Abulia

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 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.

Evaluation

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]
(B3)

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.

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. Bedsores
5. Deep vein thrombosis