Hong Kong Journal of Psychiatry (1997) 7 (2) 40-46


Gabor S. Ungvari, Helen F.K. Chiu & Linda C.W. Lam

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Syndromes of apathy, demoralization and social breakdown in the elderly are long known but neglected concepts recently re-emerging as differential diagnostic possibilities to depression particularly among the elderly. The definition and brief description of these largely ignored syndromes are provided together with two case vignettes of apathy to illustrate the diagnostic difficulties in geriatric depression.

Keywords: geriatric depression, demoralization, apathy, social breakdown in the elderly.


Reliable ascertainment of geriatric depression has farreaching implications for several reasons. First, depression is not only a socially disabling psychiatric condition but it significantly contributes to an increase in mortality (Depression Guideline Panel, 1993). Second, depression affects around 10- 15 % of the general population in the western world (Tiemens et al, 1996) and at least 3 % of the population in Hong Kong (Chen et al. 1993). Last, but not least, depression is a tormenting subjective experience causing immeasurable suffering to patients and also their relatives. It is, therefore, of utmost importance to keep abreast with the new developments in the diagnosis of depression.

This paper attempts to explore a diagnostic conundrum at the borderland of depressive illness in the elderly. While dementia has been, and still is, the main differential diagnostic problem in geriatric depression (Mcloughlin & Levy, 1996), recently increasing attention has been paid to apathy (Marin, 1991), demoralization (Figueiredo, 1993) and the social breakdown syndrome (Radebaugh et al, 1987). These psychopathological entities are frequently encountered in geriatric and psychogeriatric clinical practice but probably go unnoticed or treated as depression since they are not wellknown enough among even psychiatrists let alone geriatricians and general practitioners. The aim of the following case histories is to highlight the difficulties in the diagnosis of geriatric depression and to call attention to the clinical concepts of apathy, demoralization and the social breakdown syndrome.



Ms A, a 79-year old widowed Chinese housewife, was admitted from a nursing home for lack of motivation to the extent of neglect of personal hygiene, poor food intake, paucity of spontaneous speech and retarded movements. She preferred to stay in bed all day. When prompted she related multiple somatic complaints like headache and epigastric and back pain. In an uncertain and inconsistent manner she mentioned spirits disturbing her. No obvious psychosocial stressor was ever identified; she had a long and apparently happy marriage and up to recently she had lived an emotionally balanced and financially secure life. Following the death of her husband, her three daughters provided good support.

Over the past 3 years Ms A had three admissions to our psychogeriatric unit with similar presentation. In addition to an always prominent core symptomatology of loss of motivation, vague somatic complaints and motor slowness, she variously presented with a number of short-lived symptoms of insomnia, loss of appetite or hyperphagia, dysphoric mood and what appeared to be attention-seeking behaviour. She became increasingly detached even from her immediate family. During all her admissions, although alert, fully oriented and coherent in speech, she refused to comply with psychological testing.

Apart from longstading hypertension well-controlled with 40 mg/day nifedipine, Ms A's medical history was unremarkable. Physical examination yielded no abnormal findings. Routine laboratory tests including full blood picture, liver, thyroid and renal function tests, serum electrolytes and VDRL were within normal limits. EEG showed no abnormality. During her first admission a CT scan of the brain revealed generalized cerebral atrophy and hypodense areas in the right basal ganglia suggestive of old infarcts.

Ms A's initial diagnosis of major depressive illness with psychotic features was changed after the brain CT scan to organic mood disorder. Subsequent trials with prothiaden and fluoxetine were unsuccessful despite adequate doses and duration of treatment. Twelve courses of electroconvulsive treatment (ECT) with seizure duration of at least 15 seconds each also failed to improve her condition. A noticeable, albeit transient, increase in motivation was observed with meclobamide 450 mg/day. Eventually, however, all psychotropic medication was stopped and currently she is managed with simple measures of behaviour therapy in a longstay care facility.


Ms B was a 87-year old single Chinese woman who had resided in a nursing home for 4 years prior to her first psychiatric evaluation and subsequent admission. She was the only child in a poor family. She worked as a maid all her life and, being an assertive and determined person, managed to live alone independently until the age of 83. She maintained a good relationship with relatives who remained supportive throughout her illness. Ms B's family and medical history were unremarkable except for a recent digoxin-responsive atrial fibrillation.

