involved the right motor cortex, frontal eye
fields, frontal and parietal operculum, inferior
parietal lobule, and the anterior portion of the
inferior middle and superior temporal gyrus. There
was also some involvement of the insula, a
substantial portion of the frontal white matter, and
the globus pallidus (sparing the internal capsule).
IW was left with a substantial left hemiparesis,
largely sparing the face and involving the arm and
leg equally. The paresis had undergone a limited
recovery. When he was assessed (from 20-24
months after the stroke) he retained a substantial
paresis - such that he could move the upper arm
and shoulder well, but had no movement in the
distal portion of the arm and hand.
IW had shown marked anosognosia for his
paresis in the acute period after the stroke. When
assessed at 20-24 months this situation had
improved slightly, but was variable. There were
times when he was frankly anosognosic. On other
occasions he appeared to be aware of his
hemiparesis, but was wildly inaccurate about the
severity: for example claiming that it was “95%
returned to normal” (i.e. anosodiaphoria). At these
times his presentation resembled the dissociation
between awareness of disability and handicap
reported by House and Hodges (1988, pp. 114115), such that he could be made aware of his
paresis on direct questioning, but denied that it was
causing him any real handicap. Finally, there were
occasions where he showed far greater awareness
of his hemiparesis and its implication. At such
times he felt enormous frustration at his disability,
and such episodes often led to brief episodes of
tearfulness. However, when questioned later during
the same session on this topic, he typically
returned to the argument that his disability was
minor. Thus, IW was anosognosic or
anosodiaphoric during each assessment, with brief
periods of awareness of deficit during three of the
five testing sessions. A possible explanation of the
apparent differences in the level of his
anosognosia, for at least some of the instances,

Neglect and Extinction on confrontation
(Heilman et al., 2003, pp. 297-298): IW showed no
signs of hemi-spatial neglect on confrontation
testing in any sense modality (visual, auditory and
tactile). However, he showed clear signs of
extinction of the leftward stimulus on bilateral
stimulation. In 5/6 ‘bilateral’ trials in the visual
modality he reported the event as ‘right-sided’ only.
A similar effect was seen in 5/7 ‘bilateral’ trials in
the tactile modality. There were no signs of
extinction in the auditory modality.
Line cancellation (Albert, 1973): IW showed no
signs of neglect on the Albert line cancellation
task.
Line bisection (Heilman et al., 2003): IW
bisected 3/4 lines right of center. However, the
effect of lateral bias was small, his errors (on lines
of 12cm) being 2%, 3% and 8% right of center,
with his one leftward errors being 2% left of
center.
Rey Complex Figure Recall: IW’s memory of
this figure showed good recall of the basic
elements, though it was impoverished in terms of
detail (15/36). It was also rotated through 90
degrees relative to the original (see Solms et al.
1998; Turnbull et al., 1997a; 1997b for further
discussion of this sign).
Topographical orientation: IW drew a map of
his home town, which showed a clear
understanding of relative spatial relations.
However, it seems to have been inaccurate in
several details, and was rated as 7/10 by a member
of IW’s family familiar with the layout of the
town. He accurately located a number of British
cities on an outline map of the country.
EXECUTIVE FUNCTION
Block Design: IW performed very poorly on the
Block Design subtest of the WAIS-R, failing to
correctly complete any items successfully before
the test was terminated after item 6. His errors were
of three types: (i) failure to complete the figures
into the ‘square’ pattern of the model (items 1-4),
(ii) producing the correct overall ‘square’ shape, but
with a single block rotated or incorrectly chosen,
and (iii) a clear 90 degree rotation of one item.
Picture Completion: IW performed within
normal limits (Scaled Score 11).
Rey Figure Copy: IW produced a reasonable
final version of the figure, scored as 30/36. He
used a poor (Type 3) strategy and omitted the

