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The Emotional Impact of Aphasia

Article in Seminars in Speech and Language · February 1999

DOI: 10.1055/s-2008-1064006 · Source: OAI

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1 Emotional Impact (Code et al)

The Emotional Impact of Aphasia.

1, 2) 1) 3)
Chris Code , Gayle Hemsley and Manfred Herrmann

1) Brain Damage and Communication Research, School of Communication Sciences and Disorders,
University of Sydney, Australia
2) Department of Psychology, University of Exeter, England
3) Division of Neuropsychology and Behavioural Neurology, Otto-von-Guericke University Magdeburg,
Germany

Seminars in Speech & Language

Vol 20, (1999) PP.19-31.

Key Words aphasia, emotion, depression

Running title: Emotional Impact

Address for correspondence: Chris Code, PhD

Department of Psychology
Washington Singer Laboratories
Exeter University
Perry Road
Exeter, EX4 4QG
UK

Email: [email protected]
Tel: ++ 44 (0) 1392 264642
Fax: ++ 44 (0) 1392 264623

Words=6700 (inc.refs)
2 Emotional Impact (Code et al)

Acknowledgments:

During the preparation of the manuscript Manfred Herrmann spent a sabbatical at the School of

Communication Sciences and Disorders, Brain Damage and Communication Research, University of

Sydney which was supported by a visiting scholarship from the Faculty of Health Sciences, University of

Sydney, Australia. He wishes to express his gratitude to Professor Vicki Reed and staff for their support

during the stay

3 Emotional Impact (Code et al)

ABSTRACT

In this paper we review the negative impact of aphasia on emotional well-being. Depression is the

emotional response which has been examined most and we examine the different causes of depression for

people with aphasia. We discuss the relationships between recovery and emotional state and the clinical

implications of these relationships and review briefly issues of drug treatment for depression. We conclude

that the emotional impact of aphasia can have a marked negative impact on recovery, response to

rehabilitation and psychosocial adjustment.

4 Emotional Impact (Code et al)

INTRODUCTION

This paper examines what we know about the causes of emotional and psychosocial change for people with

aphasia. It seems obvious that aphasia and other neurological and neuropsychological disorders following

brain damage can lead to considerable emotional stress and psychosocial disturbance for patients and their

families. Emotional experience is what essentially defines our existence. It is what makes us human.

Without it we are the monodimensional Mr Spock who never experiences an emotional high or low. With it

we are the complex Captain Kirk, sometimes indulging and other times battling to control his emotions.

Our personal, subjective sense of well-being is derived from our current experience of life as a whole

(Campbell, 1976). Our emotional life, both positive and negative, emerges from our interaction with

society and how we perceive this is what determines the quality of our life experiences. Most of our

happiness and sadness comes from our interactions with others, whether directly or vicariously through the

media, music, reading, TV, art, and so on. The term 'psychosocial' refers to this grounding of emotional

experience within social context. Emotional disturbances, therefore, might be considered a relatively well

understand psychological reaction to the impairment, disability and handicap that accompanies aphasia.

But, until recently it was unclear what caused emotional changes that aphasic people often showed and how

these impacted, if at all, on recovery and how to treat them. Our understanding is improving, and this paper

aims to present an overview of that current understanding.

THE EMOTIONAL RESPONSE TO APHASIA

Before we examine the nature of emotional disturbance in people with aphasia, we must seek an answer to

the question, what is emotion? Although there are a number of perspectives on the nature of emotion and
5 Emotional Impact (Code et al)

its function in our lives, there is some consensus that we can identify a range of recognizable emotions

(Kleinginna & Kleinginna, 1981; Oatley & Johnson-Laird, 1987; Scherer, 1993; Power & Dalgleish, 1997).

Each emotion is accompanied by widespread bodily signals and cognitive impulses to behave in particular

ways, allowing us to experience and recognise emotions and changes in them. A range of views exist on the

number of human emotions which can be experienced, but five basic emotions are generally accepted,

mainly based on their existence across cultures, the association of a distinguishing facial expression and

the physiological changes which accompany them (Ekman, Friesen & Ellsworth, 1982; Oatley & Johnson-

Laird, 1987; Power & Dalgleish, 1997). These five common emotions are happiness, anger, anxiety,

disgust and sadness. Other emotional complexes are thought to be combinations of these, emerging as an

individual emotional balance between positive and negative mood shifts.

Aphasia following stroke impacts significantly on emotional state. Although similar broad patterns of

emotional response to stroke and aphasia have been described, as we will see, there appears to be no

necessary and fixed schedule of emotional responses which uniformly exist across patients. Starkstein and

Robinson (1988) reviewed the range of emotional reactions accompanying aphasia. These are adapted and

outlined in Table 1. In aphasic people we can observe what we can call positive emotional reactions (e.g.,

mania, delirium, anosognosia, denial) and negative reactions (e.g., depression, anxiety). Each of these

emotional states in their extreme form is inappropriate; the ‘ideal’ is a balance between positive and

negative mood state.

The person with aphasia experiences a sudden and unexpected inability to function in the complete range of

activities of everyday life; in cognitive, behavioural, leisure, occupational, social and family activities.

Negative emotional reactions to this frequently manifest as depression, both for individuals with aphasia as

well as for those who are close to them. It is not surprising, therefore, that depression is the most reported

and investigated mood state following brain damage, and consequently the main focus of our discussion.
6 Emotional Impact (Code et al)

[TABLE 1 ABOUT HERE]

THE NATURE OF DEPRESSION

Everyone experiences sadness in their lives. Depression, however, is more than a transient unhappiness,

and manifests as a distinct and lasting decline in normal mood. Depression extinguishes the spark of life

and eliminates the possibility of joy, laughter, empathy, happiness, and love. It reduces contact with the

outside world, leaving the individual alone and isolated (Browning, 1995).

