APATHY SCALE STARKSTEIN PDF

Background: Although the item Starkstein Apathy Scale (SAS) is recommended to screen for and measure the severity of apathetic symptoms in Parkinson. Although the item Starkstein Apathy Scale (SAS) is recommended to screen for and measure the severity of apathetic symptoms in Parkinson disease (PD). Items 9 – 14 breviated version of the AES, known as the Apathy Scale. Copyright © SciRes. .. [6] Starkstein, S.E. and Leentjens, A.F.G. () The noso-.

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Apathy is currently defined as diminished motivation as expressed in poor goal-oriented behaviours and cognitions. A structured clinical interview and a specific set of diagnostic criteria to diagnose apathy in dementia have been recently validated.

There are several valid and reliable scales to measure the severity of apathy in adults with neuropsychiatric disorders. Among patients with Alzheimer’s disease, apathy is significantly associated with older age, the presence of depression, and more severe cognitive and functional deficits, and also predicts a faster cognitive and functional decline.

The mechanism of apathy in neuropsychiatric disorders is still unknown, but several studies suggest an important role for frontal lobe and basal ganglia dysfunction. There are no specific randomized controlled trials of psychoactive compounds to treat apathy in neuropsychiatric disorders.

Evidence from case reports and small case series suggest the usefulness of psychostimulants to treat apathy in traumatic brain injury, whereas pharmacological trials for behavioural and psychological problems in dementia suggest that anticholinesterases may have some efficacy.

The prevalence, clinical correlates and treatment of apathy in Alzheimer’s disease

Dementia, Alzheimer’s disease, Geriatric Psychiatry, Apathy. Introduction Diminished motivation is one of the most frequent behavioural changes among patients with neuropsychiatric disorders.

Apathy is most frequently associated with depression and severe dementia. AD patients with apathy are more impaired in basic activities of daily a;athy and their caregivers report significantly higher levels of distress as compared to AD patients without apathy Landes et al. In starlstein of the strong negative impact of apathy in AD, treatment studies for this frequent behavioural condition are surprisingly few. Our group and others have also reported a relatively high frequency of apathy among patients with stroke lesions, traumatic brain injury, Parkinson’s disease, and Huntington’s disease Burns et al.

Nevertheless, the frequency starksteij apathy is highest among individuals with dementia, and the present review scape mainly focus on the frequency and clinical correlates of apathy in AD. We will briefly discuss the neurobiological basis of apathy, and also review pharmacological and etarkstein treatment modalities.

Diagnosis of Apathy Marin scal apathy as the absence or lack of feeling, emotion, interest or motivation Starkstsin Starkstein Starkstein standardized Marin’s construct into a set of criteria based on the presence of diminished goal-directed behaviour, diminished goal-directed cognition, and diminished concomitants of goal-directed behaviour Table I. These diagnostic criteria have been validated for patients with Alzheimer’s disease, starksteim their validity in other neuropsychiatric conditions remains to be established.

One of the main diagnostic dilemmas is how to separate apathy from depression. Marin Marin et al. Several studies from our group demonstrated that apathy is a common feature of depression among individuals with or without AD, although apathy and depression may also occur independently of each other Starkstein et al.

Several instruments are now available to rate the severity of apathy. Marin and coworkers were the first to validate the Apathy Evaluation Scale for use with patients with stroke, Parkinson’s disease, or Alzheimer’s disease Marin et al.

This instrument consists of 18 items scaale can be administered as a self-rated scale, as a caregiver scale, or as a clinician administered test. Starkstein and coworkers developed a aapathy Apathy Scale Table IIwhich is an abridged and slightly modified version of Marin’s instrument Starkstein et al.

The Apathy Scale was validated for use in stroke, Parkinson’s disease, and Alzheimer’s disease. Cummings developed the Neuropsychiatric Inventory as a multidimensional instrument administered to an informant Cummings This assessment includes a specific module to measure apathy, which consists of 8 items that are rated as present or absent.

Scores on the apathy module provide a measure of the frequency and severity of apathy, as well as caregiver distress. Roberts and coworkers designed the Apathy Inventory based on the format of the Neuropsychiatric Inventory Robert et al. The Apathy Inventory also includes separate assessments for the starktsein of emotional blunting, lack of initiative, and loss of interest.

