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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, requiring further evaluation and treatment. This activity outlines the presentation of abulia, evaluation, and management and highlights the interprofessional team's role in improving outcomes for patients with this condition. Objectives: Evaluate the etiologic factors associated with the development of abulia. Identify the typical signs and symptoms of abulia. Assess 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 derives from the Greek 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 of abulia include: Conditions causing basal forebrain damage: Trauma, anterior cerebral artery territory infarction, 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 supposed to occur because of a brain’s dopamine-dependent circuitry malfunction. 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 a neurological phenomenon in which damage in 1 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: Anterior cingulate cortex: Most common, produced by anterior cerebral artery infarction and produces abulia minor [3] Unilateral anterior cerebral artery lesions produce transient abulia often associated with contralateral motor neglect because of damage to the medial premotor area. Bilateral lesions in the medial frontal lobes, basal ganglia, supplementary motor areas, caudate nuclei, and cingulate gyri lead to persistent abulia. Frontal convexity damage Focal subcortical lesions of the caudate nucleus, anterior thalamus, globus pallidus, internal capsule, and midbrain Disconnections of limbic tracts projecting from the anterior thalamus to the cingulate 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. Bilateral lesions at or rostral to the meso-diencephalic junction or bilateral damage to the frontal lobes can lead to abulia major. Pressure on the bilateral frontal periventricular white matter can cause abulia in hydrocephalus.

Classification and Clinical Features Abulia minor (apathy) Patients with abulia minor may comply with the requests of others and participate in activities that others initiate but do not initiate plans or activities of their own. Enjoyment and motivation may or may not be present. They may say little spontaneously but respond briefly when others speak to them. Some patients may “talk a good game,” telling others about some plans, but never follow through. Initiation is dissociated from volition. Abulia major (a kinetic mutism) The patient initiates nothing, including speaking and eating, and may 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. Speech and agitation to unpleasant stimuli may develop in lesions involving the anteromedial lobes. 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 appropriate responses 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: Decreased spontaneity of activity and speech Prolonged latency in responding to queries, directions, and other stimuli and Reduced ability to persist with a task

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

Differential diagnoses include the following: 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, slow movement, and difficulty 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.[7][8]

Healthcare workers should be familiar with abulia because it has a varied presentation that may lead to very high morbidity. The primary care provider 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 treat these patients with occupational therapists and physicians. Pharmacists review prescribed medications and educate the patients and their families about side effects and compliance. The interprofessional team can improve outcomes.