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leftmost item from the figure, in spite of specific
prompting to be certain that he had completed the
entire figure.
Reitan’s Word Finding Test (Reitan, 1972). IW
performed well within normal limits (50/75) on this
test of verbal problem solving. The task requires
that the participant make a ‘guess’ at the meaning
of a nonsense word (‘grobnick’) after consecutive
clues (see Walsh, 1985, pp.155-156 for clinical
examples). E.g.: Without the grobnick we would
not live very long. The grobnick is very big. The
grobnick is very far away. We cannot see the
grobnick at night. The grobnick is hot and bright.
Austin Maze: IW showed a clear ability to learn
the route through the maze, but with a shallow
learning curve. He scored 12, 11, 10, 3, 10, 5,
5, 3 before testing was terminated. He showed
no impulsivity, and no systematic errors on
choice points, so that his poor performance seemed
more a result of visuo-spatial than executive
difficulties.
Comment
IW suffered a large right middle cerebral artery
infarction, and showed a range of neurological and
neuropsychological deficits consistent with this
lesion site: a substantial left hemiparesis, some
neglect-related and visuo-spatial disorders, and
denial of deficit (anosognosia). He did not appear
to be impaired on tests of executive function. IW’s
visuo-spatial deficits appear to be relatively minor,
and seem unlikely to be playing a substantial role
in generating his anosognosia.

From the perspective of IW’s family, the most
striking effect of his stroke was a change in
personality. His family reported that IW was easily
moved to tears. For example, when singing “sad
laments and other sad songs” in the church choir, IW
was frequently overcome with sadness, most notably
when he had returned for his first post-morbid
concert with his choir. IW burst into tears at the
beginning of a song, was incapable of joining in, and
merely stood still in the midst of his fellow
choristers, with tears streaming down his face, for
the remainder of the song. At the start of the next
song he was able to regain his composure and
continue to sing. When asked what the song in
question had been, he said that it was about
‘autumn’, with the leaves falling from the trees. IW
then clearly suggested (though he could not quite say
this out loud, for fear of becoming overcome with
emotion again when describing the event) that the
associated thought was one of the end of life. IW and
his family described many other examples of this
sort – such as when he read or saw a television report
of someone being involved in an accident. He was
notably more anxious when a member of his family
might be exposed to danger, such as his daughter
driving long-distances in her car.
There were no reports of IW behaving in a
disinhibited way (i.e. suddenly acting on impulse).
However, there were times when his behaviour
seemed fully planned, but ill-judged. Thus, on one
occasion he began telling a joke of a sexual nature
to a group of women. His sister and wife were
horrified, and said that such an event would have
been unimaginable to him pre-morbidly.
Affective Neuroscience Personality Scale

ASSESSMENT OF EMOTION AND PERSONALITY
A variety of approaches were adopted in order
to establish the nature of the changes to IW’s
emotional life. These consisted of (1) a self-rating
measure of emotion (Affective Neuroscience
Personality Scale), (2) a series of memory probes
relating to different classes of emotion (Affective
Story Recall), and (3) interviews with two
members of IW’s family, attempting to establish
the nature of IW’s pre-morbid personality, and
personality changes.
Interviews with IW’s family (his wife and
daughter) suggested a man who placed great
emphasis on authority figures, and on the
institutions of society in general. He had always
believed that there was a ‘right’ way to do things,
and that one should constantly strive to become a
better person. This account is of some interest
given that denial of deficit has been reported to be
more common in those who were pre-morbidly
“conscientious, highly work-oriented, orderly,
disciplined people” (Prigatano and Weinstein, 1996,
pp. 318-319; Weinstein, 1996; Weinstein and Kahn,
1953; see also Gainotti, 1975).

IW was asked to complete a multi-dimensional
emotion and personality inventory (Davis and
Panksepp, 1999; Davis et al., 2003), derived from
the basic categories of emotion that have emerged
from the recent neuroscience literature (Damasio et
al., 2000; Cloninger, 1994; Le Doux, 1996; Phan et
al., 2002; Panksepp, 1998; Rolls, 1999). This
measure is especially useful in the present
circumstances because it tracks negative emotions of
three separate types. The negative emotions are (1)
Anger: e.g. “When I am frustrated I often get angry”,
“If I am blocked from getting what I want, I usually
just accept it”; (2) Fear: e.g. “people who know me
well would say I am an anxious person”, “I am
frequently more tense inside than others realize”; and
(3) Sadness: e.g. “I often feel sad”, “Moving away
from my friends would not upset me”.
The scale also includes one category for
positive emotion, nowadays well-understood to be
related to dopamine - motivating us to investigate
our environment, with the expectation of reward
(e.g. Robbins and Everitt, 1992). The system has
been variously referred to over the years as a
‘reward’ (Schultz, 2001), ‘preparation’ (Hobel,

