Abulia is a pathological lack of will in a person. The word "Abulia" is of ancient Greek origin and consists of two particles a - the universal negative particle, and boulia - will.
The patient becomes extremely passive and uninitiative. All this happens due to lack of will. But what is will and what is its role in our lives?
Will is a very important mental function. Without it, we turn into passive, as they say, plants that cannot satisfy even their basic needs. It is an independent component of mental activity, and the most important component in the structure of the psyche for the implementation of many mental processes (memory, attention, thinking, motor activity). With the help of will, a person can control his behavior, take purposeful actions, satisfy his needs and move towards goals.
The first function of the will is incentive. With its help, we can take action, move towards a goal, provide for our needs and overcome obstacles that arise along the way. The incentive function manifests itself both in large-scale situations and in the most ordinary ones. The moment you get up from the couch to grab a bite to eat and the moment you spend years moving to the top of the career ladder - all this is an incentive function of the will.
But it is important to understand that not all human activity is dictated by will. For example, when a stone flies at you and you dodge it, this is not will, but a defensive reaction. This action of yours is determined by the situation that has arisen, and not by your will. The difference between volitional action is its arbitrariness and goal orientation.
The second function of the will is inhibitory. Its main task is to stop those desires and impulses that are undesirable for a person’s behavior in a particular situation. That is, with the help of volitional inhibition, a person can stop or prevent those of his actions that contradict his beliefs, worldview and upbringing. I.P. Pavlov believed that volitional inhibition requires more significant effort from a person than active action.
Signs of abulia
The main signs of abulia are lack of will. What happens to a person whose willpower is significantly reduced?
Abulia is a medical term for a painful state of lack of will in a person. He cannot perform even basic actions and does not find the strength to make a decision. Even if this decision is extremely necessary, and he realizes it.
A less pronounced condition, characterized by a decrease in desires, motives and volitional activity, is called hypobulia. Compared to abulia, in this case the will is not completely absent, but is only in a weakened state. Patients have difficulty choosing a goal and concentrating on it. They are lethargic, passive, indifferent and can also remain in one position for a long time, as with severe abulia.
It is important to note that abulia is not an independent disease. Experts always consider a painful lack of will as part of certain mental or neurological diseases.
These are neurological diseases such as organic brain lesions: tumor, traumatic brain injury and brain atrophy. In rare cases, this syndrome may occur in people who have had a stroke. Abulia can be caused by a lack of blood circulation to the brain, damage in the frontal lobe, anterior cingulate cortex or basal ganglia.
Abulia is observed in mental illnesses such as depression, schizophrenia, and atrophic processes in the brain.
There are also cases of congenital abulia with severe mental retardation, the so-called. apathetic oligophrenia.
Causes of lack of will
In severe manifestations, impaired will can be a symptom of various neurological and mental disorders: schizophrenia, depression, Parkinson's disease, head injury and other ailments. In this case, we can talk about abulia - lack of will, which has physiological causes. It is caused by brain problems that need to be treated. When diagnosing, it is imperative to exclude these factors. It is worth consulting a doctor if weak will has never been a feature of your personality, but has only begun to appear recently and is accompanied by other symptoms.[1]
But we will talk about weakness of will as a stable model of behavior. Modern psychology claims that, like many other behavioral disorders, it originates in childhood. If, as in the story of our hero, parents always made decisions for the child, then it is not surprising that in adulthood a person does not have such a skill - after all, there were simply no conditions for its formation. The person seems to continue to expect that they will still decide for him what to do, who to meet, and even what to cook for breakfast.
Sometimes lack of will develops as a reaction to a protracted crisis. For example, if a person found himself in a difficult financial situation, tried several times to correct it and failed each time. Unfortunately, the brain quickly learns that another attempt will lead to failure, which means it’s not worth trying. The result is apathy and passivity, which means almost zero chances of improving your life. This condition is called learned helplessness.[2]
There is also a point of view that the tendency to weak will or, conversely, to strong will depends on the body’s ability to absorb glucose. Scientists conducted experiments that showed that people whose glucose metabolism mechanism does not work well cope worse with intellectual work and are more prone to impulsive actions. And this mechanism is genetically embedded in a person, it is almost impossible to influence it. True, the ability to control your will can still be trained, it’s just that it will be more difficult for people who are not very lucky with their genes.[3]
Abulia with depression
Typically, as already mentioned, abulia is observed in depression, schizophrenia, dementia, and sometimes after a stroke.