The American Psychiatric Association recognises different types of depressive disorders. These are

operationally defined in the Diagnostic and Statistical Manual of Mental Disorders (DSM) of which the

current version is the DSM-IV (American Psychiatric Association, 1994). The most often investigated

categories in stroke research are major depression and dysthymia. The differential diagnosis of the two

forms of depression is particularly difficult, since the two disorders share the same symptoms and differ

mainly in duration and severity. Major depression usually consists of one or more distinct major depressive

episodes lasting for at least two weeks. At least five major symptoms must be present during the same two

week period, representing a change from previous functioning. Essential to diagnosis of major depression is

the presence of depressed mood most of the day, nearly every day with markedly diminished interest or

pleasure in all, or almost all, activities most of the day and nearly every day. These two major criteria must

be accompanied by at least three of the following associated symptoms present nearly every day for the

diagnosis of major depression: 1. significant weight loss or gain when not dieting or decrease or increase in

appetite; 2. insomnia or hypersomnia; 3. psychomotor agitation or retardation; 4. fatigue or loss of energy;

7 Emotional Impact (Code et al)

5. feelings of worthlessness or excessive or inappropriate guilt; 6. diminished ability to think or

concentrate, or indecisiveness; 7 recurrent thoughts of death or suicide or a suicidal attempt.

Dysthymic disorder requires the presence of depressed mood for at least two years for most of the day,

more days than not, together with at least two of the criteria listed for major depression (DSM-IV, 1994). .

Most research studies ignores the two year duration criterion. Dysthymic disorders, therefore, are often

operationally defined as minor depression. The mild or moderate impairment in social and occupational

functioning experienced with minor depression is considered to be associated mainly with the chronicity

rather than the severity of depression. Such people do not experience full blown depressive episodes, yet

are impaired by persistent disordered mood

DEPRESSION FOLLOWING STROKE

Depression following a stroke, called post-stroke depression (PSD), is defined by the presence of clinically

significant major or minor depression, as diagnosed by the criteria outlined above. Lipsey, Spencer, Rabins

and Robinson (1986) showed that symptom clusters noted in the DSM-III-R were almost identical for

patients suffering from PSD and functional depression without neurological damage. Criteria for diagnosis,

however, specifically note that organic factors should not initiate or maintain the disturbance, an issue

which will be addressed below. However, we can at this point question the validity of using DSM criterion

to identify PSD because changes in energy levels, weight, appetite and sleeping patterns following stroke

can result not only from depression, but also from other neurological and neuropsychological deficits

associated with stroke (Herrmann & Wallesch, 1993). Also, neurological deficits can impair facial
8 Emotional Impact (Code et al)

expression and the expression of emotion through motor speech and vocal tone, erroneously suggesting the

presence of depression (Code & Muller, 1992; see Stern, this issue, for fuller discussion of these issues).

There is some disagreement as to the proportion of people who will acquire some form of clinically

significant PSD, although most studies agree that PSD is very common. Figures vary from 50-60% (Lipsey,

Robinson, Pearlson, Rao & Price, 1985; Starkstein & Robinson, 1988) to 5-11% (House, Dennis, Warlow,

Hawton & Molyneux, 1990). This variation is at least partially due to the complexity of comparing studies,

each using different sample selection criteria, operationalisation of emotional-mood disorders, as well as

different measures of depression (Herrmann & Wallesch, 1993).

However, recent evidence shows that, when present, depression persists in stroke patients well into the

chronic stages of rehabilitation. Åstrom, Adolfsson and Asplund, (1993) examined the prevalence and

course of PSD for three years post-onset. A major depressive syndrome found in 25% of patients during

acute stages rose to 31% of patients at three months post-onset. It was present in 16% at 12 months but

increased again over the next two years to 29%, a level higher than at 3 months post-onset. At this time,

patients also demonstrated reduced life satisfaction and involvement in activities of daily living. Although

such evidence regarding the presence of PSD is convincing, some degree of confusion and controversy

remains in the literature as to the cause, or causes of PSD.

Causes of Depression in Aphasia

The person with aphasia can be faced with depression, communicative and social isolation, occupational

frustrations and reduced involvement in everyday living and leisure activities (Friedland & McColl, 1987;
9 Emotional Impact (Code et al)

Herrmann & Wallesch, 1989; Code & Muller, 1992; Taylor Sarno, 1993; Gainotti, 1997). An early survey

of the social and emotional problems of aphasia noted many effects of stroke on the individual's emotional

well-being. These were considered to be natural and 'reactive', arising from low self-esteem and an inability

to "give up emotional attachment to the pre-morbid self concept and accept...a less adequate, disabled

image" (Biorn-Hansen, 1957; page 56). This in turn produced difficulties with interpersonal relationships,

sometimes leading to withdrawal from others.

Subsequent writers frequently viewed PSD as a natural and reactive response to physical impairment and

speech and language disturbances (Fisher, 1961; Tanner, 1980; Tanner & Gerstenberger, 1988) although it

is now well established that emotional disorders can be directly caused by the nature, severity and site of

brain damage, causing disruption of the neurobiochemical processes underlying normal emotion (Gainotti,

1972; Starkstein & Robinson, 1988).

The classical model derived from neurology, the anterior-posterior characterization, is built on observations

of brain damaged patients, and mainly left-hemisphere damaged patients (Gainotti, 1972; Benson, 1973;

Benson & Geschwind, 1976; Brown, 1975; see Code, 1986, for discussion). On this model, patients with

anterior left-hemisphere damage, with nonfluent aphasia, agrammatism and good comprehension,

predominantly present with a negative, depressive affect. This is sometimes referred to as catastrophic

reaction. While some feel that true and full-blown catastrophic reaction (Goldstein, 1948) is rare, others

have used the term in a wider sense to characterize the broad negative mood state we observe in aphasic

people (Gainotti, 1997). In contrast, patients with posterior left-hemisphere damage with fluent paraphasia

and poor comprehension often present with an abnormally positive, sometimes euphoric, affect. These

patients apparently have poor understanding of there true condition. They appear to deny the severity and

even the existence of any condition. This is referred to as an anosognosic indifference or denial.
10 Emotional Impact (Code et al)

Robinson and Benson, (1981) compared fluent, non-fluent and global aphasic patients with matched

controls on physical and cognitive impairments, several months post-onset of brain damage. They found

that non-fluent patients with more frontal damage had a significantly higher frequency and severity of

depression. As degree of depression was not found to advance with increasing cognitive impairment,

results were not attributable to awareness of disability, but rather suggested that the site of the lesion was

the probable cause of depression (Starkstein & Robinson, 1988). A range of studies confirm an organic

aetiology to PSD (Folstein, Maiberger & McHugh, 1977; Finkelstein et al., 1982; Robinson & Price, 1982;

Robinson et al., 1984; Sinyor et al., 1986).