We have recently published the validity and reliability of the Structured Clinical Interview for Apathy Starkstein et al. This instrument includes questions assessing the domains of lack of motivation relative to the individual’s previous level of functioning, lack of effort to perform every day activities, dependency on others to structure activities, lack of interest in learning new things or in new experiences, lack of concern about one’s personal problems, unchanging or flat dcale, and lack of emotional response to positive or negative personal events.

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Based on answers to specific questions, symptoms are scored as either absent, subclinical, or definitely present. This is, to our knowledge, the only standardized instrument to assess the presence of symptoms of apathy using a semi-structured format.

In conclusion, whilst apathy is one of the most frequent behavioural changes in neuropsychiatric disorders, its clinical assessment is still problematic.

Diagnostic criteria for apathy have been validated for Alzheimer’s disease only. There is a variety of scales that are both valid and reliable to rate the severity of apathy, but these instruments are also used to diagnose apathy based on cut-off scores. This procedure may result in apathy groups with different syndromic clusters.

There is also a structured clinical interview for apathy, but its validity and reliability has been established for patients with dementia only. We examined the frequency of apathy in a study that included a consecutive series of patients with probable AD Starkstein et al.

Scores on this item are 0: Patients with scores of 2 or higher were considered apathetic. Based on this diagnostic scheme, 46 of the patients with Alzheimer’s disease had apathy. In the next study we diagnosed apathy based on the diagnostic criteria described in Table 1 Starkstein et al.

Clinical information was obtained from caregivers, who filled the Apathy Scale about the patient. Briefly, apathy was diagnosed whenever patients had 1 Poor or no motivation as rated with item 7 on the Apathy Scale2 Poor or no interests as rated with items 1 and 2 or effort as rated with items 4 and 9and 3 Feelings of indifference or lack of emotions most or all of the time as rated with items 10 and About two thirds of the AD patients with apathy were also depressed either major or minor depression.

Apathy was diagnosed using the diagnostic criteria listed in Table I Starkstein et al. Thirteen of these 29 patients also had major depression, 5 patients had minor depression, and 11 patients were not depressed.

Taken together, our findings suggest that the frequency of apathy in AD is lower when assessed with a structured interview and diagnosed with standardized criteria as compared to using arbitrary cut-off points on a severity rating scale. In a study that included patients with AD, Landes and coworkers diagnosed apathy based on a cut-off score on the Dementia Apathy Interview and Rating Landes et al.

First, apathy has been diagnosed using a variety of rating instruments and different strategies. Second, the source of patients varied widely, from patients living in the community to those admitted to specialized dementia units.

Finally, those apathu that included patients with relatively more severe dementia showed a higher frequency of apathy than studies that included patients with milder dementia. Clinical correlates and course of apathy in AD Most studies on apathy in AD have been cross-sectional, and all of them demonstrated a stadkstein association between more severe apathy and more severe dementia. In a recent study we assessed the longitudinal evolution of apathy in a consecutive series of patients with probable AD attending a memory clinic Starkstein et al.

Apathy was assessed with the Apathy Scale and diagnosed using the diagnostic criteria shown in Table I. Patients with apathy were significantly older, had more severe cognitive deficits and more severe impairments in activities starksteln daily living than patients without apathy. To examine whether apathy should be considered a mere symptom of depression in dementia, we first examined whether the onset of depression during the follow-up period was associated with increasing apathy.

The results showed a significant overall increment in apathy scores during the follow-up period, but there was no depression by apathy interaction i. These findings suggest that apathy in Alzheimer’s disease should not be considered as a symptom of severe depression only. We next examined whether apathy at baseline may predict more severe depression at follow-up.

We found a significantly greater increase in depression scores during the follow-up period for patients with apathy as compared to those without apathy, suggesting that apathy is a significant predictor of depression in AD.

Finally, we also found that patients with apathy at baseline or those that developed apathy during the follow-up period had a faster cognitive and functional decline than patients with no apathy at baseline or at follow-up.

In conclusion, apathy in Alzheimer’s disease is associated with older age, more severe deficits in activities of daily living, and a faster progression of cognitive and functional impairments. In cross-sectional studies apathy was found to be significantly associated with depression, whereas in longitudinal studies apathy was found to be a significant predictor of more severe depression.

