Apathy and depressed mood in acquired brain 
damage: relationship to lesion localization and 
psychophysiological reactivity

Andersson, Stein; Krogstad, J. M.; Finset, Arnstein

doi:10.1017/s0033291798008046

Cited by 206 publications

(147 citation statements)

References 49 publications

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“…Finally, a functional study has reported a relationship between apathy and hypoperfusion of both frontal lobes after stroke [29]. Interestingly, Andersson et al [5] reported that Apathy Evaluation Scale (AES) mean score was higher in right damaged patients, but that only in left damaged patients it was correlated to the severity of depressive symptoms.…”

Section: Psychiatric Historymentioning

confidence: 99%

See 1 more Smart Citation

Post-Stroke Depression: Main Phenomenological Clusters and their Relationships with Clinical Measures

Quaranta

Marra

Gainotti

2012

Behavioural Neurology

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Abstract. Objectives:To investigate the principal psychopathological dimensions of post-stroke depression (PSD) through the assessment of the factorial structure of the Post-Stroke Depression Rating Scale (PSDRS). Methods: We enrolled ninety-eight subjects with PSD, who underwent the PSDRS, MMSE and Barthel Index. Information about demographic, clinical, and neuroanatomical factors was collected.Results: The factor analysis extracted three factors accounting for 63.4% of the total variance, and identified as: 1) "Depressive and Anxious Symptoms" (DAS); 2) "Lack of Emotional Control" (LEC); 3) "Reduced Motivation" (RM). On multivariate statistics, DAS severity was predicted by previous history of mood disorders and Barthel Index; LEC severity was predicted by Barthel Index; RM severity was predicted by age. Conclusions: The PSDRS displayed a reliable factor structure that agreed with previous interpretation of PSD. In particular, core depressive symptoms seem to be related to premorbid personality and functional status, whereas apathy/anhedonia may be connected to brain aging.

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Section: Psychiatric Historymentioning

confidence: 99%

“…The association between older age and apathy has been generally interpreted as the expression of the physiological involution of dopaminergic circuitry in normal aging [5,26], or as a "consequence of response to uncontrollable stress and problems associated with ascending age" [5].…”

Section: Psychiatric Historymentioning

confidence: 99%

Post-Stroke Depression: Main Phenomenological Clusters and their Relationships with Clinical Measures

Quaranta

Marra

Gainotti

2012

Behavioural Neurology

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“…Kant et al (69) found that it occurred (mixed with depression) in 60% of their sample. Andersson et al (70) found that almost half of their individuals with TBI had significant degrees of apathy. Deficits in motivated behavior can occur in association with injury to the circuitry of "reward" (68,71).…”

Section: Changes In Personalitymentioning

confidence: 99%

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

2008

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Traumatic brain injury (TBI) is a universal public health problem. A recent review of epidemiological studies in Europe suggests an incidence of 235 hospitalized cases (including fatalities) per 100,000 population (1). In the US, the incidence is estimated at 150 per 100,000 population (2). Less data is available from other regions of the world, but TBI is acknowledged as a significant problem worldwide. Of note is that the incidence rates are calculated from hospitalized cases only, and do not include injured individuals who do not seek or have access to care. Thus, the actual incidence of injury is probably 3 to 4 fold larger than the quoted numbers. Most studies suggest that the incidence rates for TBI are greatest in the second and third decades of life, with a secondary increase in the elderly stemming from falls (2,3). Males are more likely to suffer a TBI than females (2,3).In developed countries, there has been a reduction in the mortality rates associated with TBI over the last several decades, generally attributed to improved systems of trauma care and improved motor vehicle safety design. Many individuals with mild traumatic brain injury and virtually all individuals who survive moderate and severe TBI are left with significant long-term neurobehavioral sequelae (4-6). Thus, the reduction in TBI-associated mortality rates (7) has led to a significant increase in the number of individuals with long-term neurobehavioral disorders related to TBI (8,9).Brain trauma can be caused in a number of ways, including mechanisms which penetrate the substance of the brain (e.g., projectiles) and those that do not. This paper focuses on non-penetrating injuries. Despite different contexts and instruments, the physics and biomechanics underlying damage to the brain from non-penetrating injuries have some common features. This results in certain brain regions being at greater risk for damage than others and allows for some general statements to be made about typical profiles of brain injury associated with trauma. The assessment and treatment of the neurobehavioral sequelae of TBI follow logically from an understanding of this injury profile. RELATIONSHIP OF PROFILE OF INJURY TO NEUROBEHAVIORAL SEQUELAEThere are two broad categories of forces that result in brain injury: contact (or impact) and inertial (acceleration or deceleration). Contact injuries result from the brain coming into contact with an object (which might include the skull, or some external object). Contact mechanisms often result in damage to scalp, skull, and brain surface (e.g., contusions, lacerations, hematomas) (10). Frequent sites of such injury are the anterior temporal poles, lateral and inferior temporal cortices, frontal poles, and orbital frontal cortices.Inertial injury results from rapid acceleration or deceleration of the brain that produces shear, tensile, and compression forces. These forces have maximum impact on axons and blood vessels, resulting in axonal injury, tissue tears, and intracerebral hematomas. These mechanisms also produc...