Studies have also found a significant positive correlation between adjacency of left hemisphere lesions to

the frontal pole and increasing frequency and severity of depression (i.e., lesions closer to the frontal pole

are more likely to result in depression). Conversely, euphoric reaction, or abnormally positive affect, has

been linked with more posterior, and right hemisphere lesions (Finkelstein et al., 1982; Sinyor et al., 1986;

Starkstein & Robinson, 1988). However, there are some limitations to the research concerning the

neurobiochemical background of PSD and in the ways that depression is assessed in aphasic patients

(Stern, this issue). The majority of studies have come from the same group of researchers and not all results

have been replicated by independent researchers. But taken together, there is good evidence that depression

in an individual following stroke and aphasia can have an organic basis - at least in the post-acute stage.

While the view that anterior damage causes depression and posterior damage causes indifference or

euphoria in aphasic peoples is widely espoused in the literature, it would be a mistake to assume that

particular emotional responses inevitably follow specifically localized brain damage.

11 Emotional Impact (Code et al)

A Model of Depression in Aphasia

It appears that multiple factors are involved in determining presence or absence of depression in aphasic

people, and that causation may vary as a function of progress through different stages of recovery

(Gainotti, 1997). Depression in the acute stage following a stroke appears to be most related to site of

lesion in many people with aphasias, rather than degree of cognitive and physical impairment or quality of

social support (Robinson, Bolduc and Price, (1987a). In the six months immediately following stroke,

however, the relationship between depression and cognitive and physical impairment increases to become

almost as significant as lesion location (Robinson, Starr, Lipsey, Rao & Price, 1984). Starkstein and

Robinson conclude that ‘while the presence of post-stroke depression mainly depends on the location of the

lesion ... there is an important interaction between physical impairment and depression’ (1988, page 13).

Currently, research supports the view that depression can have a direct organic cause and can also occur

reactively, as a naturally occurring form. These two forms of depression have been termed primary and

secondary, respectively. Herrmann and his colleagues (Herrmann, Bartels & Wallesch, 1993; Herrmann &

Wallesch, 1993) have added a third separate form to make primary, secondary and tertiary forms; each

related to different stages of recovery and rehabilitation. The relationship between them is illustrated in

Figure 1.

On this general model primary depression has its onset in the acute stage (0-3 months) following stroke and

results directly from the brain-damage itself. It is caused by structural lesions resulting in neurobiochemical

changes, although other contributing factors include pre-morbid disposition to depression (psychiatric

history, alcohol abuse, dementia), site of lesion and configuration of lesion. People with middle cerebral

artery infarction (causing damage to the frontal pole and basal ganglia) appear to be especially vulnerable.
12 Emotional Impact (Code et al)

During the acute period, there is apparently only a minor relationship between natural emotional reactions

to loss and degree of depression.

As time passes, however, a reactive or secondary depression may develop, usually within the first six

months during chronic stages of recovery. This is a more natural, or reactive depression to psychosocial,

neuropsychological and functional impairment caused by stroke. Herrmann and Wallesch suggest that there

are two types of people s specifically at risk for secondary reactive depression: those who ‘denied the

consequences of stroke in the initial period and are now confronted with the whole spectrum of their

functional, neurological and neuropsychological disabilities, or, those who primarily hoped for rapid

restitution and reintegration and now realise that they may suffer from their disabilities for a long period of

time’ (Herrmann & Wallesch, 1993; page 62).

[FIGURE 1 ABOUT HERE]

The third form, tertiary depression, has its onset during the transition to outpatient rehabilitation. This may

develop as ‘patients and their relatives realise the psychosocial consequences of their disabilities when they

attempt to re-integrate into their pre-morbid social structure. The patients' social role changes from that of

'patient' to 'disabled' with all its negative connotations. This may cause tertiary depression or increase

already existing depression’ (1993; page 63).

Secondary Depression and the Grieving Process

Their are individual differences in the way people respond to stroke and aphasia and it is important to focus

on each individual as unique, according to their functional communicative abilities, emotional and
13 Emotional Impact (Code et al)

psychosocial well-being, and overall life situation. Type and severity of secondary depression relates

strongly to the value and meaning attached to language by the individual in their pre-morbid occupational

and familial roles (Benson, 1973; Starkstein & Robinson, 1988; Wahrborg, 1991). Also contributing to

individual response will be the coping style, coping resources and social network brought to bare when

readjusting to aphasia (Friedland & McColl, 1987; Code & Muller, 1992; Taylor-Sarno, 1993; Hemsley &

Code, 1996).

The response of the individual with aphasia to secondary depression has been examined with reference to

the classic grief model developed to characterize reaction to losing a loved one (Kubler-Ross, 1969). This

model has been widely applied in many areas, including individuals with acquired neurogenic

communication disorder (Tanner, 1980; Tanner & Gerstenberger, 1988). Tanner and Gerstenberger

describe grieving as a natural and expected reaction for the individual faced with loss which they describe

as a ‘complex progression of emotional and intellectual adjustments to separation from something or

someone valued’ (Tanner & Gerstenberger, 1988; page 80).

They apply the three dimensions of loss from the grief model to the experience of people with aphasia.

These are loss and separation involving person, self and object. Each of these dimensions can be viewed

symbolically as providing meaning associated with losses experienced: ‘The symbolic aspects of loss are

those unique aspects which are person-specific and intangible such as loss of role, prestige and identity’

(Tanner & Gerstenberger, 1988; page 79).