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Starkstein Apathy Scale (SAS)

Mechanism of apathy in AD The current view on the mechanism of apathy in neurological disorders is mostly mechanistic: In a recent review, Habib summarized the main clinical features of apathy which he termed “athymormia” after brain damage, and stressed the over-representation of basal ganglia lesions among these patients. Recent studies emphasized the potential importance of parallel and segregated cortico-subcortical loops originating from and terminating in the frontal lobes for the mechanism of neuropsychiatric disorders Cummings One of these circuits originates in the anterior cingulate cortex, connects with the ventral globus pallidus and the dorsomedial thalamus, and projects back to the anterior cingulate.

Habib speculated that this cingulate circuit may mediate “the process of converting motivation into action”, and that apathy may result from the bilateral disruption at different levels of this circuit or from lesions in limbic areas outside the striato-pallidal complex. This would explain why some patients with orbito-frontal lesions who mostly show disinhibited behaviours, also feature a concomitant loss of motivation.

Habib concluded that “athymormia” is the result of a striatal-limbic disconnection syndrome characterized by deficits converting past or present emotional experience into action. Habib’s proposal is certainly interesting and fits nicely with the current model of segregated basal ganglia-frontal lobe loops for the modulation of behaviour. However, Habib’s model partially rests on the dubious assumption that action is causally dependent on motivation. The problem with this hypothesis is how to avoid the Cartesian dilemma of psychological states motivation and past or present emotional experiences producing a physical state action.

They further suggested that apathy may result from the disruption of prefrontal cortex-basal ganglia circuits, considered to play a critical role in the generation and control of self-generated purposeful behaviour. They hypothesized that disruption of an “emotional-affective” process may produce apathy due to the inability to associate affective and emotional signals with overt behaviour; disruption of the “cognitive” process may result from impairments on cognitive functions that are “needed to elaborate the plan of actions”; whereas the “auto-activation deficit” may result from “difficulties in activating thoughts or initiating the motor program necessary to complete the behaviour”.

They suggest that apathy may result from a faulty elaboration of “plans of action” and from the disruption of “activating thoughts” in the initiation of motor programs, which are both psychological concepts.

Finally, whereas a strong association between apathy and cognitive impairments has been consistently demonstrated, it is uncertain whether apathy may result from deficits restricted to executive functions.

In conclusion, current theories explain apathy as the behavioural expression of the disruption of cognitive modules that deal with the organization of human action, drive and motivation. These modules are considered to engage independent frontal-subcortical circuits. Future studies are needed to clarify the association between apathy and lesions in specific brain areas, as well as the role of executive dysfunction in the mechanism of apathy. Treatment of apathy There are few randomized controlled trials of pharmacological or non-pharmacological treatments for apathy in AD.

Politis and coworkers Politis et al. The control treatment consisted on one-to-one meetings with an activity therapist. The authors found a significant improvement on apathy measures over the course of the study, but there were no significant differences between the treatment groups on any of the outcome measures.

Lee and coworkers Lee et al. However, the magnitude and temporal course of their therapeutic effect is still controversial Whyte et al. A recent double blind, placebo controlled study evaluated the effects of methylphenidate on diverse cognitive functions in a group of 24 patients who had moderate to severe head injuries Whyte et al. Finally, there is some empirical evidence that cholinesterase inhibitors such as donepezil may improve cognitive functioning, motivation and general well being of patients with traumatic brain injury Arciniegas et al.

In a study that included men with Parkinson’s disease Ready and coworkers Ready et al. The authors suggested that testosterone replacement therapy may constitute a helpful treatment of apathy for these patients. Several treatment studies suggested that anticholinesterase compounds may improve apathy among patients with dementia.

In a recent study, Cummings and coworkers Cummings et al. After 26 weeks of treatment there was a significant improvement of apathy, as measured with the Neuropsychiatric Inventory. It is important to stress that the effect of rivastigmine was not specific for apathy, since improvements were also noticed on other neuropsychiatric disturbances. Furthermore, changes on the Starksteib Inventory were rather small and may not have been clinically relevant.