Negative emotions and anosognosia

1997), ‘seeking’ (Ikemoto and Panksepp, 1999)
system (see also Davidson and Irwin, 1999). We
refer to it using the phrase (4) Seeking: e.g.
“almost any little problem or puzzle stimulates my
interest”, “I do not get much pleasure from looking
forward to special events”. The Davis et al. (2003)
scale also includes ratings of other more complex
emotional states (care, playfulness, spirituality) but these are not discussed in the present study.
The Davis et al. (2003) paper also reports norms
based on 171 controls, against whose scores IW’
performance was compared.

71

enrolled in a study of patients with lesions to the
pulvinar of the thalamus. Each participant had a
hemiparesis (two with a right hemiparesis, and one
with a left hemiparesis) that had followed from a
stroke involving the thalamus and internal capsule.
None of the patients with left-sided lesions was
aphasic (one remained mildly dysarthric and
anomic). None of these controls were anosognosic.
A ‘neurologically-normal control group’ consisted
of five participants who were matched with IW in
terms of age and education.
Results

Results
On the three negative emotion categories, IW
produced scores that were divergent from
neurologically-normal controls only in that he
reported elevated levels of emotion. On measures
of fear IW scored 33/42 (> 84th percentile), and for
sadness, IW scored 34/42 (> 98th percentile, a
higher score than any male control subject) and on
anger, IW scored 16/42 (< 16th percentile). On the
positive emotion items, IW scored 39/42 (> 98th
percentile).
Comment
IW scored highly on two of the three categories
measuring negative emotion, including an
extremely high score on the sadness measure. He
also produced a high score for the positive emotion
category. These data are not consistent with a claim
that IW has a selective disruption of negative
emotions. However, we note also that self-report
measures of emotion are readily open to bias, and
also that IW’s increased ratings may result from a
low level of insight into his own emotional state.
AFFECTIVE STORY RECALL
In addition to a questionnaire-based approach,
we also thought it appropriate to design a task that
addressed the issue of IW’s emotional experience
more indirectly. In an Affective Story Recall task,
IW was asked to recall a series of personal
experiences from events in his life, which matched
a particular emotional category. The list of such
prompts was designed around the categories used
in the questionnaire reported above. IW was asked
to recall memories of four types, following the
phrase “Try and recall an event in your life which
has caused you to feel anger or rage”. The question
was then repeated for the categories: fear or
anxiety; sadness or distress; and seeking or
expectancy. IW completed the task twice, across
two sessions, producing a list of eight stories.
The task was also administered to two types of
control groups. A neurological patient control
group consisted of three participants who had been

The stories produced by the neurological patient
control group tended to focus on the nature of their
disability, and its implications for their everyday
life. Thus, a typical patient described anger because
he could not garden any more (a previous hobby),
and sadness because of his reduced social contact.
He was also fearful because he might be knocked
over, or trip, when going up the stairs in his local
pub. His seeking stories were dominated by his
wish to return to full health, and that he had
expected to show the sort of full recovery seen in
cases of a broken leg.
Those produced by the neurologically-normal
control group tended to focus on events related to
how they felt in situations related to themselves or
close family. For example, one control described
fear when she heard on the radio that there had
been a massive explosion at her husband’s factory.
IW’s stories were dominated by emotion of
various types, but differed from those of controls in
that they focused on the disability experienced by
others. A typical example was his Anger story:
When climbing in the mountains, impending bad
weather, IW and colleagues chanced upon a
climber totally unprepared for the possible
conditions. IW warned him not to continue, but the
climber did not heed his advice. Later, at IW’s
insistence, he and his colleagues tracked back to
find that climber had slipped and been killed. IW
chose this as an example of the emotion ‘anger’,
he said, because “the climber should have taken
advice from people who knew”.
Because IW’s stories focused especially on the
serious consequences typically experienced by
others, the data were analysed in terms of the
‘object’ of the emotion, in addition to quantifying
its magnitude (see below).
The data were blind-rated by two control
subjects who had no history of neurological
disease. The raters read each story and rated it in
terms of its perceived emotional content in each of
the four categories (e.g. “How much of the content
relates to fear or anxiety”) on a 0-10 scale. They
also rated each story in terms of the object of the
emotion – i.e. whether the primary object/person
which the story referred to was that of the person
telling the story (self), or another individual. The