Loss of person is the experience of a 'psychological separation' of the person with aphasia and immediate

family or networks of support. It result s from a reduced ability to engage in meaningful verbal

communication with those close to you, an easy and natural part of pre-morbid relationships. A

consequence can be the psychological isolation of the partner.

14 Emotional Impact (Code et al)

The perception that some aspect of physical or psychological integrity has been lost is referred to as loss of

self. For the person with aphasia this results from loss of pre-morbid self as a communicator and hence the

inability to naturally perform everyday communicative functions. The person with aphasia recognises

differences in their pre- and post-stroke functioning, which is confounded by contrasting the abilities of self

and others in functional, social and occupational tasks (Brumfitt, 1993).

Loss of object involves loss of use or ownership of significant possessions related directly to handicap

caused by brain damage. Objects may be of high monetary or sentimental value and loss may be permanent

or temporary. A car and driver's license, for example, are commonly 'lost' following stroke, a possession

which is usually valued not for its cost, but for the independence it represents. Other lost objects may be a

job, an income a hobby or interest.

The grieving process is described in terms of a series of stages. These stages are labelled denial, anger,

bargaining, depression and acceptance. Acceptance is the end stage which is reached if the grieving process

is worked through positively and successfully. It occurs when the person is 'emotionally removed' from

loss, conceding to the way things are, given the effects of the stroke and aphasia. Ordering and time span

for each of these stages will vary greatly between individuals. This process can apply to both the person

with aphasia and families (Tanner & Gerstenberger, 1988), being triggered by loss of person, self or object,

or some combination of these.

This non-neurobiologically conceived form of denial may involve complete or partial ignorance of the

presence, magnitude or permanence of aphasia and is seen as acting as a buffer between the self and reality

and anxiety, providing a mechanism for avoidance until acute deficits and difficulties can be more easily

dealt with. The next stages are anger and bargaining. Tanner and Gerstenberger suggest that frustration
15 Emotional Impact (Code et al)

may manifest as anger or bargaining with health professionals, with God or with self. In complete contrast

to denial, frustration results from full awareness of disability and realisation of powerlessness to

significantly change the course of events and therefore an unwanted and distressing reality.

As conscious awareness of the degree and permanence of deficits increases, a majority of people will

experience a (secondary) depression, arising from the full realisation of the value of the losses of person,

self and object. As mentioned earlier, this reaction may last for weeks or months, or can become fixated

within the individual for years. The grieving model sees depression as a necessary stage of emotional

recovery that must be worked through before true acceptance can be achieved.

The grieving model is powerful in its ability to explain some of the emotional and psychosocial aftermath

of stroke and aphasia, but researchers have complained that it is too powerful and its applicability to

aphasia has not been researched. A particular problem some critics have is that the grieving process is seen

as a static ‘stages’ model, and does not reflect the dynamic nature of emotional response to aphasia

(Gordon, Hibberd & Morganstein, 1988; Jackson, 1988).

The characteristics of the stages of grief - denial, anger, depression, etc., are certainly emotions that brain

damaged people experience and clinicians observe very often, but it is far from clear that these reactions

occur in stages or are sequentially related to each other, as the model tends to imply. A particular problem

with the model is that it was not developed with brain damaged people and aphasia in mind and it is unable

to deal with the fact that emotional changes following brain damage, including denial, anger and

depression, can have neurobiological causes too.

The future should see some progress towards combining what we know about different forms of emotional

change in aphasic people. We need to be able to distinguish, for instance, between primary and secondary
16 Emotional Impact (Code et al)

depression and between denial which has a neurobiological cause, a primary denial, with denial which is

caused by psychological protective mechanisms, a secondary denial. We need clear understanding of

different causes in order that we approach our intervention appropriately. There are indications that we may

be able to distinguish between primary and secondary depression (Herrmann & Wallesch, 1993). Lazarus

(1993) proposed that people react to particular negative life events through a subjective interpretation and

evaluation of the event and its meaning for them. Gainotti (1997) has recently suggested that this model

could form a useful framework for research into the complex interaction between the different kinds of

emotional response to aphasia.

THE EFFECTS OF EMOTIONAL FACTORS ON RECOVERY

AND RESPONSE TO REHABILITATION.

The dramatic and disabling effects of physical impairment accompanying stroke often takes priority in

treatment. This emphasis on physical recovery reflects the dominance of the medical model in our health

care systems (Taylor-Sarno, 1993). In its most radical form, the medical model has little time for emotional

experience and personal perspectives which are neither objective nor easy to measure and is not concerned

with social roles and psychosocial perceptions, factors not traditionally seen as well suited to experimental

investigation. This means that issues of personal experience are often neglected during the course of

rehabilitation. As a result, while emotional and psychosocial adjustment may have been acknowledged,

‘less emphasis has been placed on it, and little progress has been made on either addressing it’s causes or in

formulating treatment strategies" (Friedland & McColl, 1987; page 145).

17 Emotional Impact (Code et al)

It may be that the view that emotion is under the control of higher cognitive processes has caused

researchers to ignore evidence that emotional state can have a significant impact on motivation, physical

performance, cognitive and language processing (Tucker, 1981; Oatley & Johnson-Laird, 1987; Power &

Dalgleish, 1997). With positive mood and well-being, motivation increases and language and cognitive

performance improves. When emotional balance is disrupted, cognitive performance can decline. For this

reason, mood state may play a significant role in recovery from brain damage, helping to improve

individual psychosocial well-being.

Although there are few studies on the interactions between emotional and psychosocial factors with

recovery of language, evidence is now accumulating which suggests a significant effect on rehabilitation

outcome, through attention to these factors. Peoples with positive mood states respond better to therapy

than those who are depressed or express negative attitudes toward their disabilities. Robinson, Lipsey, Rao

and Price (1986) conducted a longitudinal study of post-stroke mood disorders, and concluded that

depression, if present, interacted with disability and had negative effects on medical and psychosocial

rehabilitation. Similarly, Sinyor et al. (1986a) compared rehabilitation outcome in depressed and non-

depressed stroke patients, and found that individuals suffering depression were less likely to progress in

physiotherapy, frequently reducing functional status during the first month post-onset (where non-

depressed peoples showed slight increases or no change in functional status).

