Abulia: what is it, symptoms, causes, treatment, prognosis

What is abulia?

In neurology, abulia(from Greek: ἀ- - negative particle and βουλή - will), refers to a lack of will or initiative and can be considered as violation of the motivational sphere. Abulia is in the middle of the spectrum of weakened motivation, with apathy less pronounced and akinetic mutism more pronounced than abulia. The condition was initially considered a disorder of the will, and the abulist cannot act or make decisions on his own; and their condition can range from subtle to overwhelming.

Symptoms and Signs

Clinical condition indicated as abulia, was first described in 1838; however, a number of different, conflicting definitions have emerged since then. Abulia is described as a loss of movement, expression, behavior, and speech production, with a delay and prolonged delay in speech, as well as a decrease in spontaneous thought content and initiative. The clinical signs most commonly associated with abulia include:

• difficulty in initiating and maintaining purposeful movements;
• lack of spontaneous movement;
• decreased spontaneous speech;
• increased response time to requests;
• passivity;
• decreased emotional responsiveness and spontaneity;
• decreased social interactions;
• decreased interest in regular activities.

The disorder may affect feeding, especially in patients with progressive dementia. Patients can continue to chew or hold food in their mouth for several hours without swallowing. This behavior may be most evident after these patients have eaten some of their food and no longer have a strong appetite.

Differentiation from other disorders

Both neurologists and psychiatrists recognize abulia as a separate clinical entity, but its status as a syndrome is unclear. Although abulia has been known to clinicians since 1838, it has undergone various interpretations - from “pure absence will "in the absence of motor paralysis before, recently, considered" a decrease in the emotions of action and knowledge". As a result of the change in the definition of abulia, there is currently debate over whether abulia is a sign or symptom of another. illness or illness of one's own that seems to manifest itself in the presence of other, more well-studied disorders, such how Alzheimer's disease.

A 2002 survey by two movement disorders experts, two neuropsychiatrists, and two specialists in rehabilitation, did not shed light on the issue of differentiating abulia from other disorders of motivational spheres. The experts used the terms "apathy" and "abulia" interchangeably and debated whether abulia was a separate subject or just a hazy gray area in the spectrum of more specific disorders. Four experts said abulia was a sign and symptom, and the group was divided over whether it was a syndrome. Another survey, which consisted of true and false questions about what abulia differs from, whether it is a sign, symptom or syndrome, where there are lesions during abulia, what diseases are usually associated with abulia and what modern methods of treatment were used, was referred to 15 neurologists and 10 psychiatrists. Most experts agreed that abulia is clinically distinct from depression, akinetic mutism, and alexithymia. However, only 32% believe that abulia is different from apathy, 44% said they are not different, and 24% are not sure. Once again, there was controversy over whether abulia was a sign, symptom, or syndrome.

The study of motivation has mainly dealt with how stimuli acquire meaning in relation to animals. Only recently has the study of motivational processes been expanded in order to integrate biological stimuli and emotional states into explaining purposeful human behavior. Given the number of impairments attributed to lack of will and motivation, it is very important that abulia and apathy are more precisely formulated to avoid confusion.

Causes

Many different reasons for abulia have been suggested. Despite the fact that there is some controversy about the legality of abulia as a separate disease, experts are mostly agree that abulia is the result of damage to the frontal lobe, and not damage to the cerebellum or brain stem. As a result of a growing body of evidence showing that mesolimbic and mesocortical dopamine system are key to motivation and response to reward, abulia can be a dysfunction associated with dopamine. Abulia can also result from various brain injuries that cause personality changes, such as illness, mental illness, injury, or intracerebral hemorrhage (stroke), especially stroke causing diffuse damage to the right hemisphere.

- Damage to the basal ganglia.

Injuries to the frontal lobe and / or basal ganglia can affect a person's ability to initiate speech, movement, and social interaction. Studies have shown that 5–67% of all patients with traumatic brain injury and 13% of patients with lesions of the basal ganglia suffer from some form of decreased motivation.

This can complicate rehabilitation if the stroke patient is not motivated to perform tasks such as walking, despite being able to do so. It should be distinguished from apraxia, when a patient with a brain injury has impaired understanding. movements necessary to perform a motor task, despite the absence of paralysis that interferes with the performance of this tasks; this condition can also lead to the fact that the activity does not start.

- Injury to the knee of the inner capsule.