Abulia, that is, a decrease and loss of impulses, is not only an element of a mental defect in schizophrenia, but no less expressively occurs during a period of depression. Here, abulia is reversible synchronously with the elimination of the depressive syndrome. With depression, abulia is much better understood by patients than with schizophrenia, and, moreover, it differs in that it is painfully experienced by patients, accompanied by complaints and a desire to get rid of it. Often, depressed patients, when describing their condition, put abulia first and say that they cannot bring themselves to do even the most basic things - get up, get dressed, cook something, wash, and everything else. Thus, the independent nature of this symptom, which is not at all an integral part of the apathetic defect, becomes clear. And the reversibility of abulia demonstrates that this disorder can, in principle, be corrected in patients with apato-abulia defect. In the self-esteem of depressed patients, the reversibility of abulia is usually perceived by them as an encouraging sign of upcoming recovery, which indeed reflects the parallelism of the severity of abulia and hypothymia (depressive affect or low mood).
Diagnostics
Detection of abulia is part of a comprehensive diagnosis of mental and neurological diseases. The examination is carried out by a neurologist, psychiatrist, psychologist. An important point is to distinguish a pathological syndrome from laziness, the consequences of improper upbringing. The set of diagnostic procedures includes:
- Conversation, inspection. A survey of the patient's relatives is carried out: anamnesis, complaints are clarified, and the duration and severity of symptoms are clarified. A conversation with a patient often turns out to be uninformative. The neurologist performs an examination: assesses the integrity of reflexes, motor skills, and sensitivity. Based on the data obtained, doctors make an assumption about the underlying disease and determine a list of further procedures.
- Observation. Direct detection of abulia symptoms occurs during the consultation and while the patient is in the hospital. There is a lack of interest in communicating with a doctor, medical personnel, passivity, slowness, and refusal to perform daily rituals.
- Instrumental examination. Prescribed to confirm the diagnosis and differentiate neurological pathologies. Common examination methods are computed tomography and magnetic resonance imaging of the brain. Abulia is characterized by the presence of pathological signs in the prefrontal zone.
- Psychodiagnostics. A clinical psychologist conducts research on the cognitive and emotional-personal spheres. In most cases, a full diagnosis is impossible (the volitional component of activity is impaired). Separate tests are performed for thinking, memory and emotional state, which make it possible to distinguish between schizophrenia, depression, manic-depressive psychosis, and dementia.
The stage of the disorder in question can have varying degrees of severity - from mild to overwhelming. Most often, this condition is perceived as a pathology of volitional regulation of behavior. The difficulty of diagnosis is due to the fact that abulia is an intermediate state between different mental disorders.
As the most effective methods, it is customary to use MRI diagnostics to determine organic pathologies in the central nervous system, as well as clinical observation of the patient.
In such a situation, competent differential diagnosis is important, since banal laziness should not be ruled out, especially when it comes to treating a child. When a child refuses to put his toys in order at the behest of his parents, you should not immediately suspect a pathology.
The destruction of one's own toy world at the first request from adults is difficult for a child, so one can find a completely logical explanation for such behavior. It’s another matter when a child spends too long reading the same page in a book or even imitates reading. Solving the problem on your own can be problematic, so contacting a specialist is the best solution.
Abulia. Symptoms
What are the symptoms of abulia? Patients may be aware of their lack of initiative, passivity, lack of desires and motivation. In the early stages, abulia can be perceived as ordinary laziness. Therefore, this decrease in volition, as a symptom of the disease, must be diagnosed by a doctor.
Patients suffering from abulia do not experience any urges. They are partially or even completely weak-willed, have no motivation for action, are passive, and do not show initiative in activity. Their actions and thinking are essentially slowed down. If you ask a patient with abulia a question, he will answer it not immediately, but after some time. It gets to the point that a person in this condition cannot even eat, drink, take a shower or wash himself. Lack of will can develop to the point of inability and unwillingness to provide all one’s basic vital needs.
Abulia is classified according to its dynamics. It is this approach to classification that helps to better select the optimal treatment and give a prognosis for the development of the disease. Pathological lack of will is divided into short-term, periodic and permanent.
With short-term abulia, the patient retains the will and awareness of actions, but it is difficult for him to do something. It is diagnosed with asthenic syndrome, neurotic disorders and adynamic depression.
Periodic abulia is observed in depression and depressive-delusional symptoms in schizophrenia.
With constant abulia , as the name implies, lack of will accompanies the patient constantly, and it is difficult to treat. Persistent abulia occurs with increasing schizophrenic apatho-abulic defect, traumatic brain injury and atrophic processes in the brain.
Diagnosis of abulia is carried out by a psychiatrist. For diagnosis, observation of the patient and his behavior is necessary. Collecting information can take a long time, from several days or more. To clarify the diagnosis, computed tomography (CT) and magnetic resonance imaging (MRI) are also performed. Using these methods, organic brain lesions can be detected.
The syndrome and symptom of apathy are of great interest to psychiatrists and neurologists, since, as a model of interdisciplinary research, they also affect the field of gerontology.
