Review

Abulia in the elderly

Geraldine D’Souza MRCPsych, Alex Kakoullis MRCPsych, Nibha Hegde MRCPsych, George Tadros MD, MRCPsych

Recognition and management

of abulia in the elderly
Abulia is a state of diminished motivation in which an individual may appear apathetic, disinterested, asocial
and emotionally remote. There is currently a lack of information on the recognition and management of
abulia in elderly patients, despite the fact that it occurs in conjunction with many conditions that are
associated with ageing. Here, the authors review the current literature and describe three cases of abulia
in elderly patients that responded well to treatment with bromocriptine.
Mini-Mental State Examination (MMSE).5 Abulia was

T
The word abulia means absence of volition. The symp-
tom of abulia is described by the Oxford Medical
Dictionary as ‘the absence or impairment of will-
power’ where ‘an individual still has desires but they
are not put into action’. Alternatively, it can be defined
as a state of diminished motivation not attributable to
a decreased level of consciousness, cognitive impair-
ment or emotional distress.1 It can range from subtle
to overwhelming in severity, and some consider it as
part of a spectrum of diminished motivation in which
akinetic mutism is the most extreme form.2 Terms
that have been used synonymously with abulia include
apathy and amotivational states. It can exist independ-
ently but more commonly occurs as part of a constel-
lation of symptoms accompanying a specific disorder,
either neurological or psychiatric.
An individual with abulia may appear not to have the
will or motivation to pursue activities or initiate conver-
sation. They may seem apathetic, disinterested, asocial,
quiet or mute, physically slowed and emotionally remote.
Abulia has significant clinical implications as it is poten-
tially treatable and is associated with poor function and
increased carer stress.3 Despite this, it seems to receive
little clinical attention and is rarely acknowledged. It has
associations with a number of conditions, including
schizophrenia, Huntington’s disease and acquired brain
injury. Also, although it is not caused by ageing per se,4
abulia has been observed in a number of conditions asso-
ciated with ageing. These include Alzheimer’s disease,
vascular dementia, stroke, Lewy body dementia,
Parkinson’s disease and frontotemporal dementia.
Abulia and dementia
Abulia tends to occur in the advanced stages of
Alzheimer’s dementia when limbic areas such as the
frontal lobe, amygdalae and cingulate gyrus become
affected. It also appears to be associated with a worse
outcome in Alzheimer’s disease: a faster rate of decline
in cognitive function was noted in apathetic outpatients
versus a non-apathetic group as assessed using the
24 Progress in Neurology and Psychiatry
also found to be more common in patients who did not
show a behavioural response to donepezil.6
Abulia is also seen in vascular dementia, frontotem-
poral dementia and subcortical dementias. In vascular
dementia, it is more commonly associated with right
hemispheric lesions.7 In frontotemporal dementia,
abulia is thought to be related to dysfunction of the
medial frontal lobe.8 In subcortical dementias, disor-
ders of the basal ganglia have been mainly implicated
as the cause of abulic symptoms.
Abulia and depression
Many studies have documented the occurrence of abulia
in depression, and in fact, clinicians often misleadingly
regard depression as a disorder model to define abulia.
The literature, however, suggests that abulia and depres-
sion are two separate entities. They may be associated
in part due to the fact that some items on depression
scales are consistent with abulia. Another possible expla-
nation given is that similar cerebral circuits (limbic-
fronto-subcortical) could be involved in both abulia and
depression but that the neurotransmitter involvement
could differ. Serotonergic agents relieve depression but
may increase apathy whereas dopaminergic agents may
relieve apathy.9 When associated with intracranial pathol-
ogy, depression is reported to be more common with
anterior and left-sided lesions whereas abulia appears to
be more common with right-sided lesions.10
In a cross-sectional study of 154 patients with demen-
tia of varying aetiology, abulia did not correlate with
depression. Abulia, but not depression, correlated with
lower cognitive function as measured by the MMSE.11
A number of other studies also do not suggest a strong
correlation between depression and apathy.7,12 Abulia
is therefore seen as a specific neuropsychiatric syn-
drome that is distinct from depression, and distinguish-
ing these two syndromes has therapeutic implications.