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Oliver H. Turnbull and Others

neurological-normal controls
neurological-patent controls
IW

Fig. 2 – Performance on Affective Story Recall, for all
emotion classes, in IW and two control groups. IW’s
performance is close to that of the controls for all emotion
classes, especially for negative emotions. The measure of
variance is a standard error.

scores for each emotion, in each category of story,
were averaged across raters.

neurological-normal controls
neurological-patent controls
IW

Absolute Levels of Emotion
An important preliminary analysis focuses on
whether the absolute levels of emotion differ
between IW and two control groups (Figure 2).
The levels of emotion did not differ greatly across
the four emotion categories, though IW’s level of
rated emotion were lower than those of the two
control groups for three of the four emotion
categories, but higher for separation-distress. Using
ANOVA to compare the magnitude of overall
emotion across categories, IW was not significantly
different to the to the neurological patient control
group [F (1, 14) = 0.036, p > 0.05], or the
neurologically-normal control group [F (1, 22) =
1.387, p > 0.05].
The ‘Object’ of the Emotion
While IW’s overall level of emotion did not
differ from those of controls, it is of some note that
the object of the emotions experienced by IW
appeared to differ from those of controls. In each
case, the emotions experienced by controls
appeared to be rated more highly in relation to
their self, for example in that they felt anger,
anxiety, and feelings of loss in relation their paresis
(see Figure 3) – a result that we have reported
based on data from another group of patients
(Turnbull et al., 2002). However, IW’s profile
showed that such feelings was far more commonly
directed at others.
When comparing IW to the neurological patient
control group, ANOVA showed no main effect of
self vs. other [F (1, 14) = 2.29, p > 0.05], no main
effect of group [F (1, 14) = 2.22, p > 0.05],
however, there was a substantial interaction [F (1,
14) = 34.5, p < 0.001]. Post-hoc analyses showed a
significant difference between IW and controls for
both self [t (14) = – 4.6, p < 0.001] and others [t
(14) = – 4.2, p < 0.001].

Fig. 3 – Performance on Affective Story Recall, for all
emotion classes, as related to ‘self ’ versus ‘others’. The
difference between IW’s performance on the ‘self’ and ‘others’
categories is evident for all emotion classes. The measure of
variance is a standard error.

When comparing IW to the neurologically
normal control group, ANOVA showed a main
effect of self vs. other [F (1, 22) = 23.51, p <
0.001], a main effect of group [F (1, 22) = 109.5,
p < 0.001], and an interaction [F (1, 22) = 8.84, p
< 0.01]. Post-hoc analyses again showed a
significant difference between IW and controls for
both self [t (22) = – 7.5, p < 0.001] and others [t
(22) = – 11.8, p < 0.001].
Analysing these data at the level of individual
emotion types would result in a loss of statistical
power. However, as can be seen in Figure 3, a few
general trends are evident. Firstly, as regards the
tendency for IW to have lower ratings than controls
on ‘self’ items, this trend was evident for all four
emotion classes, relative to both the neurological,
and the neurologically normal control group. In
each case IW’s performance was in the lower 10th
percentile, and was below the 1st percentile relative
to neurologically normal controls in terms of
sadness, fear and seeking. As regards the tendency
for IW to have higher ratings than controls on
‘other’ items, this trend was also evident for all
four emotion classes, relative to both the
neurological, and the neurologically normal control
group. Again, IW’s performance was always in the
lower 10th percentile, and was again below the 1st
percentile relative to neurologically normal controls
in terms of sadness, fear and seeking.
Comment
The overall magnitude of emotion in Affective
Story Recall for IW was not significantly different