Ms B adapted well to the nursing home accepting even restrictive regulations like vegetarian diet. She was alert and lively, needed no supervision with activities of daily living and had a reasonable appetite and a good memory. Approximately 1 year before the initial psychiatric assessment, she gradually became more and more withdrawn and quiet, reduced her daily activities and food intake and barely spoke. She gave no reason why she changed her usual pattern of behaviour.

On the first psychiatric examination Ms B was found cachectic, slow in motion but alert and orientated. She answered questions but did not initiate conversation or offered any complaints. She was calm, indifferent and completely detached displaying a marked lack of concern towards her fate or the surroundings. She neither wished to die nor minded if it happened. No feelings of guilt, remorse or self-blame were reported. She did not feel hungry. She refused to complete the Mini Mental State Examination due to lack of interest. Although she did not feel ill, she accepted psychiatric admission. The provisional diagnosis was major depressive episode while the possibility of a dementing process was also entertained.

Routine diagnostic workup was non-contributory; full blood picture, liver, thyroid and renal function tests, serum electrolytes, VDRL were all normal. Ms B did not cooperate with EEG and MRI scan investigations. In view of her frailty and the lack of physical signs suggesting progressive intracranial lesion, we decided not to involve legal measures to pursue further these investigations against her will.

Over the next 7 months until her death, Ms B's condition remained essentially unchanged. Treatment attempts with antidepressants included nortriptyline (30 mg/day), paroxetine (20 mg/day), citalopram (20 . mg/day), and buspirone (20 mg/day). Treatment emerging side effects and later bronchopneumonia prevented the implementation of more vigorous therapeutic measures such as higher doses of antidepressants, augmentation strategies or ECT.

As a consequence of persistently poor food intake her weight fluctuated between 27 and 29 kg so eventually she required tube-feeding. She stayed in bed most of the time showing absolutely no interest in herself or the environment although remaining fully alert. She never voiced suicidal or other ideas even vaguely suggestive of depression. Nor did she reveal any hallucinations or delusional thinking. Later she became incon-tinent but, while fully aware of her plight, remained indifferent as before. After 5 months in the hospital she succumbed to bronchopneumonia. Autopsy was not performed.



First a depressive illness was suspected in both our cases. However, prolonged observation showed a consistent pattern of mood state distinctly different from that of depression and characterized by lack of concern and motivation and an impenetrable detachment. Depressed mood, sadness, despondency never surfaced throughout both patients' illness, nor were there any signs of depressive cognition including guilty feelings, self-blame, remorse or nihilistic delusions. Other features of depressive illness (feeling of worthlessness, helplessness, suicidal ideation, diurnal variation, etc.) were also lacking. Failure to respond to antidepressant treatment in Ms A's case is another, although admittedly weak, argument against depressive disorder. Although neither of the clinical presentations met ICD- 10 or DSM-N criteria for major depressive episode at any time, an element of diagnostic uncertainty obviously remains. With the lack of identifying biological markers for depressive illness, an atypical, apathetic depression (see below) cannot be ruled out purely on the basis of symptoms, course and outcome.

Ms A's illness, namely a slowly progressing apathy resembling chronic depression, was consistent with basal ganglia pathology (Burns et al, 1990; Cummings, 1993; Bhatia & Marsden, 1994;). Ms B's illness posed a more serious diagnostic dilemma that eventually remained unresolved. Her case history depicts a realistic clinical situation for two reasons; first, not all the necessary investigations could be done and second, only insufficient history could be gathered. Yet, oftentimes, clinicians have to proceed even under such circumstances with some form of treatment or utilize treatment response to a well-known therapeutic intervention as an aid in diagnosis. That was why we repeatedly launched antidepressant treatment although the diagnosis of depression was only one of the unverifiable possibilities. In the absence of extensive diagnostic evaluation in Ms B's case, we had to rely solely on clinical observation and examine the differential diagnosis offered by modem descriptive psychopathology.