Starkstein and Robinson (1988) concluded that depressed aphasic individuals show a lower rate of recovery

and significantly greater cognitive impairment. Similarly, Herrmann and Wallesch (1993) conclude from

their review that ‘it has been demonstrated that the success of rehabilitation may depend on early diagnosis

and adequate therapy of depressive changes. Not only the overall prognosis, but the specific effect on

neurological and neuropsychological impairment have been shown to correlate negatively with the

presence of depressive changes’ (1993; page 55). Hartman and Landau, (1987) compared the effects of
18 Emotional Impact (Code et al)

traditional aphasia therapy and counselling (addressing the emotional trauma of stroke) in language

recovery. Both were potentially valuable, indicating that positive psychosocial adjustment to trauma may

significantly improve cognitive state, and possibly impact upon the rate and degree of language recovery.

Hemsley and Code (1996) examined the relationships between recovery from aphasia and emotional and

psychosocial changes at 3 months and 9 months post-onset in 5 individuals and their spouses. They found

wide individual variability. There appeared to be a relationship between degree of awareness of the reality,

perception of severity of problems and degree of optimisim for the future. For one there was a decline in

well-being after 9 months with improvement on aphasia tests, resulting from improved comprehension and

awareness of the nature of the deficits. For one carer there was a decline in well-being at 9 months as she

began to realise that improvement was going to be little and slow. One mildly impaired patient was

severely depressed while another severely impaired patient showed no depression. One patient was not

depressed but his wife was significantly depressed. Relatively high optimism for the future, which was a

feature for several at 3 months post-onset, was reduced at 9 months.

Depression following brain damage responds to specific pharmacotherapeutic intervention. Different

antidepressant drugs have been trialed with patients with PSD: the effects of classic tricyclic

antidepressant, nortryptiline (Lipsey, Robinson, Pearlson, Rao & Price, 1984; Finklestein, Weintraub &

Karmouz, 1987; Balunov, Sadov & Alemasova, 1990), selective serotonin re-uptake inhibitors (Andersen,

Veestergard & Lauritzen, 1994; Andersen, 1996), and dextroamphetamine or methylphenidate (Lingam,

Lazarus, Groves & Oh, 1988; Masand, Murray & Pickett, 1991; Johnson, Roberts, Ross & Witten, 1992;

Lazarus, Winemiller, Lingam, et al., 1992; Masand & Chaudhary, 1994) have all been examined. Also,

electroconvulsive therapy has been successfully combined with antidepressant drugs (Murray, Shea &

Conn, 1986; Currier, Murray & Welch, 1992). Nearly all studies indicate that antidepressant drug treatment

improves the emotional state of depressed stroke patients and has a positive effect upon daily life activities
19 Emotional Impact (Code et al)

(Reding, Orto, Winter, Fortuna, DiPonte & McDowell, 1986). What we have been less clear about is

whether different approaches to intervention may be required at acute stages when individuals may be

experiencing primary depression as compared to more chronic secondary or tertiary stages. Antidepressants

are rarely prescribed for aphasic people. Probably, physicians have been reluctant to prescribe

antidepressants because they believed the patient’s depression was of the reactive kind we have described

above as well as unacceptable side effects (Andersen, 1997). However, drug trials have shown that the

selective serotonin re-uptake inhibitor citalopram is well tolerated and has only mild side effects (Andersen

et al, 1994). We need to investigate further how drug therapy, counselling and psychotherapy may be

combined at appropriate times and in different ways for different individuals. For fuller discussion of the

application of drugs to depression in aphasic patients see Wallesch, Müller & Herrmann (1996) and

Andersen (1997).

Taken together the research suggests an obligation to closely monitor the effects of emotional changes and

the way in which they impact on the ability of the aphasic people we work with to respond to rehabilitation

and to adjust to their disabilities. (Methods for assessing mood in aphasic people are reviewed by Stern in

this issue.) There is now indication that emotional factors must be addressed in rehabilitation and that

rehabilitation programs based purely on the medical model are simply not adequate or appropriate.

However, what is also becoming clear is that emotional response to aphasia is complex and seems to be

highly individualistic. Emotion probably interacts with other factors as well as the individual’s own

perceptions of their problems and their significance. Comprehensive rehabilitation must include a

significant social frame of reference which converges on emotional and psychosocial factors (Code &

Muller, 1992; Brumfitt, 1993; Taylor-Sarno, 1993; Muller, 1992).

20 Emotional Impact (Code et al)

References

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders, Fourth

Edition. Washington, DC: American Psychiatric Association.

Andersen, G. (1997). Post-stroke depression and pathological crying: Clinical aspects and new

pharmacological approaches. Aphasiology, 11, 651-664.

Andersen, G., Veestergard, K. & Lauritzen, L. (1994). Effective treatment of poststroke depression with

the selective serotonin reuptake inhibitor citalopram. Stroke, 25, 1099-1104.

Åström, M., Adolfsson, R. & Asplund, K. (1993). Major depression in stroke patients - A 3-year

longitudinal study. Stroke, 24, 976-982.

Balunov, O.A., Sadov, O.G. & Alemasova, A. Yu. (1990). Therapy of depressions in post-stroke patients.

Alaska Medicine, 32, 27-29.

Barry, S. & Dinan, T.G. (1990) Alpha-2 adrenergic receptor function in post-stroke depression.

Psychological Medicine, 20, 305-309

Benson, D.F. (1973). Psychiatric aspects of aphasia. British Journal of Psychiatry, 123, 555-566.

Benson, D.F. (1979). Aphasia, Alexia, Agraphia. New York: Churchill Livingstone.

