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Last Update: March 9, 2023.

Continuing Education Activity

Abulia, also known as apathy, psychic akinesia, and athymia, refers to a lack of will, drive, or initiative for action, speech and thought, and is felt to be related to dysfunctions with the brain's dopamine-dependent circuitry. Treatment depends on etiology but often is geared toward increasing dopamine levels. Interprofessional team members should be familiar with the presentation, evaluation, and treatment of abulia. It can have several different etiologies, many of which require further evaluation and treatment. This activity outlines the presentation, evaluation, and management of abulia and highlights the interprofessional team's role in improving outcomes for patients with this condition.


  • Review the etiologic factors associated with the development of abulia.
  • Summarize the typical signs and symptoms of abulia.
  • Describe important treatment considerations and psychosocial considerations in managing this condition.
  • Outline strategies for the interprofessional care team to employ for optimal management and counseling to patients with abulia.
Access free multiple choice questions on this topic.


The Dictionary of Neurological Signs defines abulia as a "syndrome of hypofunction," characterized by lack of initiative, spontaneity, and drive, apathy, slowness of thought (bradyphrenia), and blunting of emotional responses and response to external stimuli.

In other words, abulia refers to a lack of will, drive, or initiative for action, speech, and thought. This term is derived from the Greek word aboulia, meaning “non-will.” This has to be distinguished from the inability to perform an activity due to cognitive or physical disability. This phenomenon has been known since 1838.[1] Several terms have been used interchangeably with abulia: apathy, psychic akinesia, loss of psychic self-activation, and athymia.


Potential causes include:

  • Conditions causing basal forebrain damage: Trauma, anterior cerebral artery territory infarct, and ruptured anterior communicating artery aneurysms
  • Closed head injury
  • Parkinson disease
  • Other causes of frontal lobe disease: tumor, abscess, frontal lobotomy
  • Metabolic and electrolyte disorders: hypoxia, hypoglycemia, hepatic encephalopathy


Abulia is thought to be a common problem, but the national and international frequency is not reported.


Abulia is supposed to occur because of a malfunction of the brain’s dopamine-dependent circuitry. Lesions anywhere in the "centro-medial core" of brain frontal-subcortical circuitry, from frontal lobes to the brainstem, may produce this condition.[2]

Diaschisis is the neurological phenomenon in which damage in one part of the brain results in functional impairment in a remote but interconnected location. This can be the mechanism behind the appearance of abulia in basal ganglia and thalamic lesions because of the complex frontal-basal ganglia-thalamic circuits. 

The following structural lesions have been attributed as factors in the etiology of abulia:

  1. Anterior cingulate cortex:[3] Most common, produced by anterior cerebral artery infarction and produces abulia minor
  2. Unilateral anterior cerebral artery lesions produce transient abulia often associated with contralateral motor neglect because of damage to the medial premotor area.
  3. Bilateral lesions in the medial frontal lobes, basal ganglia, supplementary motor areas, caudate nuclei, and cingulate gyri lead to persistent abulia.
  4. Frontal convexity damage
  5. Focal subcortical lesions of the caudate nucleus, anterior thalamus, globus pallidus, internal capsule, and midbrain
  6. Disconnections of limbic tracts projecting from the anterior thalamus to the cingulate
  7. Embolism occurring in the subthalamic-thalamic penetrating artery of Percheron leading to bilateral meso-diencephalon infarct may damage the medial thalamus and upper mesencephalon. This can lead to abulia.
  8. Bilateral lesions at or rostral to the meso-diencephalic junction or bilateral damage to the frontal lobes can lead to abulia major.
  9. Pressure on the bilateral frontal periventricular white matter can cause abulia in hydrocephalus.

History and Physical

Classification and Clinical Features

Abulia Minor (Apathy)

Patients with abulia minor may comply with requests of others and participate in activities that other initiate but will not initiate plans or activities of their own. Enjoyment and motivation and may or may not be present. They may say little spontaneously but give brief responses when others speak to them. Some patients may “talk a good game,” telling others about some plans, but never follows through on them. Initiation is dissociated from volition.

Abulia Major ( Akinetic Mutism)

The patient will initiate nothing at all, including speaking and eating, and may ultimately require total personal care. Akinetic mutism is a state of limited verbal and motor responsiveness to the environment in those without paralysis and coma. Patients may have open eyes and brief movements. In lesions involving the anteromedial lobes, speech and agitation to unpleasant stimuli may develop. The eyes of these patients are open and follow objects, and they are more alert than those with mesencephalic or thalamic lesions. The patients may also make brief, monosyllabic, but an appropriate response to questions.

"Miller Fisher's telephone effect" - Patients with abulia may sometimes talk at length fluently and animatedly over the telephone.


Diagnosis is mainly based clinically. Fisher’s “telephone test,” where the patient responds during a telephone conversation but not during personal face-to-face contact, may be used to diagnose abulia minor.