Negative emotions and anosognosia

from that of controls, suggesting that IW has a
relatively normal range of emotional report, at least
as measured by this task. It is of especial note that
the negative emotions (sadness-distress, anger-rage
and fear-anxiety) did not differ from controls.
Indeed, in the category of separation-distress, IW
exhibited higher levels than both control groups.
This suggests that IW continues to experience a
magnitude of negative emotions that is consistent
with that of others, including neurological patients
with hemiparesis.
However, there was some evidence that IW’s
emotions appear to be more commonly directed at a
different object – such that emotional content of the
story is directed far more at others than at himself.
As shown in Figure 3, this effect seems to be
consistent across each of the categories of emotion.
DISCUSSION
The primary goal of the investigation was to
formally establish the magnitude of emotions
experienced by IW, and in particular whether he
experienced negative emotions. His emotional
experience, measured by self-report questionnaire
(the Affective Neuroscience Personality Scale),
produced scores at the higher end of the normal
range for three of the four emotion categories (only
anger was low), and was especially high for the
category of sadness. A more indirect assessment of
his emotional state, using the same categories of
emotion (Affective Story Recall), again produced
scores not significantly different from two control
groups across all emotion categories. Indeed, it was
lowest on the positive emotion category of seeking.
Thus, across two quite different assessment
methods, IW shows a range of emotional
experience that is consistent with that of controls,
especially for negative emotions (anger, fear and
sadness). Taken together with other reports of
negative emotion, and even frank depression, in
anosognosics (Kaplan-Solms and Solms, 2000;
Starkstein et al., 1990), this result runs counter to
the argument that anosognosia might result from a
loss of negative emotions. However, given that
anosognosia is a diverse phenomenon (e.g. Marcel
et al., 2004) the more general role of negative
emotions in the disorder remains uncertain.
Negative emotions may not always be preserved in
anosognosia, and the pattern of emotional
preservation may be an important factor in the
many ways in which anosognosia can present
clinically. It may, for example, include the selective
loss, or even the enhancement, of certain classes of
emotion – as in instances of explicit hatred of the
paretic limb (e.g. Critchley, 1974; Moss and
Turnbull, 1996). Certainly, some formal assessment
of the incidence and diversity of emotional changes
in anosognosia would be a welcome topic for
future research.

73

An interesting aspect of IW’s performance on
the task of Affective Story Recall was his tendency
to produce the same magnitude of emotion as
controls, but for this to be directed at an external
‘object’ – a finding that we have reported
elsewhere (Turnbull et al., 2002). For example,
IW’s production of emotion-related stories carry a
recurring theme of loss (especially death and
injury), almost regardless of the emotional topic
suggested to him. One explanation of this finding
might be that IW’s attempts to consciously link his
feelings of sadness with his hemiparesis are
aversive and/or intolerable to him (c.f. Anderson
and Green, 2001). Arguments of this type have
previously been proposed (Goldstein, 1939;
Schilder, 1935; Weinstein, 1991; Weinstein and
Kahn, 1955), and have been revived more recently,
suggesting that anosognosia might be a form of
defense (Marcel et al., 2004; Kaplan-Solms and
Solms, 2000; Ramachandran, 1996; Turnbull et al.,
2002). Were this true, then at least some
anosognosic patients would have a demonstrable
implicit awareness of their disability (see Feinberg,
1997, p.384 for further discussion). However, the
evidence for this claim remains indirect, and more
explicit attempts to measure the extent of
awareness of disability would form a further useful
topic for future research.
Acknowledgements. We would like to thank Bob Rafal,
for his referral of the patient, and providing details of the
neurological examination. Also Steve Jackson, Giuseppe
Di Pellegrino, and Jaak Panksepp for their comments on
earlier drafts, and notably Tony Marcel for his meticulous
reviews. Dr. Turnbull’s research is supported by grants
from NARSAD and the Wellcome Trust.