In the literature, the term “apathy” is used to describe various conditions. Thus, it can be a special personal characteristic, manifested in low social and professional activity and be an important characteristic of normal development and aging [1, 2], a clinical variant of depression [3, 4], a specific negative disorder in schizophrenia [5, 6], component of the clinical picture of somatic and neurological diseases (AIDS, Lyme disease, endocrine disorders, Pick's disease, Alzheimer's disease (AD), various dementias, etc.), part of neuroleptic-induced akinesia [7], a consequence of long-term treatment with SSRIs - “SSRI-induced indifference "[8-11]. It forms the basis of the psychopathological concept of “beautiful indifference” (la belle indifference) [12]. Apathy can be observed under certain conditions and in healthy people [13].
Below is a summary of neurological, mental and somatic diseases in which apathy can develop.
The first difficulty that arises in assessing apathy is the question of the term used to designate the disorder in question. Like any complex mental phenomenon, apathy does not have a single canonical definition, which leads to a variety of approaches to its interpretation.
For many psychiatrists, apathy is a symptom that involves diminished interests and emotions. It is usually considered a sign of depression or a nonspecific symptom of other diseases. This definition is given in many psychiatric dictionaries [14] and in the works of some authors [15]. When considering apathy in this way, its most characteristic features are lack of interests, feelings, indifference, flattening of affect and emotional insensitivity.
However, the absence of emotions or interests, according to R. Marin (1996) [16], does not fully correspond to its definition. Firstly, considering apathy in this understanding is not entirely correct, since emotions and interest, although related, are different concepts. Secondly, the term “apathy” is often used to describe patients whose condition differs significantly from this definition. Thus, if in schizophrenia the concept of apathy is applicable to patients with negative symptoms, for whom a lack of emotions and interests is a characteristic feature, then patients with depression may report a lack of interests, but at the same time show strong negative emotions (which cannot be regarded as their complete absence) or, conversely, be characterized by flattened emotional reactions, but retain interests and hobbies.
According to R. Marin [16], the emphasis in understanding apathy should be placed on a decrease in goal-directed behavior, which moves this term into the area of motivation-related psychological functioning of a person. In this understanding, the term “apathy” represents an inversion of motivation, and in a clinical sense, a lack of motivation. At the same time, motivation includes not only issues of conscious and intentional mental act, but also unconscious psychological and biological processes responsible for goal-directed behavior. Lack of initiative, ambition or persistence, despite intact intelligence and physical capabilities, and decreased responsiveness to rewards or incentives are some of the main psychological characteristics that suggest impaired motivation. Given the central role of motivation in human behavior, diagnosing a patient as apathetic implies clinical deterioration at the level of dysfunction of many body systems, which is fundamental to adaptation processes [17].
Apathy is a common symptom of depression, which, along with anhedonia and motor retardation, is reflected in multivariate analytical studies [18, 19]. Apathy is often present in cases of depression in adolescence [20], anaclitic depression in children [21], depressive disorders of the involutionary period, as well as in elderly people [22-24], whose depression, as a rule, does not meet the criteria for major depressive disorder [25] and are considered subsyndromal depression or subdepressive disorders.
The range of opinions regarding the psychopathological structure, typology, and nosological affiliation of apathetic depression is extremely wide. Some authors [26-29] consider apathy as one of the main variants of depressive affect, the clinical picture of which is dominated by a lack of motivation with a drop in vitality, and the remaining activity partly masks the emerging “flaw” (outwardly, the lifestyle and nature of activity do not change significantly, but at the same time, all actions seem to lose their inner meaning, they are performed out of necessity, “out of habit,” “automatically”). Other researchers [30] point to apathy as “the initial, basic manifestation of endogenous depression” or the main personality trait of patients with depression [31]. Still others [32] focus on “motivational oppression” within the framework of a melancholy-apathetic decline in mood. S.Yu. Tsirkin [15] classifies apathy as a disorder of emotions, considering it a modification of anhedonia and sadness. The decrease in motivation is explained by the inability to anticipate the fruits of one’s activities, i.e. anhedonia. A.B. Smulevich [33], within the framework of the psychopathological model of depression, based on the correlation of psychopathological formations belonging to two categories that are polar in clinical significance, considers apathy as a symptom related to the negative spectrum of affective pathology with alienation phenomena.
Apathetic depression is assessed [34, 35] as one of the components of the structure of complex depression with various outcomes, or is considered [36-39] as unfavorable protracted forms of depression.
Since the 90s of the last century, much attention has been paid in the literature on psychiatry to apathy as an independent clinical disorder that can occur in many diseases of the central nervous system: stroke, PD, progressive paralysis, Huntington’s disease, AD, vascular and frontotemporal dementia [40 ]. It has been noted [41, 42] that dysfunction in the frontal-subcortical pathways, especially those connecting the ventromedial prefrontal cortex with the basal ganglia, plays a leading role in their pathogenesis.