Clinically, patients with abulia do not disclose any sign
of sadness or negative thoughts. Instead, they show an
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Review
Abulia in the elderly
Case 1
A 73-year-old male patient, who was premorbidly active and sociable
with no previous psychiatric history, presented to psychiatric
services with a profound loss of motivation, energy and interest, and
poor concentration. He was an ex-smoker with hypercholesterol-
aemia, hypertension and ischaemic heart disease, having had a myo-
cardial infarction and a triple bypass operation at the age of 66 years.
A major complaint was of difficulty in getting up every morning. At the
time, the patient would sometimes stay in bed as late as 5pm despite
going to sleep at midnight.The patient denied low mood.
The patient was given various diagnoses including generalised
anxiety disorder, depression with somatic symptoms and hypo-
chondriasis. He was treated with various antidepressants with little
or no effect. He also received cognitive behavioural therapy with
similarly poor results. He scored 30 out of 30 on the MMSE. Neuro-
psychological testing did not support a diagnosis of dementia but
showed a degree of frontal lobe dysfunction. An MRI scan showed
changes consistent with previous vascular accidents and minor
diffuse cortical atrophy with minimal dilatation of the ventricles.
obvious lack of concern about their condition or the rel-
atives around them. Patients with abulic symptoms at
baseline respond poorly to antidepressants.13
Role of dopamine
Although the pathological changes that might explain
abulia are unlikely to be restricted to one neurotrans-
mitter, the dopaminergic system in the brain has
received the most attention. Damage to frontal sub-
cortical circuits linking the anteromedial frontal lobe
to the thalamus and basal ganglia is associated with
abulia.14,15 This is thought to be a result of damage to
the dopaminergic system.16 In animals, mesocorticol-
imbic dopaminergic circuits have been found to medi-
ate reward and motivation, and their damage is
associated with apathy.14 It has been hypothesised that
such areas and pathways in the brain are what allow
us to turn our impulses into actions. Their malfunction
‘is the fundamental cause of all slowness in the CNS’.2
Pharmacologically, agents that have an effect on the
dopaminergic system produce intriguing changes in
motivation. Dopamine antagonists in rats impair motor
activity, spontaneity and behavioural responsiveness.
Higher doses can induce catalepsy. Conversely, amphet-
amines increase stimulation-seeking activity in rats. In
humans, cocaine and amphetamine withdrawal can com-
monly be associated with apathy and poor motivation.
This can be reversed with bromocriptine treatment.14
As a result of the above findings and theories, drugs
that affect the dopaminergic system have been looked
26 Progress in Neurology and Psychiatry
The patient continued to deteriorate without any treatment
success. Two years after first presentation, he was thought to be
abulic probably as a result of cerebrovascular disease. His anti-
depressant was discontinued and, with his consent to try an off-
licence medication, he was started on bromocriptine 2.5mg twice
daily. This was incrementally increased over a month to 10mg twice
daily. Treatment response was recorded by charting behaviour and
sleep. Slight improvements in his time of waking were noted at each
dose increase. The patient was monitored for side-effects, including
blood pressure and mental state, but none were reported.
Over three months, the patient continued to improve on
bromocriptine 10mg twice daily. He began to get out of bed as early
as 8am and take part in social activities. Although there were some
reports of minor problems in his short-term memory, neither he
nor his wife felt that there was any significant cognitive impairment.