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“…however, apathy can occur without depression in Ad and when depression and apathy co-occur in Ad patients, it has been shown that they are clinically and anatomically independent [20][21][22] . Indeed, in order to discriminate apathy from depression, several scales have been designed to quantify apathy, which wisely exclude symptoms such as sadness and negative thoughts, typically observed in depressive syndromes 15,[23][24][25][26][27] .…”

mentioning

confidence: 99%

Neurobiology of apathy in Alzheimer's disease

Guimarães

Lévy²,

Teixeira

et al. 2008

Arq. Neuro-Psiquiatr.

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-Apathy is considered the most frequent neuropsychiatric disturbance in dementia and its outcome is generally deleterious. Apathy can be related to a dysfunction of the anatomical-system that supports the generation of voluntary actions, namely the prefrontal cortex and/or the prefrontal-subcortical circuits. In Alzheimer's disease, pathological and neuroimaging data indicate that apathy is likely due to a dysfunction of the medial prefrontal cortex. Accordingly, in this review article, we propose a pathophysiological model to explain apathetic behavior in Alzheimer's disease, combining data from neuroimaging, neuropathology and experimental research on the role of orbito-frontal cortex, anterior cingulate cortex, basal ganglia and dopamine in decision-making neurobiology.Key words: apathy, Alzheimer's disease, decision-making, orbito-frontal cortex, anterior cingulate cortex, basal ganglia, dopamine. Neurobiologia da apatia na doença de alzheimerResumo -Apatia é considerada a alteração neuropsiquiátrica mais freqüente nas demências e suas conseqüências são habitualmente deletérias. Apatia pode ser relacionada à disfunção do sistema anatômico responsável pela geração de ações voluntárias, conhecido com córtex pré-frontal e/ou circuitos pré-frontais-subcorticais. Na doença de Alzheimer, evidências neuropatológicas e de neuroimagem funcional indicam que a apatia é provavelmente decorrente da disfunção do córtex pré-frontal medial. Assim, neste artigo de revisão, apresentamos uma proposta de um modelo fisiopatológico para explicar o comportamento apático na doença de Alzheimer, combinando dados de neuropatologia, neuroimagem e experimentação animal sobre o papel do córtex órbito-frontal, cíngulo anterior, núcleos da base e dopamina na neurobiologia da tomada de decisão.PAlAvrAs-chAve: apatia, doença de Alzheimer, tomada de decisão, córtex órbito-frontal, córtex cingulado anterior, núcleos da base, dopamina.

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Apathy and depressed mood in acquired brain damage: relationship to lesion localization and psychophysiological reactivity

Cited by 206 publications

References 49 publications

Post-Stroke Depression: Main Phenomenological Clusters and their Relationships with Clinical Measures

Post-Stroke Depression: Main Phenomenological Clusters and their Relationships with Clinical Measures

Neurobehavioral sequelae of traumatic brain injury: evaluation and management

Neurobiology of apathy in Alzheimer's disease

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