The first definition of apathy as a syndrome occurring in various mental and neurological disorders was given by R. Marin [23, 43]. According to his definition, apathy is a syndrome of loss of motivation, i.e. initiatives not associated with emotional or cognitive impairment or decreased level of consciousness. To diagnose it, conditions such as abulia, akinesia and akinetic mutism, depression, dementia, and delirium must be excluded. The main signs of apathy, according to R. Marin, are 1) loss or weakening of motivation; 2) absence or weakening of spontaneous goal-directed activity” (lack of initiative, effort, persistence and productivity); 3) loss or weakening of purposeful cognitive activity” (lack of independent ideas, interest in news, events in the lives of friends or loved ones, one’s condition, financial problems); 4) loss or weakening of emotional reactions to positive and negative stimuli, dulling of affect, emotional indifference. R. Marin [16] identified several subtypes of the syndrome: cognitive, motor, sensory and affective. In his opinion, they are determined by various pathogenetic mechanisms. The author identified three directions for further research on apathy: 1) studying the patient’s behavior with the absence or decrease in its focus; 2) assessing the reduction in the level of emotional reactivity and emotional experiences; 3) assessment of cognitive functioning associated with the process of goal setting (lack of plans for the future, inability to form and put forward goals in any activity).
In contrast to the considered definition of apathy syndrome by D. Stuss et al. [44] paid attention to a decrease in spontaneous behavior (absence of a self-initiated reaction). R. Levy and B. Dubois [45] believed that apathy syndrome is not just a “decreased motivation,” which, in their opinion, is a subjectively interpreted, vague psychological concept. Studying the mechanisms of apathy, these authors identified three pathogenetic processes underlying its development: 1) “emotional-affective” (associated with a disruption of the relationship between emotional-affective signals and ongoing or upcoming behavior caused by damage in the midfrontal prefrontal cortex and associated with its areas - the limbic system within the basal ganglia); 2) “cognitive” (in which there are difficulties in developing a plan for current or upcoming actions), possibly due to disturbances in the dorsolateral prefrontal cortex and associated areas of the basal ganglia (“associative territory”); 3) “decreased self-activation” (an inability to “self-activate” thoughts or actions is noted, with a relatively intact ability to respond to motivating stimuli from the outside). This most severe variant, caused by lesions in the two areas of the brain mentioned above, was called “mental akinesia” by the authors.
In 2009, a special group of scientists was created in France [46] to develop diagnostic criteria for apathy syndrome that should be widely used in clinical practice. Based on the results of her work, apathy was defined as a decrease in motivation that persists for a long time and meets the following requirements: 1) the basic symptom (decreased motivation) must be present for at least 4 weeks; 2) two of the other three symptoms of apathy must be present—decreased goal-directed cognitive activity, decreased goal-directed behavior, and decreased emotional responsiveness; 3) identifiable functional impairment must be recorded. To facilitate the identification of apathy, it has been proposed to use a special scale, the Apathy Evaluation Scale (AES).
The identification of apathy syndrome led to the emergence of a large number of epidemiological studies aimed at studying its prevalence in various diseases. Thus, S. Starkstein et al. [47] examined 164 patients with PD. 52 (32%) of them met diagnostic criteria for apathy, 83% of patients with apathy had concomitant depression, and 56% had dementia. Only 5% of patients had apathy without concomitant depression or dementia. Similar results were obtained by other authors [48]: of 232 people with PD, 38% had apathy, 11% had it combined with depression and dementia, 10% had depression only, 6.5% had dementia only, and in 9% it was without depression or dementia. We also examined 175 patients with a newly diagnosed PD and 165 without it (controls). Apathy was diagnosed using the NPI (Neuropsychiatric Inventory) scale. The results of this study showed that of 22.9% of patients with PD, 37.5% had clear depressive symptoms. In the control group, not a single case of apathy was identified.
As a result of a 4-year follow-up [49] of 79 patients with PD, 29 showed no symptoms of apathy, 11 had apathy constantly, and 39 developed it during the observation period.
The connection between apathy and AD was established many years ago [50]. It was later found [2, 51-53] that its prevalence in this disease is high and amounts to 29-88%. One such study examined 150 patients with AD and found that 20% had disorders that met criteria for both apathy and depression, 7% had apathy only, and 31% had depression only. At the same time, apathy did not have a significant effect on the severity of depressive disorder, but was associated with more severe cognitive impairment [53]. In another study [54], in a study of 734 patients with AD, the prevalence of depression was 47.9% of cases, apathy - 41.6%, comorbidity of depression and apathy - 32.4%.
In vascular dementia, apathy syndrome was identified in 41% of cases [55]. S. Starkstein et al. [56], using a shortened version of the AES, found that 11% of patients with acute cerebrovascular accident had apathy, 11% had major depression with severe apathy, and 23% had depression only without apathy. Summary data on the prevalence of apathy are presented in Table. 1
.