After six months of treatment, he and his wife reported that he was
back to his ‘normal’ self and had resumed going on family holidays. A
year later, he remained very well.
at as possible treatments for abulia, although no treat-
ment is currently licensed for this. Most of the research
has involved small numbers of case studies. L-dopa was
successfully used to treat severe abulia caused by
encephalitis lethargica.17 Unfortunately, the effects were
transient. Stimulants such as methylphenidate and, to a
lesser degree, dexamphetamine have also shown prom-
ise as treatments for apathy.14 Carbidopa/levodopa has
improved abulia in at least four case studies. 18
Amantadine has shown benefit in a number of case stud-
ies.3,19 The antidepressant bupropion, which inhibits
dopamine reuptake, has also been effectively used for
apathy even when dopamine agonists have failed.20
Use of the dopamine agonist bromocriptine in the
treatment for abulia has only been reported in 17 pub-
lished cases. This excludes reports of its use in akinetic
mutism. In 1988, Catsman-Berrevoets and von
Harskamp described response in a 38-year-old woman
with bilateral thalamic infarctions, who had developed
severe memory disorder, severe apathy and a compul-
sive tendency to assume a sleeping position.21 Barrett
described abulia in four cases ranging between the
ages of 28 and 62 years; two had brain damage second-
ary to alcohol consumption, one had Wilson’s disease
and one had an infarction in the basal ganglia. All cases
showed improvement in motivation and self-care but
one patient developed a depressive episode and was
tried on lisuride instead.16 Parks et al. described apathy
and psychomotor slowing in a 51-year-old following a
subarachnoid haemorrhage. Bromocriptine produced
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Case 2
A 72-year-old ex-professional man who was premorbidly assertive,
active and driven was referred to psychiatric services with a history
of lack of motivation and energy, anhedonia and a general change in
personality. He had a history of mild reactive depression on three
previous occasions. There was nothing of note in his past medical
history. There were no predominant negative cognitions. His GP
described him as ‘flat, slow and meagre with responses’ and his wife
found him ‘difficult’ as he was not interested in any activities and was
going to bed early every night. There was no evidence of significant
cognitive deficit. An MRI scan showed periventricular and subcortical
ischaemia, greater in the right hemisphere than left, with additional
ischaemia in the brainstem.
a sustained improvement followed by deterioration on
stopping the drug.22 Powell et al. treated 11 patients
(six men and five women between the ages of 26 and
55 years) who had previously had traumatic brain
injury or a subarachnoid haemorrhage. Bromcriptine
improved motivation and cognitive function, but not
mood.23 No studies have specifically looked at its use
in the treatment of abulia in the elderly.
Case studies
Case studies 1-3 focus on our experience of the treatment
of abulia with bromocriptine in three elderly patients.
The first case is a classical example of a patient with pure
abulic symptoms who showed a good response to
bromocriptine. The second case is an example of the
overlap between abulia and atypical features of depres-
sion. The third case demonstrates the complexity and
dilemma of using dopaminergic treatment in a patient
with vascular dementia and psychotic symptoms. All
three cases show an underlying vascular pathology.
Discussion
Abulia has been receiving increasing clinical recognition
and research attention in recent years. In the elderly, it
remains under-recognised in its own right, but it may
be an important prognostic factor. In a recent survey
aiming to explore the knowledge of British neurologists
and psychiatrists on the topic ‘diminished drive and
motivation’, less than a half of these specialists believed
that these disorders were distinct from depression. Only
52 per cent of them considered it could indicate damage
to the basal ganglia.24 Even though there has been grow-
ing interest in the subject in recent years, the number
of publications on the topic is relatively sparse. This is
probably due to the fact that milder forms are more com-
mon than the ‘pure cases’ and abulia is more often asso-
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Review
Abulia in the elderly
The patient was treated with several antidepressants and with
cognitive behavioural therapy. All treatments had either little or no
benefit. A couple of years later, it was felt that although his mood had
not been particularly an issue, his motivation levels had remained poor
and he did not initiate conversation. He was thought to be abulic
rather than depressed. He was also started on bromocriptine 2.5mg
twice daily.This was incrementally increased to 10mg twice daily. He
was monitored for clinical response and side-effects but no significant
problems were experienced. He became progressively more motivated
with each increase in dose, and after several months was driving his
car, resuming his regular swimming exercise, socialising far better than
before and had successfully organised his golden wedding anniversary.
ciated with cognitive dysfunction, mood disorders, psy-
chotic or other neurological and medical conditions.