Benson, D.F. & Geschwind, N. (1975). Psychiatric conditiuons associated with focal lesions of the central

nervous system. In: M.F. Reiser (ed.), American Handbook of Psychiatry, Vol 4: Organic Disorders and

Psychosomatic Medicine. New York: Basic Books.

Berthier, M.L. & Starkstein, S.E. (1987). Acute atypical psychosis following a right hemisphere stroke.

Atca Neurologica Belgica, 87, 125-131.

21 Emotional Impact (Code et al)

Biorn-Hansen, V. (1957). Social and emotional aspects of aphasia. Journal of Speech and Hearing

Disorders, 22, 53-59.

Brown, J.W. (1975). The neural organization of language: aphasia and neuropsychiatry. In: M.F. Reiser

(ed.), American Handbook of Psychiatry, Vol 4: Organic Disorders and Psychosomatic Medicine. New

York: Basic Books.

Browning, M.A. (1995). Depression. In Hogstel, M.O. (Ed). Geropsychiatric Nursing. St Louis: Mosby

Year Book Inc.

Brumfitt, S. (1993). Losing your sense of self: what aphasia can do. Aphasiology, 7, 569-574.

Bryer, J.B., Starkstein, S.E., Votypka, V., Parikh, R.M., Price, T.R. & Robinson, R.G. (1992) Reduction of

CSF monoamine metabolites in postrstroke depression: A preliminary report. Journal of

Neuropsychiatry and Clinical Neurosciences, 4, 440-442.

Campbell, A. (1976). Subjective measures of well being. American Psychologist, 31, 117-124.

Carnwath, T.C.M. & Johnson, D.A.W. (1987). Psychiatric morbidity among patients with stroke. British

Medical Journal, 294, 409-411.

Code, C. (1986). Catastrophic reactions and anosognosia in anterior-posterior and left-right models of the

cerebral control of emotion. Psychological Research, 48, 53-55.

Code, C. & Muller, D.J. (1992). The Code-Muller protocols: Assessing Perceptions of Psychosocial

Adsjustment to Aphasia and Related Disorders. Whurr: London.

Currier, M.B., Murray, G.B. & Welch, C.C. (1992) Electroconvulsive therapy for post-stroke depressed

geriatric patients. The Journal of Neuropsychiatry and Clinical Neurosciences, 4, 140-144.

Cutting (1978). A study of anosognosia. Journal of Neurology, Neurosurgery and Psychiatry, 41, 548-555.
22 Emotional Impact (Code et al)

Damasio, A.R. & Van Hoesen, G.W. (1983). Emotional disturbances associated with focal lesions of the

limbic frontal lobe. In Heilman, K.M. & Satz, P. (Eds). Neuropsychology of Human Emotion. New

York: Guillford Press.

Ekman, P., Friesen, W.V. & Ellsworth, P. (1982). What emotion categories or dimensions can observers

judge from facial behaviour. In Ekman, P. (Ed). Emotions in Human Face. (2nd ed). Cambridge:

Cambridge University Press.

Finklestein, S., Benowitz, L.J., Baldessarini, R.G., Arana, G.W., Levine, D., Woo, E., Bear, D., Moya, K.

& Stoll, A.L. (1982) Mood, vegetative disturbance and dexamethasone suppression test after stroke.

Annals of Neurology, 12, 463-468.

Finklestein, S.P., Weintraub, R.J. & Karmouz, N. (1987) Antidepressant drug treatment for post-stroke

depression: A retrospective study. Archives of Physical Medicine & Rehabilitation, 68, 772-776.

Fisher, S. (1961). Psychiatric considerations of cerebral vascular disease. American Journal of Cardiology,

7, 379.

Folstein, M.F., Maiberger, R., & McHugh, P.R. (1977). Mood disorders as a specific complication of

stroke. Journal of Neurology, Neurosurgery, and Psychiatry, 41, 470-473.

Friedland, J. & McColl, M. (1987). Social support and psychosocial dysfunction after stroke: buffering

effects in a community sample. Archives of Physical Medicine and Rehabilitation, 68, 475-480.

Gainotti, G. (1972) Emotional behavior and hemispheric side of the lesion. Cortex, 8, 41-55.

Gainotti, G. (1997) Emotional, psychological and psychosocial problems of aphasdic patients: an

introduction. Aphasiology, 11, 635-650.

Goldstein, K. (1948) Language and language disturbances. New York: Grune and Stratton.
23 Emotional Impact (Code et al)

Gordon, W.A., Hibbard, M.R. & Morganstein, S. (1988) Response to Tanner and Gerstenberger.

Aphasiology, 2, 85-87.

Hartman, J. & Landau, W.M. (1987). Comparisons of formal language therapy with supportive counselling

for aphasia due to acute vascular accident. Archives of Neurology, 44, 646-649.

Heilman, K.M. (1979). Neglect and related disorders. In Heilman, K.M. & Valenstein, E. (Eds). Clinical

Neuropsychology. New York: Oxford University Press.

Heilman, K.M., Scholes, R. & Watson, R.T. (1975). Auditory affective agnosia: disturbed comprehension

of affective speech. Journal of Neurology, Neurosurgery and Psychiatry, 38, 69-72.

Hemsley, G. & Code, C. (1996). Interactions between recovery in aphasia, emotional and psychosocial

factors in subjects with aphasia, their significant others and speech pathologists. Disability &

Rehabilitattion, 18, 567-584

Herrmann, M., Bartels, C., Schumacher, M. & Wallesch, C.W. (1995). Poststroke depression: Is there a

pathoanatomical correlate for depression following the postacute stage of stroke? Stroke, 26, 850-856.

Herrmann, M., Bartels, C. & Wallesch, C.W. (1993). Depression in acute and chronic aphasia - Symptoms,

pathoanatomo-clinical correlations, and functional implications. Journal of Neurology, Neurosurgery,

and Psychiatry, 56, 672-678.

Herrmann, M. & Wallesch, C.W. (1989). Psychosocial changes and psychosocial adjustment with severe

aphasia. Aphasiology, 3, 513-526.