Criteria for the diagnosis of abulia:

  1. Decreased spontaneity of activity and speech
  2. Prolonged latency in responding to queries, directions, and other stimuli and
  3. Reduced ability to persist with a task

Treatment / Management

The treatment of abulia is by treating the underlying cause, if possible. Otherwise, it depends mainly on the drugs that increase the dopamine levels in the dopaminergic circuitry. These include:

  1. Carbidopa/levodopa
  2. Amantadine
  3. Bupropion, a dopamine reuptake inhibitor
  4. Bromocriptine, a dopamine agonist and
  5. Nefiracetam, a new cyclic-aminobutyric compound that has been shown to enhance neurotransmission[4]
  6. Olanzapine[5]
  7. Agomelatine[6]

Differential Diagnosis

Differential diagnoses include the following[7][8]:

  • Post-stroke depression: This is a mood disorder. Patients have a persistent sad mood and negative thought content. Such patients may have a history of depression.
  • Aphasia: This is a language disorder. Patients appear to be well with normal mood and behavior. They attempt to communicate but with difficulty. They socialize appropriately.
  • Parkinson's disease: This is a movement disorder. Patients exhibit rigidity, tremors, slowness of movement, and difficulty in walking. Cognitive and behavioral problems occur at a later stage of the disease.
  • The condition may be confused with the psychomotor retardation of depression and is sometimes labeled "pseudo-depression." It is important to differentiate abulia from depression as antidepressants are not effective in abulia.
  • Catatonia: In mild cases, it can be difficult to differentiate this condition from abulia.


The prognosis depends on the underlying condition causing abulia. 


Patients with abulia may suffer from the following complications due to lack of initiative:

  1. Malnutrition
  2. Dehydration
  3. Electrolyte imbalance
  4. Bedsores
  5. Deep vein thrombosis

Deterrence and Patient Education

Patients with abulia are difficult to motivate. Still, an active role played by a neuroscience nurse, rehabilitation physician, neurologist, and psychiatrist can bring an effective outcome to the patient.

Enhancing Healthcare Team Outcomes

Healthcare workers should be familiar with abulia because it has a varied presentation that may lead to very high morbidity. Both the primary care provider and nurse practitioner should refer these patients to a mental health worker because the management is complex and long-term. The treatment generally depends on the cause, but not all treatments work. For treatments to work, the patient must also be compliant and have a mindset of improvement. Besides medications, cognitive behavior therapy has been used, but relapse rates are high. To date, there is no way to prevent abulia, and the disorder can affect any individual irrespective of age, race, gender, or ethnicity. Neuroscience and rehabilitation nurses work with occupational therapists and physicians to treat these patients. Pharmacists review prescribed medications and educate the patients and their families about side effects and compliance. The interprofessional team can improve outcomes. [Level 5]

Review Questions


Vijayaraghavan L, Krishnamoorthy ES, Brown RG, Trimble MR. Abulia: a delphi survey of British neurologists and psychiatrists. Mov Disord. 2002 Sep;17(5):1052-7. [PubMed: 12360558]
Hastak SM, Gorawara PS, Mishra NK. Abulia: no will, no way. J Assoc Physicians India. 2005 Sep;53:814-8. [PubMed: 16334629]
Siegel JS, Snyder AZ, Metcalf NV, Fucetola RP, Hacker CD, Shimony JS, Shulman GL, Corbetta M. The circuitry of abulia: insights from functional connectivity MRI. Neuroimage Clin. 2014;6:320-6. [PMC free article: PMC4215525] [PubMed: 25379445]
Jorge RE, Starkstein SE, Robinson RG. Apathy following stroke. Can J Psychiatry. 2010 Jun;55(6):350-4. [PubMed: 20540829]
Spiegel DR, Chatterjee A. A case of abulia, status/post right middle cerebral artery territory infarct, treated successfully with olanzapine. Clin Neuropharmacol. 2014 Nov-Dec;37(6):186-9. [PubMed: 25384076]
Thome J, Foley P. Agomelatine: an agent against anhedonia and abulia? J Neural Transm (Vienna). 2015 Aug;122 Suppl 1:S3-7. [PubMed: 24311062]
Naik VD. Abulia following an episode of cardiac arrest. BMJ Case Rep. 2015 Jul 01;2015 [PMC free article: PMC4493212] [PubMed: 26135487]
Muqit MM, Rakshi JS, Shakir RA, Larner AJ. Catatonia or abulia? A difficult differential diagnosis. Mov Disord. 2001 Mar;16(2):360-2. [PubMed: 11295797]

Disclosure: Joe Das declares no relevant financial relationships with ineligible companies.

Disclosure: Abdolreza Saadabadi declares no relevant financial relationships with ineligible companies.

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Bookshelf ID: NBK537093PMID: 30725778


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