It is currently believed [13] that neurological diseases of any etiology, the focal symptoms of which are associated with damage to the frontal lobes of the brain, lead to changes in personality and behavior associated with a lack of motivation, which can be designated as apathetic syndrome [13]. Multiple sclerosis, Pick's disease, other non-Alzheimer's type frontal dementias, frontal tumors, strokes and hydrocephalus, etc. are examples of pathological processes leading to the development of frontal syndrome [90]. Lack of initiative and persistence, decreased interaction with the social environment and lack of empathy, which are clinical manifestations of damage to the frontal lobes, contribute to the development of apathy syndrome. According to J. Campbell et al. [91] and M. Mega et al. [92], three subtypes of frontal syndromes are associated with apathy. Mesencephalic-frontal damage and destruction of the cingulate gyrus lead to the apathy syndrome itself. In dorsolateral frontal lesions, apathy is associated with impairment of executive cognitive abilities needed to plan and control goal-directed behavior. Patients with damage to the lateral orbitofrontal cortex experience personality changes (irritability, angry outbursts, or sexual disinhibition) that occur “against a background of abulia or apathy” [93]. The “indifference reaction” occurs in approximately 25% of patients with right hemisphere stroke [94, 95] and approximately 10% with left hemisphere stroke [94].
Being associated with a decrease in the functional activity of patients, apathy is of great importance for their adaptive behavior [96, 97], affecting the effectiveness of treatment of the underlying disease, aggravation of the condition and difficulty in caring for patients [98]. Apathy can accelerate the development of cognitive impairment in neurodegenerative diseases, worsen the quality of life, reduce patients’ awareness of their condition and motivation for treatment [53, 97, 99-101]. In the works of K. Pedersen et al. [48, 49] confirmed the association of apathy with more severe depressive symptoms and more severe motor symptoms in PD.
Despite the similar understanding of apathy by various researchers, there is still no unified approach to defining the corresponding term that would be acceptable for psychiatric and neurological practice. In DSM-IV [100], apathy is not included in the glossary at all and is mentioned only as a symptom that occurs in various disorders. Many authors [47, 102, 103] point out the insufficiency of diagnostic criteria for apathy and the need to create additional diagnostic scales.
From the point of view of clinical practice, it is significant that apathy syndrome and depression (including apathetic) often accompany each other, have similar manifestations [96] and therefore their differential diagnosis is required. This is especially true for elderly patients, in whom depression and apathy are variables that correlate with each other [22-24, 104]. Some studies have shown that apathy is associated with a high score on the depression scale [79, 88, 89, 105-107], while it is noted [25] that apathy syndrome is most often observed in the structure of subsyndromal depression, and some symptoms (decreased interests , psychomotor retardation, lack of energy) is common to these conditions. The accuracy of diagnosis of such subsyndromal depressions and their differentiation from apathetic syndrome are important for determining therapeutic tactics.
The work of O.S. is devoted to the issues of differential diagnosis of depression and apathy. Levin [108], in which the difference between apathy as an independent syndrome and depression is seen in the absence of melancholy and anxious affect in the first disorder. Differential diagnosis of depression and apathy according to O.S. Levin is presented in table. 2
.
S. Ishii et al. [100] provide slightly different differential diagnostic criteria for the syndrome of apathy and depression, highlighting their features and common features (Table 3)
.
The authors include a blunted emotional response, indifference, low social activity, decreased motivation and inertia as symptoms characteristic only of apathy.
For depression, differential diagnostic criteria are dysphoria, suicidal and pessimistic thoughts, feelings of guilt, and feelings of hopelessness. The most used differential zone in diagnosing either apathy or depression is the assessment of the patient's emotionality and his thinking.
J. Ishizaki et al. [40] consider depression to be a “disorder of emotion,” while apathy is a “disorder of impulse.” Patients with apathy show weakened emotional reactions in response to both positive and negative stimuli, while patients with depression react selectively to negative stimuli. A similar situation is observed in the area of thinking: patients with depression are characterized by negative thoughts about the past, present and future [109], while with apathy there is a lack of such concern and a general decrease in interests. A decrease in interests in patients with depression is associated with a pessimistic assessment of their capabilities and the expectation of failure; in patients with apathy, on the contrary, the importance of the goals themselves is devalued. Patients with apathy rarely come to the doctor with complaints about their well-being; rather, this will worry those caring for such patients [16], while for patients with depression, their condition is subjectively intolerable, for which they usually seek help.
