In neurology, abulia refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). 

Abulia is a form of insanity characterized by an inertness, torpor, or paralysis of the will.

Abulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than abulia.

It is considered to be a disorder of the will.

Abulia has been described as a loss of drive, expression, behavior and speech output, with slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative, a reduction in action emotion and cognition.

Aboulic individuals are unable to act or make decisions independently.

The condition may range in severity from subtle to overwhelming. 

In the case of akinetic mutism, patients describe that an attempt to movement, a resistance rises up to meet them.

Abulia is a of loss of drive, expression, behavior and speech output, with slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative.

Considered a reduction in action emotion and cognition.

The clinical features associated with abulia :

Difficulty in initiating and sustaining purposeful movements

Lack of spontaneous movement

Reduced spontaneous speech

Increased response-time to queries


Reduced emotional responsiveness and spontaneity

Reduced social interactions

Reduced interest in usual pastimes

With progressive dementia, it may affect feeding.

Patients may chew or hold food in their mouths for hours without swallowing it.

It is considered a process of reduction in action emotion and cognition.

As a result of the changing definition of abulia, there is currently a debate on whether or not abulia is a sign or a symptom of another disease, or its own disease that seems to appear in the presence of other more well-researched diseases, such as Alzheimer’s disease.[6]

Whether it is clinically distinct from depression, akinetic mutism, and alexithymia, and there is disagreement about whether or not abulia is a sign, symptom, or syndrome.

The study of motivation has been mostly about how stimuli come to acquire significance for animals. 

There is a number of disorders attributed to a lack of will and motivation.

Many different causes of abulia have been suggested. 

Abulia is the result of frontal lesions-not with cerebellar or brainstem lesions, may be a dopamine-related dysfunction.

Abulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage, especially stroke causing diffuse injury to the right hemisphere.

5-67% of all patients with traumatic brain injuries and 13% of patients with lesions on their basal ganglia experience some form of diminished motivation.

Abulia may complicate rehabilitation when a stroke patient becomes uninterested in performing tasks like walking despite being capable of doing so. 

It should be differentiated from apraxia, when a brain injured patient has impairment in comprehending the movements necessary to perform a motor task despite not having any paralysis that prevents performing the task; that condition can also result in lack of initiation of activity.

Abulia may exist independently of depression as its own syndrome.

The anterior cingulate circuit consists of the anterior cingulate cortex, (Brodmann area 24), and its projections to the ventral striatum which includes the ventromedial caudate, the ventral pallidum, which connects to the ventral anterior nucleus of the thalamus. 

The anterior cingulate circuit is essential for the initiation of behavior, motivation and goal orientation, which are the very things missing from a patient with a disorder of diminished motivation. 

Unilateral injury or injury along any point in the circuit leads to abulia regardless of the side of the injury.

Bilateral damage in patients exhibit a more extreme case of diminished motivation, akinetic mutism.

The caudate nucleus is involved in degenerative diseases of the central nervous system such as Huntington disease. 

In acute caudate stroke patients, 48% were found to be experiencing abulia. 

Abulia falls between two other disorders of diminished motivation.

To diagnose abulia requires clinical observation of the patient to compare the patient’s new behavior to see if there is in fact a case of diminished motivation.

Imaging studies using a CT or MRI scan can localize brain lesions which have been shown to be one of the main causes of abulia.

Abulia may be present: 

Normal pressure hydrocephalus

Major depressive disorder

Persistent depressive disorder

Attention deficit hyperactivity disorder


Frontotemporal dementia

Parkinson’s disease

Huntington’s disease

Pick’s disease

Progressive supranuclear palsy

Traumatic brain injury


Alzheimer’s disease

A lack of motivation has been reported in 25–50% of patients with Alzheimer’s disease. 

Abulia is most prevalent in cases of severe dementia which may result from reduced metabolic activity in the prefrontal regions of the brain. 

Patients with Alzheimer’s disease and abulia are significantly older than patients with Alzheimer’s who do not lack motivation. 

The prevalence of abulia increased from 14% in patients with a mild case Alzheimer’s disease to 61% in patients with a severe case of Alzheimer’s disease, which most likely developed over time as the patient got older.


Most current treatments are pharmacological, with the use of antidepressants. 

Evaluation of the patient’s general medical condition and fixing the problems that can be resolved or improved: controlling seizures, headaches, arranging physical or cognitive rehabilitation, optimizing hearing, vision, and speech. 

By improved physical status there may be enhanced functional capacity, drive, and energy.

Eliminate or reduce doses of psychotropics and other agents that aggravate motivational loss.

Treat depression when present.

Increase motivation through use of stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.

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