REFERENCES
ALBERT MD. A simple test of visual neglect. Neurology, 23: 658664, 1973.
ANDERSON MC and GREEN C. Suppressing unwanted memories by
executive control. Nature, 410: 366-369, 2001.
BANDLER R and SHIPLEY MT. Columnar organization in the
midbrain periaqueductal gray. Trends in Neurosciences, 17:
379-389, 1994.
BISIACH E and GEMINIANI G Anosognosia relating to hemiplegia
and hemianopia. In GP Prigatano and DL Schacter. Awareness
of Deficit after Brain Injury: Clinical and theoretical issues.
New York: Oxford University Press, 1991, pp.17-39.
BISIACH E, VALLAR G, PERANI D, PAPAGNO C and BERTI A.
Unawareness of disease following lesions of the right
hemisphere: Anosognosia for hemiplegia and anosognosia for
hemianopia. Neuropsychologia, 24: 471-482, 1986.
BLAKEMORE SJ, WOLPERT DM and FRITH CD. Abnormalities in the
awareness of action. Trends in Cognitive Sciences, 6: 237-242,
2002.
BOROD JC. The Neuropsychology of Emotion. Oxford: Oxford
University Press, 2000.
BRIER JI, ADAIR JC, GOLD M, FENNELL EB, GILMORE RL and
HEILMAN KM. Dissociation of anosognosia for hemiplegia and
aphasia during left-hemisphere anesthesia. Neurology, 45: 6567, 1995.
CALDER AJ, LAWRENCE AD and YOUNG AW. Neuropsychology of
fear and loathing. Nature Neuroscience, 2: 352-363, 2001.
CAPPA S, STERZI R, VALLAR G and BISIACH E. Remission of
hemineglect during vestibular stimulation. Neuropsychologia,
25: 775-782, 1987.
CLONINGER CR. Temperament and personality. Current Biology, 4:
266-273, 1994.

74

Oliver H. Turnbull and Others

CRITCHLEY M. Misoplegia, or hatred of hemiplegia. Mount Sinai
Journal of Medicine, 41: 82-87, 1974
DAMASIO AR. Descartes’ Error – Emotion, Reason and the Human
Brain. London: Papermac, 1994.
DAMASIO AR. The somatic marker hypothesis and the possible
functions of the prefrontal cortex. Philosophical Transactions
of the Royal Society of London (Series B: Biology), 351:
1413-1420, 1996.
DAMASIO AR. The Feeling of what happens: Body, Emotion and the
Making of Consciousness. London: William Heinemann, 1999.
DAMASIO H, GRABOWSKI T, BECHARA A, DAMASIO H, PONTO LLB,
PARVISI J and HICHWA RD. Subcortical and cortical brain
activity during the feeling of self-generated emotions. Nature
Neuroscience, 3: 1049-1056, 2000.
DAPRATI E, SIRIGU A, PRADAT-DIEHL P, FRANCK N and JEANNEROD
M. Recognition of Self-produced Movement in a Case of
Severe Neglect. Neurocase, 6: 477-486, 2000.
DAVIDSON RJ. Towards a biology of personality and emotion.
Annals of the New York Academy of Science, 935: 191-207,
2001.
DAVIDSON RJ and IRWIN W. The functional neuronatomy of
emotion and affective style. Trends in Cognitive Science, 3:
11-21, 1999.
DAVIS KL and PANKSEPP J. Affective Neuroscience: MultiDimensional Inventory. Greesboro: Pegasus International,
1999.
DAVIS KL, PANKSEPP J and NORMANSELL L. The Affective
Neuroscience Personality Scales: Normative Data and
Implications. Neuropsychoanalysis, 5: 57-69, 2003.
DEPAULIS A and BANDLER R. The Midbrain Periaqueductal Gray
Matter: Functional Anatomical and Neurochemical
Organization. New York: Plenum Press. 1991
FEDOROFF JP, STARKSTEIN SE and FORRESTER AW. Depression in
patients with acute traumatic injury. American Journal of
Psychiatry, 149: 918-923, 1992.
FEINBERG TE. Anosognosia and confabulation. In TE Feinberg and
MJ Farah (Eds), Behavioral Neurology and Neuropsychology.
New York: McGraw Hill, pp. 369-390, 1997.
FINK GR, MARSHALL JC, HALLIGAN PW, FRITH CD, DRIVER J,
FRACKOWIACK RSJ and DOLAN RJ. The neural consequences
of conflict between intention and the senses. Brain, 122: 497512, 1999.
FRITH CD, BLAKEMORE S-J and WOLPERT DM. Abnormalities in
the awareness and control of action. Philosophical
Transactions of the Royal Society of London (Series B:
Biology), 355: 1771-1788, 2000.
GAINOTTI G. Emotional behaviour and hemispheric side of lesion.
Cortex, 8: 41-55, 1972.
GAINOTTI G. Confabulation of denial in senile dementia.
Psychiatric Clinic (Basel), 8: 99-108, 1975.
GAINOTTI G. Emotional disorders in relation to unilateral brain
damage. In TE Feinberg and MJ Farah (Eds), Behavioural
neurology and neuropsychology. New York: McGraw Hill,
1997, pp. 369-390.
GOLDSTEIN K. The organism: A Holistic Approach to Biology
Derived from Pathological Data in Man. New York: American
Book Company, 1939.
HALLIGAN PW, MARSHALL JC and WADE DT. Unilateral
somatoparaphrenia after right hemisphere stroke: A case
description. Cortex, 31: 173-182, 1995.
HEILMAN KM, BARRETT AM and ADAIR JC. Possible mechanisms
of anosognosia: A deficit in self-awareness. Philosophical
Transactions of the Royal Society of London (Series B:
Biology), 353: 1903-1909, 1998.
HEILMAN KM, WATSON RT and VALENSTEIN E. Neglect and related
disorders. In KM Heilman and E Valenstein (Eds), Clinical
Neuropsychology. New York: Oxford University Press, pp.
296-346, 2003.
HOBEL BG. Neuroscience and appetitive behaviour research: 25
years. Appetite, 29: 119-133, 1997.
HOUSE A, DENNIS M, WARLOW C, HAWTON K and MOLTNEUX A.
Mood disorders after stroke and their relation to lesion
location. Brain, 113: 1113-1129, 1990.
HOUSE A and HODGES J. Persistent denial of handicap after
infarction of the right basal ganglia. Journal of Neurology,
Neurosurgery and Psychiatry, 51: 112-115, 1988.
IKEMOTO S and PANKSEPP J. The role of nucleus accumbens
dopamine in motivated behaviour: A unifying interpretation
with special reference to reward seeking. Brain Research
Reviews, 31: 6-41, 1999.
JORGE R and ROBINSON RG. Mood disorders following traumatic
brain injury. Neurorehabilitation, 17: 311-324, 2002.
KAPLAN-SOLMS KL and SOLMS M. Clinical Studies in