Many of these are more common in older people.
Abulia is best thought of as one potentially disabling
symptom within the context of a whole clinical picture.
When assessing patients in whom abulia presents as the
predominant symptom, other psychiatric, neurological
and medical conditions should be borne in mind and
excluded first. Although depression may not present typ-
ically, especially in the elderly, it can be differentiated
from abulia through the presence of negative thought
content, somatisation or a previous history of depression.
Socio-environmental and biological factors also play a
role in motivation and emotional response. The elderly
are particularly prone to socio-environmental changes,
which puts them at a greater risk for presenting with
abulic symptoms; institutionalisation in a nursing home
is one such example. Biological factors such as sensory
loss or physical disability may also produce a gradual
decrease in motivation due to a perceived lack of envi-
ronmental incentives. It is, therefore, important to eval-
uate the effects of such factors in contributing to abulic
symptoms. A thorough neurological and psychosocial
assessment is required to rule out an underlying cause
especially in the case of an initial presentation in older
adults. Brain imaging may help to identify the conditions
associated with abulia, but it is important to recognise
that imaging may be normal initially and that changes
on functional brain imaging (SPECT, PET) may precede
any abnormality on structural imaging such as MRI.
Conclusion
It is important for clinicians to recognise abulia early and
consider treatment. Dopaminergic medication may be
beneficial but it would be difficult to recommend one
agent over another due to the current lack of evidence.
Progress in Neurology and Psychiatry 27
Review
Abulia in the elderly
Case 3
An 80-year-old man presented with a significant lack of motivation to
engage in day to day activities. He had an established diagnosis of
vascular dementia, following a series of strokes eight years previously.
A CT scan at that time showed white matter ischaemic changes with
lacunar infarcts in the upper internal capsule, coronal radiation and
right lentiform nucleus. It also showed calcification in the carotid
siphons and basal ganglia. Since the strokes, the patient suffered with
recurrent depressive and psychotic symptoms. Up to one year prior
to presenting with lack of motivation, he had been treated with
various antidepressants, antipsychotics, anticonvulsants and ECT.
On presentation, he was free of depressive or psychotic
symptoms. His symptoms of diminished motivation were unusual for
Caution is required, because of potential side-effects, and
previously psychotic patients may be at risk of a relapse.
However, no adverse effects were experienced in our
three cases. The possible risks and benefits must be eval-
uated in each individual before treatment is decided
upon. However, it is important to remember that worse
outcomes may be seen in abulia and, in many cases, sev-
eral other treatments will have already been unsuccess-
fully tried. Hopefully, this review makes a case for an
increased awareness of abulia in clinical and research
settings. Although this applies across all age groups, one
needs to be particularly vigilant in the elderly.
Declarations of interest
None.
Dr D’Souza and Dr Kakoullis are Specialist Registrars
in Old Age Psychiatry and Dr Hegde is Staff Grade in
Old Age Psychiatry, Birmingham and Solihull Mental
Health Foundation Trust; Professor Tadros is a
Consultant in Old Age Psychiatry, Birmingham and
Solihull Mental Health Foundation Trust and Professor
of Mental Health and Ageing, Staffordshire University
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Key points
• Abulia mainly presents as lack of motivation and varies in severity
• Abulia is associated with a number of psychiatric and neurological
disorders, some of which are more common in the elderly
• Abulia affects quality of life of patients and carers and has negative
effects on outcomes of many disorders
• It is important to differentiate abulia from depression as
antidepressants do not seem to be effective
• Abulia can be successfully treated with a number of different
strategies, in particular dopaminergic medication
• The case studies presented here suggest that using bromocriptine
in the treatment of abulia is effective and safe
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