There are a number of diagnostic possibilities when analyzing Ms B's case history. First is the question of organic pathology. Had an MRI scan been done, we might have discovered an advanced frontal lobe or basal ganglia pathology frequently mentioned as being responsible for similar clinical pictures (Bums et al. 1990; Bhatia & Marsden, 1994), as it probably was in Ms A's case. Alternatively, Ms B may have suffered from a rare form of atypical depression presenting with features of anhedonia, lack of concern and motivation and affective detachment and called non-participatory depression in classical psychopathological literature(Leonhard, 1979). Nonparticipatory depression has a poor treatment response to antidepressants and ECT(Leonhard, 1979). However, nonparticipatory depression has never been validated and has gradually faded away from mainstream psychiatry. Analyzing Ms B's case, further diagnostic options requiring attention include the similar, and partly overlapping, syndromes of apathy, demoralization and the social breakdown in the elderly. These old but recently re-emerging descriptive psychopathological-clinical concepts are less known, therefore they deserve a brief overview here.


In everyday parlance, apathy is usually referred to as lack of interest or emotion or activity or the combination thereof. In clinical practice, definitions of apathy vary from author to author. At present, a certain terminological and conceptual confusion reigns as neurologists and psychiatrists approach and describe the same clinical phenomenon from different angles (Rogers et al, 1987). A common interpretation of apathy in neuropsy-chiatry defines it as the absence of emotions or emotional withdrawal (Cohen et al, 1993) manifested as either "un internal feeling state of disinterest" or "a state of behavioural inaction" (Burns et al,1990). Apathy was also characterized as "indifference to surroundings" (Shader et al, 1974).

Recently Marin (1991) conceptualized apathy at the symptomatological as well as the syndromal level. Apathy as a symptom denotes lack of motivation causally related to an ongoing psychiatric illness (Marin, 1991). Apathy as a syndrome is a more tenuous concept, the clinical utility of which has not yet been extensively explored. The syndrome of apathy (primary apathy) is defined as '"primary absence of motivation, that is, lack of motivation not attributable to disturbances of intellect, emotion, or level of consciousness" (Marin, 1991). If apathy can be explained by any of the abovementioned disturbances, then apathy is regarded as a symptom and called, somewhat illogically, secondary apathy. Diminished goal-directed overt behaviour and its cognitive and emotional concomitants coupled with the lack of emotional distress constitute the main components of apathy syndrome (Marin, 1990; 1991). A wider concept of apathy syndrome comprised lack of interest and motivation, reduced activity and poor selfcare (Koplitz, 1975). In practical terms, it is extremely difficult, if not impossible or entirely arbitrary, to judge whether an intellectual or emotional or cognitive disturbance or the lack of motivation is the primary feature of a particular psychiatric disorder, hence the finer distinction between the symptom and syndrome of apathy has not gained wider recognition. Although explicitly defined, operationalized criteria for apathy have been proposed (Marin, 1991, see Appendix II), its clinical (face) validity has not yet been fully established. Yet, the concept of apathy has proved to be useful.in clinical practice owing to its frequency and certain therapeutic implications which will be briefly discussed in the following paragraphs.

The geropsychiatric literature has recently started paying more attention to the frequency of apathy in various neuropsychiatric conditions. Its recognition in clinical practice has been facilitated by the construction of two rating instruments, the Apathy Scale (Marin, 1990, see Appendix I.) and the Irritability/Apathy Scale (Burns et al, 1990). Both scales proved to be reliable and valid clinical tools (Starkstein et al, 1992). In a cohort of 735 patients suffering from either Alzheimer's disease (AD) or multi-infarct dementia or both, apathy was the third most frequent symptom following agitation and depressive mood occuring in 22-34 % of the cases (Cohen et al,1993). Avolition-apathy and social-emotional withdrawal was found significantly more frequently among patients with AD in comparison with healthy controls (Reichman et al, 1996). In 50 consecutively assessed patients with Parkinson's disease, apathy was observed in 12 % of the cases and an additional 30 % had apathy and depression concurrently (Starkstein et al, 1992). The same group reported similar findings in stroke : 22 % of a consecutive series of 80 patients presented with apathy (Starkstein et al, 1993). Apathy was significantly correlated with older age, cognitive and functional deficit. In both studies apathy and depression was reliably differentiated from each other by concurrent administration of the Hamilton Depression Rating Scale and the Apathy Scale (Marin, 1990).