Some modern instrumental techniques such as positron emission tomography (PET) have been used to differentiate apathy from depression. PET studies have shown that in patients with early onset AD, the appearance of apathy is associated with a significant decrease in glucose metabolism in the left fronto-orbital regions, while the occurrence of depression is due to hypometabolism in the prefrontal dorsolateral region [110]. It has been suggested [111] that affective apathy involves neural pathways involving the cingulate cortex, amygdala, while cognitive apathy is hypothesized to reflect pathways involving the lateral posterior frontal cortex, and finally motor apathy involves pathways involving the motor components of the “motivational pathway” ( pedunculopontine nucleus, nucleus accumbens shell) or motor areas in the striatum. This suggests that apathy as a symptom of depression and apathy as a syndrome are clinically and anatomically independent [45].
Differential diagnosis of apathy within neurological diseases from apathy associated with depression is essential for the choice of therapeutic tactics. For example, antidepressants, especially those with a noradrenergic mechanism of action, may be effective for apathy that occurs as part of depression. At the same time, serotonin reuptake inhibitors have less effect, and in elderly patients, according to J. Ishizaki et al. [40], may even aggravate the manifestations of apathy.
When treating apathetic syndrome, it is important to select etiologically and pathogenetically substantiated treatment [40]. Several therapeutic strategies are being considered for this purpose. Prescription of antidepressants from the group of dopamine reuptake blockers (for example, sertraline and bupropion) leads to a reduction in vegetative symptoms and depressed mood, but the apathetic syndrome in the form of lack of interest, anergy, reduced emotional reactivity and initiative remains intact. In such cases, it is advisable to prescribe psychostimulants (methylphenidate or amphetamines) [112-114], dopaminergic agents and cholinesterase inhibitors [41, 91, 115]. This has been confirmed in a number of studies. Thus, in a randomized placebo-controlled trial [116] of methylphenidate for apathy syndrome in asthma, a marked improvement on the apathy scale was observed in 17 out of 57 patients. In another similar study [117], improvement was observed in 40% of patients. The effect of piribedil (a dopamine receptor stimulant) was studied in a placebo-controlled study [118] in 37 patients with AD. After 12 weeks of treatment, the total apathy score decreased by 34.6% in the piribedil group and by 3.2% in the placebo group. Described [119-121] are cases of marked improvement in the condition of patients after the use of ropinirole (D2/3 receptor agonist) in a patient with severe apathy after a stroke and selegeline in patients with apathy after severe traumatic brain injury. There is [98, 122] convincing evidence of the effectiveness of acetylcholinesterase inhibitors for apathy in AD and PD. Thus, rivastigmine in patients with severe and moderate apathy in PD and donepezil prescribed for asthma were superior in effectiveness to placebo [123, 124]. Another drug that has been proposed for the treatment of apathy is memantine, but it was not superior to placebo in a placebo-controlled study [125].
Regarding the effectiveness of non-pharmacological strategies for apathy syndrome, data are rather scattered. A. Lane-Brown et al. [126], having summarized the relevant data, concluded that in these cases it is preferable to use cognitive techniques that were most effective in patients with moderate cognitive impairment. In patients with severe dementia, good results have been reported with music therapy [127]. Multisensory stimulation has a certain effect in patients with apathy in the late stage of dementia [128].
Thus, research interest in the problem of apathy has increased significantly over the past decades, which is associated with significant progress in understanding some of the physiological mechanisms of the development of this clinical phenomenon, in particular in the aspect of frontal-subcortical dysfunction. Consensus in the definition of apathy and standardization of its diagnostic criteria are essential, promoting homogeneity in the conduct of relevant research, and differential diagnosis with apathetic depression is the key to choosing adequate therapeutic strategies. Treatment of apathy requires the development of interdisciplinary approaches based on an understanding of its biomedical (including neuroanatomical, psychophysiological), clinical and psychological aspects. The lack of clinical guidelines for patients with apathy may be explained by the lack of large, placebo-controlled clinical trials of potentially beneficial pharmacological and psychological interventions. Identification of modifiable factors in the development of apathy can lead to the development of effective preventive programs to prevent it.
Apato-abulic syndrome
Patients with apatico-abulic or apatico-abulic syndrome (defect) are characterized not only by abulia, but also by emotional emasculation. In the affective sphere, this is emotional impoverishment, indifference, including coldness towards loved ones, their problems or achievements. These changes that occur in a patient with schizophrenia increase gradually. The final stage of the apato-abulic defect in patients with schizophrenia, as already mentioned, is a constant stay in bed, when they are unable to provide for their vital needs and do not monitor hygiene. They may not wash, not get a haircut, and sleep in bed in outerwear. In extreme cases, they even defecate on themselves. There is no way to attract such patients to activity, because they lose not only their will, but also their desires. They speak little, or their speech is monotonous and unemotional. Interacting with other people is not at all interesting for them; they refuse to communicate under the pretext of fatigue.