Herrmann, M. & Wallesch, C.W. (1990). Expectations of psychosocial adjustment in aphasia: a MAUT

study with the Code-Muller Scale of Psychosocial Adjustment. Aphasiology, 4, 527-538.

24 Emotional Impact (Code et al)

Herrmann, M. & Wallesch, C.W. (1993). Depressive changes in stroke patients. Disability and

Rehabilitation 15, 55-66.

House, A., Dennis, M., Warlow, C., Hawton, K. & Molyneux, A. (1990). Mood disorders after stroke and

their relation to lesion location - A CT scan study. Brain, 113, 1113-1129.

Jackson, H. F. (1988). Brain, cognition and grief. Aphasiology, 2, 89-92.

Johnson, M.L., Roberts, M.D., Ross, A.R. & Witten, C.M. (1992). Methylphenidate in stroke patients with

depression. American Journal of Physical Medicine and Rehabilitation, 71, 239-241.

Kleinginna, P.R. & Kleinginna, A.M. (1981). A categorised list of emotion definitions with suggestions for

a consensual definition. Motivation and Emotion, 5, 345-379.

Kubler-Ross, E. (1969). On Death and Dying. New York: Macmillan.

Laplane, D., Baulac, M., Windlocher, D., & Dubois, B. (1984). Pure psychic akinesia with bilateral lesions

of basal ganglia. Journal of Neurology, Neurosurgery and Psychiatry, 47, 377-385.

Lazarus, L.W., Winemiller, D.R., Lingam, V.R., Neyman, I., Hartman, C., Abassian, M., Kartan, U.,

Groves, L. & Fawcett, J. (1992). Efficacy and side effects of methylphenidate for poststroke depression.

Journal of Clinical Psychiatry, 53, 447-449.

Lazarus, R. (1993) Coping theory and research: past present and future. Psychosomatic Medicine, 55, 234-

247.

Lingam, V.R., Lazarus, L.W., Groves, L. & Oh, S.H. (1988). Methylphenidate in treating poststroke

depression. Journal of Clinical Psychiatry, 49, 151-153.

25 Emotional Impact (Code et al)

Lipsey, J.R., Robinson, R.G., Pearlson, G.D., Rao, K. & Price, T.R. (1984). Nortriptyline treatment of

post-stroke depression: a double blind treatment trial. Lancet, 1, 297-300.

Lipsey, J.R., Robinson, R.G., Pearlson, G.D., Rao, K. & Price, T.R. (1985) The dexamethasone

suppression test and mood following stroke. American Journal of Psychiatry, 142, 318-323.

Lipsey, J.R., Spencer, W.C., Rabins, P.V., & Robinson, R.G. (1986). Phenomenological comparison of

post-stroke depression and functional depression. American Journal of Psychiatry, 143, 527-529.

Masand, P. & Chaudhary, P. (1994) Methylphenidate treatment of poststroke depression in a patient with

global aphasia. Annals of Clinical Psychiatry, 6, 271-274.

Masand, P., Murray, G.B. & Pickett, P. (1991). Psychostimulants in post-stroke depression. Journal of

Neuropsychiatry and Clinical Neurosciences, 3, 23-27.

Mesulam, M.M., Waxman, S.G., Geschwind, N., & Sabin, T.D. (1976). Acute confusional states with right

middle cerebral artery infarctions. Journal of Neurology, Neurosurgery, and Psychiatry, 39, 84-89.

Muller, D. (1992). Psychosocial aspects of aphasia. In Blanken, G., Dittmann, J., Grimm, H., Marshall,

J.C., & Wallesch, C.W. (Eds.), Linguistic Disorders and Pathologies: An International Handbook.

Berlin: Walter de Gruyter and Co.

Murray, G.B., Shea, V. & Conn, D.K. (1986). Electroconvulsive therapy for poststroke depression.

Journal of Clinical Psychiatry, 47, 258-260.

Oatley, K. & Johnson-Laird, P.N. (1987). Towards a cognitive theory of emotions. Cognition and Emotion,

1, 29-50.
26 Emotional Impact (Code et al)

Peroutka, S.J., Sohmer, B.H., Kumar, A.J., Folstein, M.F., & Robinson, R.G. (1982). Hallucinations and

delusions following a right temporoparietooccipital infarction. Johns Hopkins Medical Journal, 151,

256-273.

Power, M. & Dalgleish, T. (1997). Cognition and Emotion: From Order to Disorder. Hove, Sussex:

Psychology Press.

Price B.H. & Mesulam, M. M. (1985). Psychiatric manifestations of right hemisphere infarctions. Journal

of Nervous and Mental Disease, 173, 610-614.

Reding, M.J., Orto, L.A., Winter, S.W., Fortuna, I.M., DiPonte, P. & McDowell, F.N. (1986)

Antidepressant therapy after stroke: A double-blind trial. Archives of Neurology, 43, 763-765.

Robinson, R.G. & Benson, D.F. (1981). Depression in aphasic patients: frequency, severity, and clinical-

pathological correlations. Brain and Language, 14, 282-291.

Robinson, R.G., Bolduc, P.L., & Price, T.R. (1987). A two year longitudinal study of post-stroke mood

disorders: diagnosis and outcome at one and two years. Stroke, 18, 837-843.

Robinson, R.G., Kubos, K.L., Starr, L.B., Rao, K. & Price, T.R. (1983) Mood changes in stroke patients:

relationship to lesion location. Comprehensive Psychiatry, 24, 555-566.

Robinson, R.G., Kubos, K.L., Starr, L.B., Rao, K., & Price, T.R. (1984). Mood disorders in stroke

patients: importance of location of lesion. Brain, 107, 81-93.

Robinson, R.G., Lipsey, J.R., Rao, K. & Price, T.R. (1986). A two-year longitudinal study of poststroke

mood disorders: comparison of acute-onset with delayed-onset depression. American Journal of

Psychiatry, 143, 1238-1244.