Huntington's disease (HD) is another basal ganglia disorder where apathy features frequently. Caine and Shoulman (1983) found 78 % of their 30 patients with advanced HD apathetic. In Bums et al.(1990) study of 26 HD patients, 48 % was apathetic as measured by the Irritation/Apathy Scale. The same percentage of their AD group was found apathetic. However, when matched for the degree of cognitive impairment, HD patients had significantly higher scores on the apathy subscale than their AD counterparts. Apathy was not related to aggression, irritability or depressed mood (Bums et al, 1990).

Further clinical conditions that may comprise apathy syndrome include injury to the frontal, frontal-parietal or cingulate gyrus/supplementary motor areas (Damasio & Van Hoesen, 1983), hypothyroidism and "apathetic" hyperthyroidism (Brenner, 1978), chronic marijuana use (Dombush et al, 1976), amphetamine or cocaine withdrawal (Dackis & Gold, 1985), and loss of elementary sensory or motor capacity (Marin, 1991). Transient, dose-related apathy and indifference was reported in patients receiving fluvoxamine and fluoxetine (Hoehn-Saric et al, 1990). Social isolation and loss of environmental incentive may also result in apathy without the presence of any medical or psychiatric condition (Marin, 1990). There is an obvious phenomenological and conceptual overlap between apathy and such concepts as emotional blunting (Abrams & Taylor, 1978), negative symptoms (Andreasen, 1982), spontaneous and neuroleptic-induced akinesia (Rifkin et al, 1975) and psychomotor retardation (Rogers et al, 1987). Brad yphrenia, its currently used synonym is subcortical dementia, also has apathy as one of its main components in addition to slow cognitive processes and impaired concentration (Rogers et al, 1987). The syndrome of apathy is usually, but not necessarily, accompanied by psychomotor retardation although their severity is not always proportionate; marked psychomotor retardation, for instance, may present together with preserved motivation and euthymic mood in akinetic Parkinson syndrome. Conversely, profoundly apathetic individuals may go about their businesses quietly and dutifully almost acting like automatons as seen in some patients with chronic apathetic depression.

Abulla, characterized by "inability to exert the will" (Berrios & Gill, 1995) while the motivation to act is intact, has to be clearly delineated from apathy although they frequently cooccur (Foerster & Sahakian, 1991). With the lack of biological validators, the differentiation between the symptomatologically overlapping syndromes of apathy and depression is based on phenomenological characteristics of disputable accuracy. Therefore, the differential diagnosis is fairly subjective depending on the individual clinician's viewpoint. In the presence of lack of interest and motivation usually accompanied by psychomotor retardation, the diagnosis of apathy syndrome is suggested instead of depression, provided sadness, depressive cognition (e.g. guilt, self-blame, groundless remorse), suicidal ideation, anxiety and neurovegetative symptoms (insomnia, marked loss of appetite) are absent (Marin, 1991). Further studies will determine whether apathy is a distinct clinicalneurobiological entity or a subtype of depression (Duffy & Coffey, 1996).

Presently there is no specific therapy for apathy. Its management consists of the treatment of underlying neuropsychiatric or medical disorder and a measured social stimulation (Caine & Shoulson, 1983). There has been preliminary evidence that methylphenidate (Kaplitz, 1975; Maletta & Winegarden, 1993), bromocriptine . (Foerster & Sahakian, 1991; Powell et al, 1996), amantadine, selegillne, bupropion and amphetamine (Marin et al, 1995) are all effective in ameliorating apathy in some cases suggesting that dopaminergic dysfunction may be involved in its pathomechanism (Rogers et al, 1987).


Similar to apathy, the word 'demoralization' is also used in everyday language in various context. It has been defined for clinical use with special reference to its differentiation from depression. The two main components of demoralization are (1) a pervasive feeling of incompetence and (2) the accompanying distress leading to losing the grip and direction of one's own life (Figueiredo, 1993). Demoralization inflicts mostly psychiatrically non-ill individuals, in which case it is called primary demoral-ization although this usage would unnecessarily medicalize a common human Demoralization is one of the main psychological sequalea of institutionalization seen, for example, in prison, orphanage or in the army. Understandably, elderly people living alone or in poorly managed old age homes are particularly subject to demoralization. Engel coined the term "giving-up - given-up complex" for the stage of a medical illness where the patient eventually resigns to the inevitable and offers no more psychological resistance towards his/her illness (Engel, 1967).

