During the eighteenth and nineteenth centuries, disorders of motivation represented the theoretical foundation for most psychiatric classifications. The Swiss psychiatrist André Matthey wrote in 1816 that psychiatric illness was a manifestation of “perversions of the will and the natural inclinations without obvious impairment of the intellectual functions.” Matthey distinguished between a behavioral disturbance caused by a physical etiology (délire) and a behavioral disorder produced by a disturbance of the individual’s free will (fureur sans délire). According to Matthey’s nosology, behaviors such as kleptomania, ennui, melancholia, and tigridoanie (an irresistible urge to spill blood) were all considered “disorders of the will.” Matthey’s seminal writings became the foundation for the development of nineteenth-century neuropsychiatry and a clinical approach that placed disorders of will as the primary derangement in pathologic behaviors.

The German neuropsychiatrist Heinroth (1818) rejected earlier explanations for mental illness such as “bile or worms or a hundred other irritations” and suggested, “there are many involuntary movements, but not a single involuntary action, for action cannot be imagined without willing.” Heinroth went on to write that pathologic behaviors occurred when “the will separates itself from reason and is no longer determined by feeling or intellect.” By distinguishing intellect from
emotion and motivation, Heinroth laid the foundation for the triad approach of Mood, Cognition, and Conation that became the basis for psychiatric classification for the most part of the nineteenth century. The term abulia appeared in psychiatric literature as early as 1847 and was defined in medical dictionaries as “absence of will, a type of insanity in which this symptom is dominant.” Ribot described abulia as a “pure disease of will” in which the individual’s ability to act was abolished and he or she was reduced to an individual of “pure intellect.” Although most neuropsychiatrists at the end of the nineteenth century agreed on the concept of abulia, there was considerable disagreement on whether the disorder was caused by a deficit in cognition or was a consequence of a dysfunction in a specific motivational system within the brain.

By the beginning of the twentieth century, abulia had become a household word and parents were even urged to “combat the evil of abulia amongst students.” Despite this, the neuropsychiatric concept of disorders of will fell quickly into decline and by the end of World War I they had essentially disappeared from psychiatric nosology. The reasons for this shift include (i) the rise of behaviorism that posited a simple reflex response that did not require an intervening variable; (ii) psychiatry’s preoccupation with psychoanalysis and its emphasis of psychodynamic predeterminism; (iii) the burgeoning field of neurology with its emphasis on somatosensory disorders; (iv) the emergence of postmodernism and its emphasis on individuality and self-determinism (v) the reassignment of disorders of free will to diagnostic concepts such as “negative symptoms” and “executive cognition.”

A universal definition of the term motivation remains elusive. This single issue represents the most important barrier to our scientific attempts to understand the neural basis of goal-directed behavior and clinical disorders of motivation.

From a theoretical perspective, motivation is the heuristic construct that describes the amalgam of forces acting within an organism to initiate and direct behavior. Motivation serves to influence the activation, persistence, and direction of an organism’s behavioral response across different levels of behavioral complexity.

From a neuropsychiatric perspective, motivation describes the neurologically mediated variables that energize and direct an individual’s response to the environment. These variables include the following:

This approach provides a simple framework for assessing the character and etiology of behaviors that are characterized by a decrease in the expected response to a particular stimulus. It also provides a heuristic framework that is inclusive of and consistent with each of the different approaches to motivation described in the preceding text and does not fall prey to Cartesian models that attempt to separate mind-driven behaviors (i.e., free will) from homeostatic drive theories and instinctual reflex behavior patterns.

Apathy may be either a symptom or a syndrome. As a syndrome, Marin has proposed Diagnostic and Statistical Manual of Mental Disorders (DSM)-like criteria (see subsequent text). Although not yet formally accepted, these criteria do provide the framework for the clinical assessment of apathy.

As per Marin’s proposed criteria, apathy is defined as “A lack of motivation, relative to the patient’s previous level of functioning or the standards of his/her age and culture as evidenced by all three of the following”:

Apathy and the Diagnostic and Statistical Manual of Mental Disorders text revision (DSM-IV-TR)—The DSM glossary does not include the term apathy, but related symptoms such as indifference, emotional unresponsiveness, lack of symptoms, and lack of concern are included in the diagnostic criteria and symptoms of several disorders. Further examples of related symptoms in DSM-IV-TR include the following:

Apathy is explicitly included as a diagnostic criterion in only the following four disorders:

No data are currently available on apathy as a primary disorder. However, a considerable amount of research indicates that apathy is perhaps the most common behavioral syndrome associated with neurologic disease. A recent analysis of prevalence data revealed that neurologic diseases involving the cerebral cortex are associated with a point prevalence of apathy of approximately 60%, whereas disorders primarily involving subcortical structures are associated with a 40% prevalence of apathy.

Several studies have reported significant morbidity associated with the presence of apathy. Four studies in patients with Alzheimer dementia that utilized standardized assessment tools for the diagnosis of apathy, have reported an association between the presence of apathy and diminished performance on activities of daily living (independent of the presence of depression). Patients who are apathetic following a stroke have been reported to be more functionally impaired, with the comorbidity of apathy and depression having the greatest impact on functional capacity. A study of geriatric patients admitted to a nursing home found apathy to be an important predictor of functional capacity at discharge, independent of admission diagnosis.

Apathy appears to be associated with more rapid cognitive and functional decline in patients with AD. Apathy has also been reported to be an important predictor of poor prognosis in patients with major depressive disorders.