A case study was conducted with two patients suffering from an acute condition confusion and abulia to determine if these symptoms were the result of a heart attack in the knee capsule. The use of clinical neuropsychological and MRI studies at baseline and one year later showed that cognitive impairment still persisted one year after the stroke. Cognitive and behavioral changes due to infarction of the knee of the inner capsule are most likely associated with the fact that thalamo-cortical projection fibers, which originate from the ventral-anterial and medial-dorsal nuclei, pass through the inner part of the knee capsules. These tracts are part of a complex system of cortical and subcortical frontal chains through which information flows from the entire cortex to reaching the basal ganglia. Cognitive impairment could be due to a knee capsule infarction affecting the lower and anterior thalamic legs. The interesting thing about this case study was that the patients did not show functional deficits when follow-up one year after stroke and were not depressed but showed a decrease motivation. This result supports the idea that abulia can exist independently of depression as a syndrome of its own.

- Damage to the anterior cingulate gyrus.

The anterior cingulate gyrus consists of the anterior cingulate cortex, also called Brodmann's field 24, and its projections onto the ventral striatum, which includes the ventromedial caudate nucleus. The loop continues to connect to the ventral pallidum, which connects to the ventral anterior thalamic nucleus. This circuit is important for initiating behavior, motivation and goal orientation, which is what the patient with low motivation disorder lacks. Unilateral trauma or trauma at any point in the chain leads to abulia regardless of the side of the injury, but if there is bilateral damage, the patient will exhibit a more extreme case of impaired motivation, akinetic mutism.

- Acute lesions of the vessels of the caudal nucleus.

It is well documented that the caudate nucleus is involved in degenerative diseases of the central nervous system such as Huntington's disease. In a case study of 32 patients with acute caudate stroke, 48% were found to be abulia. Most cases of abulia were present when patients had a left caudate heart attackthat extended into putamens, which was seen on computed tomography or magnetic resonance imaging.

Epidemiology

Abulia is believed to be a common problem, but national and international reporting rates are not reported.

Diagnostics

Diagnosing abulia can be quite challenging as the condition sits between two other disorders of low motivation and can it is easy to see an extreme case of abulia as akinetic mutism or a lesser case of abulia as apathy and therefore not treat the patient appropriately way. If the disorder is confused with apathy, it can lead to attempts to involve the patient in physical rehabilitation. or other interventions where a source of strong motivation is needed for success, but it does not matter absent. The best way to diagnose abulia is by clinical observation of the patient, as well as by asking close relatives and loved ones to give a benchmark against which he was able to compare the patient's new behavior to see if there really was a case of decreased motivation. In recent years, it has been found that imaging studies using computed tomography or magnetic resonance imaging CT scans are very helpful in localizing brain lesions, which have been shown to be one of the main causes abulia.

- Diseases in which abulia may be present.

• normal pressure hydrocephalus (NPH);
• depression;
• schizophrenia;
• frontotemporal dementia;
• Parkinson's disease;
• Huntington's disease;
• Pick's disease;
• progressive supranuclear palsy;
• traumatic brain injury;
• stroke.

- Alzheimer's disease.

Lack of motivation was reported in 25-50% of patients with Alzheimer's disease. Although depression is also common in patients with this condition, abulia is not straightforward. symptom of depression, since more than half of Alzheimer's patients with abulia do not suffer from depression. Several studies have shown that abulia is most common in cases of severe dementia, which may result from decreased metabolic activity in the prefrontal regions of the brain. Alzheimer's and abulia patients are significantly older than Alzheimer's patients who do not lack motivation. Along with this, the prevalence of abulia increased from 14% in patients with mild Alzheimer's disease to 61% in patients with a severe case of Alzheimer's disease, which most likely developed over time, when the patient became older.

Treatment

Most of the current treatments for abulia are pharmacological, including the use of antidepressants. However, antidepressant treatment is not always successful, and this has opened the door to alternative treatments. The first step to successfully treating abulia or other motivational disorders is to assess the patient's overall health and address problems that can be easily resolved. This can mean controlling seizures or headaches, organizing physical or cognitive rehabilitation for cognitive and sensorimotor problems or ensuring optimal hearing, vision and speech. These rudimentary steps also increase motivation, as improving physical condition can increase functionality, movement and energy and thus raise the patient's expectations that initiative and effort will be successful.

Pharmacological treatment consists of 5 steps:

1. Optimize medical status.
2. Diagnose and treat other conditions more specifically associated with decreased motivation (eg, apathetic hyperthyroidism, Parkinson's disease).
3. Withdraw or reduce the dose of psychotropics and other agents that increase the loss of motivation (for example, SSRIs, dopamine antagonists).
4. Treat depression effectively when both motivational disorders and depression are present.
5. Increase motivation with stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.

Forecast

The prognosis depends on the underlying condition causing the abulia.

Complications

Abulia patients may suffer from the following complications due to lack of initiative:

• malnutrition;
• dehydration of the body;
• imbalance of electrolytes;
• bedsores;
• deep vein thrombosis.