Abulia (Aboulia)


Article Author:
Joe M Das


Article Editor:
Abdolreza Saadabadi


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John Schweitzer


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Tehmina Warsi


Updated:
6/7/2019 5:35:18 PM

Introduction

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.

Etiology

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

Epidemiology

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

Pathophysiology

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 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 in a fluent and animated fashion over the telephone.

Evaluation

Diagnosis is mainly based clinically. Fisher’s “telephone test” (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 in 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 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 as "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.

Prognosis

The prognosis depends on the underlying condition causing abulia. 

Complications

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

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

Deterrence and Patient Education

Patients with abulia are difficult to be motivated. Still, an active role played by a neuro-nurse, rehabilitation physician, neurologist, and a 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.


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Abulia (Aboulia) - Questions

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What does a patient with abulia lack?



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Which of the following is not a characteristic of abulia?



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A 34-year-old male who was in a motor vehicle accident was found to have bilateral basal frontal contusions. He underwent bi-frontal craniotomy and contusectomy. A postoperative CT scan of the brain showed no residual hematoma and a reduction in the previous mass effect. On postoperative day 2, the patient is conscious with a Glasgow coma scale score of 14 (eye opening 3, verbal response 5, motor response 6). He is not showing any initiative. He prefers to lie in bed throughout the day, refuses to eat a full meal, and answers questions reluctantly. He will get out of bed if asked by a healthcare team member. He has no neck stiffness, and his hematologic parameters are normal. What is the most likely diagnosis?



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What is the most common anatomical substrate affected in patients with abulia?



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A 17-year-old presented with a lack of initiative, reduced food intake, and preference to sleep most of the time. His history revealed a closed head injury two months ago, which was conservatively managed. He did not have any history of substance use. Which part of the brain is least likely to have been damaged?



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A 65-year-old male patient undergoes craniotomy and clipping of an anterior communicating artery aneurysm. He was fully conscious and oriented on postoperative day 1. But the next day onwards, he starts refusing food, prefers to sleep throughout the day, and is not responding nicely to questions asked. A magnetic resonance imaging scan of the brain is ordered. An infarct in which of the following regions is the most likely cause of his behavioral problem?



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A 60-year-old female patient underwent craniotomy and clipping of anterior communicating artery aneurysm. She was fully conscious and oriented on postoperative day 1. But the next day onwards, she started refusing food, preferred to sleep throughout the day, and was not responding nicely to questions asked. A magnetic resonance imaging scan of the brain was ordered, which showed an infarct involving the ipsilateral anterior cingulate region. Which of the following drugs is least likely to be beneficial in the treatment of her condition?



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A 50-year-old male presents to the clinic with a lack of initiative, reduced food intake, and preference to sleep most of the time. History reveals that he had undergone craniotomy and clipping of aneurysm two months back. Surgery of aneurysm at which of the following locations is most likely to be associated with his condition?



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Abulia (Aboulia) - References

References

Vijayaraghavan L,Krishnamoorthy ES,Brown RG,Trimble MR, Abulia: a delphi survey of British neurologists and psychiatrists. Movement disorders : official journal of the Movement Disorder Society. 2002 Sep     [PubMed]
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. Clinical. 2014     [PubMed]
Naik VD, Abulia following an episode of cardiac arrest. BMJ case reports. 2015 Jul 1     [PubMed]
Hastak SM,Gorawara PS,Mishra NK, Abulia: no will, no way. The Journal of the Association of Physicians of India. 2005 Sep     [PubMed]
Jorge RE,Starkstein SE,Robinson RG, Apathy following stroke. Canadian journal of psychiatry. Revue canadienne de psychiatrie. 2010 Jun     [PubMed]
Muqit MM,Rakshi JS,Shakir RA,Larner AJ, Catatonia or abulia? A difficult differential diagnosis. Movement disorders : official journal of the Movement Disorder Society. 2001 Mar;     [PubMed]
Spiegel DR,Chatterjee A, A case of abulia, status/post right middle cerebral artery territory infarct, treated successfully with olanzapine. Clinical neuropharmacology. 2014 Nov-Dec;     [PubMed]
Thome J,Foley P, Agomelatine: an agent against anhedonia and abulia? Journal of neural transmission (Vienna, Austria : 1996). 2015 Aug;     [PubMed]

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