There are various characteristic combinations of abulia with other disorders. For example, if a person experiences immobility with abulia, this condition is called abulic-akinetic syndrome, which may be a possible sign of a pathological process of frontal callous localization. In the case of apathy (indifference, decreased emotional reactions) with abulia, this is apathetic-abulia syndrome, which is the main variant of the schizophrenic defect.
Methods of treatment and correction of the syndrome
Apathetic-abulic syndrome is a disorder, when the first signs appear, you should immediately seek medical help. Otherwise, the patient’s mental state will first worsen, and then health problems will appear (due to poor nutrition, lack of mobility, etc.).
First, a specialist must conduct a full diagnosis and identify possible mental disorders that caused the rapid development of AAS. Most often, based on research results, complex therapeutic measures are prescribed that are aimed at mitigating the manifestations of the syndrome.
Diagnosis and treatment are carried out by a psychiatrist, physiotherapist and neurologist. Sometimes additional help from a speech therapist, psychologist or exercise therapy instructor is required. This is due to the fact that the patient will need to undergo rehabilitation if the cause of the development of AAS is a brain tumor, stroke, or injury.
The main diagnostic problem is related to the fact that the syndrome occurs without complaints from the patient. Due to the development of AAS, he is not able to independently determine the presence of abnormalities, since his condition does not bother him at all. Therefore, most often it is relatives who turn to specialists.
In most cases, a visit to a doctor takes place only after relatives almost forcefully bring the person to a medical facility or call an ambulance. Only after persistent questioning of the doctor can we achieve at least some results and obtain preliminary data on the patient’s condition.
For a more detailed diagnosis, an MRI or CT scan is required. Thanks to ultrasound methods, it is much easier to identify previous injuries or diseases that could trigger AAS. Additionally, neurological tests are performed and a laboratory blood test is done.
It is important to eliminate the negative consequences and achieve complete recovery of not only mental but also physical condition. If patients show serious signs of deep depression, then antipsychotics and antidepressants (prescribed strictly by a doctor) cannot be avoided.
Most often, the specialist prescribes:
- Penfluridol. A long-acting antipsychotic, which is explained by the slow metabolism of the drug. The effect after a single dose of the drug can last up to 1 week. Available in tablet form, sold in pharmacies only with a doctor's prescription.
- Frenolone. Prescribed for psychomotor retardation due to the development of schizophrenia. Available in the form of dragees or solution for injection. The drug is contraindicated for kidney or liver diseases. The product must be taken twice a day. The course of treatment is prescribed by a doctor.
- Triftazin. An antipsychotic is prescribed for various mental illnesses and psychomotor overexcitation. Helps cope with frequent neuroses and panic attacks. The drug must be taken twice a day. The course of treatment usually does not exceed 2-3 weeks. If you are depressed, Triftazin should not be taken.
Exercises in which the patient’s relatives and friends participate are highly effective. First, the specialist conducts a conversation with them and explains how they should react to the patient’s behavior. Their task is to eliminate as much as possible the likelihood of a conflict situation.
Various psychotherapeutic methods have found wide application in the treatment of this syndrome. Since it is necessary to correct a person’s correct behavioral model, group or individual sessions with a psychologist can be conducted.
In the case of a severe course of the disease, the patient actually has to relearn how to care for himself, restore communication skills and the ability to cope with everyday tasks.
To restore mental balance, it is recommended to take therapeutic relaxing baths and undergo a course of restorative massage. Visits to the pool are also highly effective. If there are appropriate conditions and the patient is not dangerous to others, then such classes are carried out with other patients.
An important step is the prevention of AAS, since otherwise there is a high risk that the syndrome will return.
To eliminate this possibility you need to:
- Give preference to an active life position. This should not be influenced by age or other factors and circumstances. To do this, you can perform special psychological exercises, do breathing exercises, and take relaxing baths.
- Take part in family activities. Moreover, it can affect both work skills and leisure.
- Perform daily duties. However, they must be monitored and assessed by other family members or the patient himself.
- Spot practice to train willpower as well as responsibility. Also, sporting events will allow you to keep yourself in good shape.
- Choose a creative hobby for yourself or just something that arouses interest and don’t give it up.
At the same time, the patient’s relatives should not show excessive care or, conversely, complete indifference. It is important that a person who has suffered from AAS is in a normal atmosphere and does not feel different from everyone else.
With timely treatment of apathetic-abulic syndrome and compliance with all recommendations, patients recover quite quickly. But it also depends on the stage of the syndrome. If the situation is advanced, it may take more time. Sometimes some behavioral functions are never restored.
Apato-abulic syndrome in schizophrenia
Apato-abulic syndrome most often occurs in schizophrenia. Patients who begin to develop these symptoms gradually, from mild passivity and indifference, reach complete emotional coldness and indifference.