In many instances, demoralization is the consequence of the complex interaction of longstanding major psychiatric illnesses and environmental factors (secondary demoralization ).

Demoralization should be distinguished from depression. In contradistinction to depression, in demoralization the magnitude of motivation is usually normal while the direction of action is lost and the demoralized individual perceives the cause of distress outside the self. There are no neurovegetative symptoms commonly associated with demoralization. With the loss of direction, demoralization brings about indecisiveness, puzzlement and uncertainty (Figueiredo, 1993). Demoralization does not appear in official psychiatric classifications and, to the best of our knowledge, no attempt has been made to operationalize demoralization for clinical use or to construct a reliable instrument for its measurement.


There are subtle, albeit salient, differences between demoralization and the "social breakdown syndrome of the elderly" also called as "diogenes syndrome" (Clark et al, 1975; Klosterkotter & Peters, 1985). Such patients live in an apparently self-inflicted and profound social isolation neglecting their self-care and immediate environment. They consistently refuse help. Collection of useless objects and a shameless attitude towards self-neglect are further characteristics of the syndrome. Substandard living conditions due to economic hardship are not included in the concept of social breakdown. A well-defined psychiatric illness, such as schizophrenia, affective illness or dementia are responsible for approximately half of the cases (secondary social breakdown) (Radebaugh et al, 1987) while in primary or pure social breakdown stressful life events against the background of lifelong personality abnormalities are thought to be the major causative factors (Klosterkotter & Peters, 1985; Tantam, 1988). Social breakdown in the elderly has received little attention in the geriatric and psychogeriatric literature although hospital admission (MacMillan & Shaw, 1966; Clark et al, 1975) and population-based mental health surveys (Radebaugh et al, 1987) both found it in a sizeable proportion among the elderly.


Elements of apathy and demoralization often appear in depressive illness and disappear when the depression is resolved. The differentiation between the syndrome of apathy, primary demoralization and social breakdown syndrome from depression has important practical implications. The features of depressive syndrome are well-known and the majority of depressive disorders are treatable with a combination of biological and psychological methods. Apathy, demoralization and the social breakdown syndrome are not part of official classifications and not widely known even among psychiatrists. Although there has been anecdotal evidence of successful interventions in apathy (e.g. Koplitz, 1975; Marin et al., 1995) and in the social breakdown syndrome (Klosterkotter & Peters, 1985), the description, diagnosis and management of these syndromes remain uncertain. Proponents of the concepts of apathy and demoralization argue that misdiagnosing either of these syndromes for depression may result in exposing the patient for long and usually repeated periods of antidepresssant treatment which is not only useless but may inflict disturbing side effects. At the same time concerted social and psychological efforts aiming at the apathetic or demoralized individual may be missed (Caine et al, 1978). Given the considerable number of patients with treatment resistant depressive illness and the not infrequent protracted recovery in geriatric depression (Alexopoulos et al, 1996), lack of treatment response does not help the clinician in the differential diagnosis. Since there are no well-established diagnostic and therapeutic guidelines on how to recognize and treat apathy, demoralization or social breakdown, for ethical reasons clinicians are compelled to proceed with new varieties of antidepressant treatment in cases of diagnostic confusion or doubt as it happened in our cases.


The overlapping concepts of apathy, demoralization and social breakdown in the elderly have recently emerged in the literature. Their clinical presentation resembles that of depression or they co-occur with chronic depression. At this point, only scanty information exists about their phenomenology, long-term course, pathomechanism or treatment response. Yet, these rising psychopathological entities are becoming important differential diagnostic options to chronic depression therefore psychiatrists, particularly psychogeriatricians, should be familiar with them.


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*Gabor S. Ungvari, PhD, FRANZCP, FHKCPsych, FHKAM(Psych), Associate Professor, Department of Psychiatry, Chinese University of Hong Kong
Helen F.K. Chiu, FRCPsych, FHKCPsych, FHKAM(Psych), Chairman and Associate Professor, Department of Psychiatry, Chinese University of Hong Kong,
Linda C.W. Lam, MRCPsych, FHKCPsych, FHKAM(Psych), Associate Professor, Department of Psychiatry, Chinese University of Hong Kong

*Correspondence : Dr G. S. Ungvari, Deparhnent of Psychiatry, 11/F, Prince of Wales Hospital, Shatin, N.T. Hong Kong.



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