To understand the concept of apathy – among the many definitions, the one proposed by Robert Marin conceptualizes it as a “loss of motivation not attributable to an impaired state of consciousness, cognitive impairment or emotional distress – it is necessary to find an agreement on the define what is meant by “motivation”.
Motivation could be defined as a guide to the behavior necessary to be able to implement a conduct aimed at achieving a purpose: being motivated to initiate an action can be considered the link between an idea and a behavior.
It may be strange, but apathetic individuals are not always lacking in motivation.
There are situations in which we even see very intense levels of motivation, even though we are unable to get moving. Clinicians are well acquainted with the expressions of many patients: “I wish so much… ..but I can’t”.
The motivational levels are adequate but unfortunately the steps to be taken necessary to reach an end are lacking. In many cases of apathy the process that should lead to the achievement of the goal stops immediately after the ideational phase.
The different degree of this fracture determines the different levels of severity of apathy (a diametrically opposite process we observe in the impulsivity in which thought and action appear fused).
A confusion that is often made by clinicians and non-clinicians concerns the association between apathy and depressive state . Apathy is not necessarily linked to a depressive disorder : many times apathetic subjects do not burst with happiness but neither are they particularly sad.
Certainly it is possible to observe apathetic traits in depressed subjects but in general they are accompanied by other elements: the absence of feeling pleasure in things often prevails ( anhedonia ) and the consequent sense of shame or guilt for this difficulty.
In apathetic subjects, sometimes a component of low empathy or low self-awareness prevails, making it difficult for them to experience feelings of guilt.
It is of fundamental importance to keep depressive disorders distinct from apathy pictures, not only from a conceptual point of view, as many antidepressant pharmacological treatments, which bring excellent results in the first case, can even make the latter worse.
Apathy would also see the involvement of neuroanatomical structures different from those involved in the depressive disorder : sometimes it derives from cerebral, traumatic or vascular lesions, which occur at the level of the frontal lobes or basal ganglia; at other times it can be the clinical sign of onset of a dementia picture that manifests itself even before the memory deficit or executive functions.
From a neurophysiological point of view, apathy could be the result of three different processes: a compromise in the connection between emotion and action; a cognitive inertia; a deficit of “self-activation”.
In other words, apathy can be the result of a compromise at any level of the process through which we formulate ideas, we articulate them to plan the achievement of a goal, we are able to attribute an emotional value to the goal to be achieved and, finally, we place ideas for behavioral implementation.
Let’s start with the compromise of the connection between emotion and action: from neuroimaging studies and brain lesions due to different causes, it is observed that the ventro-medial and orbitofrontal prefrontal cortex is a fundamental structure in associating emotions with the performance of a task.
This brain area is older, evolutionarily speaking, than other superficial and lateral cortical regions (such as the dorsal-lateral prefrontal areas); this is not surprising since the prefrontal cortex is anatomically located near the limbic areas (amygdala and hippocampus) that regulate appetitive drives.
In the situation defined as Cognitive Inertia, it is not the disconnection between emotion and action that generates the state of apati but rather the elaboration of the goal itself. Being able to formulate thoughts and articulate them in an articulated sequence that leads to the complete execution of a task is a high-order cognitive skill, recent from an evolutionary point of view.
A lesion at the level of the frontocortical regions or other parts connected to it in a circuit (such as the thalamus) can lead to great difficulties even in operations considered simple, such as dressing, precisely because of the difficulty in representing the cognitive sequence necessary for perform the given task correctly. These pictures can be observed following stroke or vascular or frontotemporal dementia.
Still different is the situation of an apathetic picture resulting from a Self Activation deficit. The stimuli that determine human conduct can derive from both the internal and external environment.
In subjects with focal lesions at the level of the basal nuclei, even though no motor function deficit is observed, a complete inability to perform any action can be observed: they can remain immobile in the same position or even not utter a word for long periods. This is considered the most severe form of apathy, called abulia.
Nevertheless, these subjects can respond correctly when requests are formulated or when they are guided in carrying out activities. It is believed that in these situations the inner capacity to formulate correct internal guidance to the task is lacking, something that does not happen when this comes from the outside.
The basal ganglia would be the structures responsible for adequately integrating, organizing and filtering the information coming from inside or outside. Focal lesions at the level of the basal ganglia – such as the pale globe or the thalamus – can lead to the arrival of a series of disorganized information to the prefrontal cortex that prevent the implementation of any conduct in an autonomous way.
Neuroimaging studies in apathetic subjects with basal ganglia lesions reveal a marked reduction in the activity of the prefrontal cortex, even if the latter is structurally intact. The neurotransmitter systems that would be compromised in the various forms of apathy primarily concern the dopaminergic pathways and it is precisely on dopamine-agonist drugs that research is focusing on improving apathy as a symptom.
Unfortunately, it still takes time to cure the underlying causes. So far we have talked about the forms of apathy derived from organic problems.
Different is the conceptualization of pictures in which apathetic aspects can derive from personality structures that can benefit from a cognitive behavioral intervention and for which we will dedicate a further study.