27 Emotional Impact (Code et al)

Robinson, R.G., Starr, L.B., Lipsey, J.R., Rao, K., & Price, T.R. (1984b). A two-year longitudinal study of

post-stroke disorders: dynamic changes in associated variables over the first six months of follow-up.

Stroke, 15, 510-517.

Robinson, R.G. & Price, T.R. (1982). Post stroke depressive disorders: a follow up study of 103 patients.

Stroke, 13, 635-641.

Ross, E.D. (1981). The aprosodias: functional-anotomic organization oif the affective components of

language in the right hemisphere. Archives of Neurology, 38, 561-569.

Scherer, K.R. (1993). Neuroscience projections to current debates in emotional psychology. In Watts, F.N.

(Ed). Neuropsychological Perspectives on Emotion. Hove, UK: Lawrence Erlbaum Associates.

Sinyor, D., Amato, P., Kaloupek, D.B., Becker, R., Goldenberg, M., & Coppersmith, H.M. (1986). Post-

stroke depression: relationship to functional impairment, coping strategies, and rehabilitation outcome.

Stroke, 17, 1102-1107.

Sinyor, D., Jacques, P., Kaloupek, D.B., Becker, R., Goldenberg, M. & Coopersmith, H.M. (1986). Post-

stroke depression and lesion location: an attempted replication. Brain, 109, 537-546.

Starkstein, S.E. & Robinson, R.G. (1988) . Aphasia and depression. Aphasiology, 2, 1-20.

Starkstein, S.E., Robinson, R.G. & Price, T.R. (1987) Comparison of cortical and subcortical lesions in

the production of poststroke mood disorders. Brain, 110, 1045-1059.

Starkstein, S.E., Pearlson, G.D., Boston, J., & Robinson, R.G. (1987). Mania after brain injury: a controlled

study of causative factors. Archives of Neurology, 44, 1069-1073.

Taylor Sarno, M. (1993). Aphasia rehabilitation: psychosocial and ethical considerations. Aphasiology, 7,

321-334.
28 Emotional Impact (Code et al)

Taylor Sarno, M. (1997). Quality of life in aphasia in the first post-stroke year. Aphasiology, 11, 665-679.

Tanner, D.C. (1980). Loss and grief: implications for the speech-language pathologist and audiologist.

Journal of the American Speech and Hearing Association, 22, 916-928.

Tanner, D.C. & Gerstenberger, D.L. (1988). The grief response in neuropathologies of speech and

language. Aphasiology, 2, 79-84.

Tucker, D.M. (1981) Lateral brain functions, emotion, and conceptualisation. Psychological Bulletin, 89,

19-46.

Wallesch, C.W., Müller, U. & Herrmann, M. (1997). Aphasia: role of pharmacotherapy in treatment. CNS-

Drugs7, 203-213.

Wahrborg, P. (1991). Assessment and Management of Emotional and Psychosocial Reactions to Brain

Damage and Aphasia. London: Whurr.

29 Emotional Impact (Code et al)

TABLE 1. Abnormal positive and negative emotional states accompanying aphasia (adapted from

and based on Starkstein & Robinson, 1988).

Abnormal Negative Emotional Responses Authors

generalised anxiety disorders Robinson, Kubos, Starr, Rao & Price, 1984
depression Robinson, Kubos, Starr, Rao & Price, 1984;
Sinyor et al., 1986;
Robinson, Bolduc & Price, 1987;
Starkstein, Robinson & Price, 1987
pathological crying Andersen, 1997
paranoid states Benson, 1979
psychotic states Peroutka, Sohmer, Kumar, Folstein & Robinson,
1982;
Price & Mesulam, 1985;
Berthia & Starkstein, 1987
obsessional disorders Laplane, Baulac, Windlocher & Dubois, 1984

Abnormal Positive Emotional Responses

manic syndromes Starkstein, Pearlson, Boston & Robinson, 1987;

Robinson, Bolduc & Price, 1987
delirium Mesulam, Waxman, Geschwind & Sabin, 1976
aprosodic states characterised by an inability to Heilman, Scholes & Watson, 1975; Ross, 1981
express and/or comprehend emotional intonation
apathetic states characterised by undue Damasio & Van Hoesen, 1983
cheerfulness but with a loss of drive or motivation
disorders associated with an inability to recognise Cutting, 1978;
events, objects and states, such as denial, neglect, Gainotti, 1972;
30 Emotional Impact (Code et al)

anosognosia Heilman, 1979;

31 Emotional Impact (Code et al)

Self Assessment Questions

1. Which of the following statements is true?

a. Depression is rare in people with aphasia.

b. Depression is common in people with aphasia

c. Primary and secondary depression in aphasic people are easy to distinguish.

d. Depression is unrelated to language abilities in aphasic people.

e. Depression in aphasia is easy to treat.

2. Which of the following is not a symptom of depression?

a. Reduced cognitive function..

b. Impair memory function.

c. Impaired swallowing.

d. Disturbed sleep patterns.

e. Impaired appetite.

3. Which of the following forms of depression does not exist?

a. Primary depression

b. Secondary depression

c. Tertiary depression.

d. Reactive depression
32 Emotional Impact (Code et al)

e. Vegetative depression

4. Which statement is untrue?

a. All aphasic patients with anterior brain damage will be depressed.

b. Some patients with posterior brain damage will be indifferent.

c. Some patients with basal ganglia damage will be depressed.

d. All aphasic patients are at risk for disturbed mood of some kind at some time.

e. All aphasic patients should be assessed for disturbed mood.

5. Which of the following statements is untrue?

a. Depression can be a natural consequence of illness and disability.

b. Aphasic people may grief for their lost communicative abilities.

c. Denial, anger and depression are sequentially related stages observed in aphasic people.

d. Depression can have a significant effect on recovery and response to rehabilitation.

e. Depression in aphasic people does not respond well to antidepressant medication.

33 Emotional Impact (Code et al)

Answer Key for Self Assessment Questions

1. b

2. c

3. e

4. a

5. e

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