Neuropsychoanalysis:
Introduction
of
a
Depth
Neuropsychology. London: Karnac Books, 2000.
LE DOUX J. The Emotional Brain. New York: Touchstone, 1996.
LU LH, BARRETT AM, SCHWARTZ MD, CIBULA JE, GILMORE RL,
UTHMAN BM and HEILMAN KM. Anosognosia and
confabulation during the Wada test. Neurology, 49: 13161332, 1997.
MARCEL AJ, TEGNÉR R and NIMMO-SMITH I. Anosognosia for
plegia: Specificity, extension, partiality and disunity of bodily
unawareness. Cortex, 40: 1940, 2004.
MCGLYNN SM and SCHACTER DL. Unawreness of deficits in
neuropsychological syndromes. Journal of Clinical and
Experimental Neuropsychology, 11: 143-205, 1989.
MEADOR KJ, LORING DW, FEINBERG TE, LEE GP and NICHOLS ME.
Anosognosia and asomatognosia during intracarotid
amobarbital inactivation. Neurology, 55: 816-820, 2000.
MOSS AD and TURNBULL OH. Hatred of the hemiparetic limbs
(misoplegia) in a 10 year-old child. Journal of Neurology,
Neurosurgery and Psychiatry, 61: 210-211, 1996.
PANKSEPP J. Affective neuroscience: The foundations of human
and animal emotions. Oxford: Oxford University Press,
1998.
PHAN KL, WAGER T, TAYLOR SF and LIBERZON I. Functional
neuroanatomy of emotion: A meta-analysis of emotion
activation studies in PET and fMRI. NeuroImage, 16: 331348, 2002.
PRIGATANO GP and SCHACTER DL. Awareness of Deficit after Brain
Injury: Clinical and theoretical issues. New York: Oxford
University Press, 1991.
PRIGATANO GP, WEINSTEIN EA and EDWIN A. Weistein’s
contributions
to
neuropsychological
rehabilitation.
Neuropsychological Rehabilitation, 6: 305-326, 1996.
RAMACHANDRAN VS. Phantom limbs, neglect syndromes,
repressed memories, and Freudian Psychology. International
Review of Neurobiology, 37: 291-333, 1994.
RAMACHANDRAN VS. What neurological syndromes can tell us
about human nature: Some lessons from phantom limbs,
Capgras syndrome, and anosognosia. Cold Harbour Symposia
on Qualtitative Biology, 61: 115-134, 1996.
RAMACHANDRAN VS and BLAKSLEE S. Phantoms in the Brain:
Human Nature and the Architecture of the Mind. London:
Fourth Estate, 1998.
REITAN RM. Verbal problem solving as related to cerebral damage.
Perceptual and Motor Skills, 34: 515-524, 1972
ROBBINS TW and EVERITT BJ. Functions of dopamine in the dorsal
and ventral striatum. Seminars in the Neurosciences, 4: 119128, 1992.
RODE G, PERENIN MT, HONORE J and BOISSON D. Improvement of
the motor deficit of neglect patients through vestibular
stimulation: Evidence for a motor neglect component. Cortex,
34: 253-261, 1998.
ROSS ED and RUSH AJ. Diagnosis and neuroanatomical correlates
of depression in brain damaged patients. Archives of General
Psychiatry, 38: 1344-1354, 1981.
ROLLS ET. The Brain and Emotion. Oxford: Oxford University
Press, 1999.
SCHILDER P. The Image and Appearance of the Human Body.
London: Kegan and Co., 1935.
SCHULTZ W. Multiple reward signals in the brain. Nature
Neuroscience, 1: 199-207, 2001.
SOLMS M, TURNBULL OH, KAPLAN-SOLMS K and MILLER P.
Rotated drawing: The range of performance, and anatomical
correlates, in a series of 16 patients. Brain and Cognition, 38:
358-368, 1998.
SIRIGU A, DAPRATI E, PRADAT-DIEHL P, FRANCK N and JEANNEROD
M. Perception of self-generated movement following left
parietal lesion. Brain, 122: 1867-1874, 1999.
STARKSTEIN SE, BERTHIER ML, FEDOROFF P, PRICE TR and
ROBINSON RG. Anosognosia and major depression in 2
patients with cerebrovascular lesions. Neurology, 40: 13801382, 1990.
STARKSTEIN SE, BOSTON JD and ROBINSON RG. Mechanisms of
mania after brain injury. Journal of Nervous and Mental
Disease, 176: 87-99, 1988.
TURNBULL OH, BESCHIN N and DELLA SALA S. Agnosia for object
orientation: Implications for theories of object recognition.
Neuropsychologia, 35: 153-163, 1997a.
TURNBULL OH, CAREY DP and MCCARTHY RA. The
neuropsychology of object constancy. Journal of the
International Neuropsychological Society, 3: 288-298, 1997b.
TURNBULL OH, JONES K and REED-SCREEN J. Implicit awareness of
deficit in anosognosia: An emotion-based account of denial of
deficit. Neuropsychoanalysis, 4: 69-86, 2002.