Abulia is one of the main symptoms of schizophrenia. In such patients who suffer from this mental disorder for a long time, emotional decline occurs, the schizophrenic apatho-abulic defect increases, in which a weakening of the will and an increase in abulia are observed. The longer the schizophrenic process proceeds, the more passive the patient becomes, eventually ceasing to care for himself, monitor his diet and hygiene, spending most of his time in bed. Zharikov N.M. recalls this in the “Textbook of Psychiatry” for 2002. Sometimes in these patients with a pronounced apatho-abulic defect in schizophrenia, parabulia is observed - a perversion of the will, when basic physiological drives can be disinhibited, for example, excessive sexuality and gluttony are observed.
Combination of abulia with other syndromes
Forms of abulia can be mild and temporary, which are accompanied by minor deviations, reduced motivation, as well as more severe, up to complete suppression of will. In an extreme form of lack of will, there may be no desire to perform basic actions - get out of bed, wash, and so on.
Syndromes that accompany abulia:
- A syndrome of depressive and asthenic type, which is accompanied by elements of adynamia, neuroses, and psychopathic disorders. During this disorder, a short-term absence of volitional impulses and loss of activity occurs.
- Abulia of periodic type. This form often occurs in drug addicts, alcoholics, in patients with severe somatoform disorders, in patients with schizophrenia. Repeated periods of lack of will may occur, as well as psychoses of the manic-depressive type.
- Catatonic syndrome and stupor. This form is characteristic of schizophrenics, and also manifests itself in severe organic brain damage. In this condition, there is a constant lack of motivation and volitional impulses.
- Abulia can often be combined with mutism - a complete lack of desire to talk. Verbal contact with patients is disrupted, and it is impossible to get answers to questions from them.
- Apato-abulic syndrome. With this syndrome, emotional insufficiency and automaticity of movements occur. Patients experience complete withdrawal into themselves, they have a lack of desire to communicate, they show with their appearance complete indifference to the interlocutor, to close people, they have a complete loss of interest in their favorite activities and entertainment.
- Abulic-akinetic syndrome. With this disorder, there is a combination of lack of will with partial or complete immobility. This may often be accompanied by inhibition in the thinking process.
Abulia. How to treat the disease
How to treat abulia? Treatment for abulia is aimed at the underlying disease of which it is a symptom. Medications used in the treatment of abulia include antidepressants, antipsychotics, nootropics, and cholinesterase inhibitors.
To treat apato-abulic syndrome (defect) in schizophrenia, antipsychotic drugs with an activating spectrum of action are used. Some authors recommend psychostimulants. However, in this case you need to be extremely careful, because the use of these drugs can lead to exacerbation (resumption) of productive symptoms, increase delusions and hallucinations. A psychiatrist must select the correct drug treatment that will have a beneficial effect on apatho-abulic manifestations in patients with a mental disorder.
Modern medicine has learned to cope with many diseases, and a good specialist can help most patients. The main thing is to seek help in time and not delay. Then the chances of returning to your usual lifestyle and enjoying every new day increase.
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Approaches to the treatment of abulia
There is no treatment for abulia as a separate symptom of the disease. It is important to carry out treatment comprehensively and individually. The patient’s age, his physical condition, the duration of the mental disorder and its nature are always taken into account. Drug therapy is usually combined with psychotherapy. You need to understand that treatment should be carried out long-term and continuously, only under the supervision of the attending physician.
Medicinal effects
Abulia in schizophrenia is treated with antipsychotics. There is a group of atypical antipsychotics that appeared relatively recently. These drugs can prevent the development of negative symptoms in schizophrenia, maintain social and labor status, and increase the patient’s rehabilitation potential.
As a rule, antipsychotics in this group are highly effective and have minimal side effects. This group includes drugs such as Olanzapine, Quetiapine, Risperidone, Invega, Clopixol, Alimemazine. The dosage is selected by the doctor based on the clinical picture of the disease.
Depressive disorders can also be accompanied by the development of abulia, especially in severe cases. These conditions are difficult to treat; treatment with antidepressants should be carried out for a long time - from 6 months. Preference is given to the group of selective serotonin reuptake inhibitors (SSRIs): Sertraline, Paroxetine, Escitalopram, etc.
Psychotherapy
Any option and method of psychotherapy is used only after the necessary correction of the condition with medications. If we are talking about simple laziness, the question is only about increasing motivation to achieve desired goals, learning to plan work and your leisure time, and taking full responsibility for failure to complete tasks. Self-discipline and occupational therapy, primarily on oneself, bring positive results.
For abulia caused by a mental disorder, the method of work is selected individually by the psychotherapist. Cognitive behavioral, family and group therapies are well suited for this purpose. It is very important for depressed people to feel supported and understood by other people.
In the family, it is necessary to form the correct attitude of all its members towards this type of mental disorder, to create a favorable and calm environment for the patient. Psychotherapy is usually carried out throughout the year in courses of 10-15 sessions.