Negative emotions and anosognosia
VALLAR G, STERZI R, BOTTINI G, CAPPA S and RUSCONI ML.
Temporary remission of left hemianesthesia after vestibular
stimulation. Cortex, 26: 123-131, 1990.
WALSH KW. Understanding Brain Damage: A Primer of
Neuropsychological Evaluation. Edinburgh: Churchill
Livingstone, 1985.
WEINSTEIN EA. Anosognosia and denial of illness. In GP Prigatano
and DL Schacter (Eds), Awareness of Deficit after Brain
Injury. Oxford: Oxford University Press, 1991.
WEINSTEIN EA. Symbolic aspects of confabulation following brain

75

damage: Influence of premorbid personality. Bulletin of the
Menninger Clinic, 60: 331-350, 1996.
WEINSTEIN EA and KAHN RL. Personality factors in denial of
illness. American Medical Association Archives of Neurology
and Psychiatry, 69: 355-367, 1953.
WEINSTEIN EA and KAHN RL. Denial of illness: Symbolic and
physiological aspects. Illinois: Charles C. Thomas, 1955.
Oliver Turnbull, Centre for Cognitive Neuroscience, School of Psychology, University
of Wales, Bangor, Wales, LL57 2AS, UK. e-mail: o.turnbull@bangor.ac.uk

(Received 25 September 2002; reviewed 2 December 2002; revised 31 October 2003; accepted 7 November 2003)