Abulia
A disorder of diminished motivation and will.
Abulia is a neurological condition characterized by a lack of volition, will, or initiative, falling on a spectrum of diminished motivation between apathy and akinetic mutism. It was originally considered a disorder of the will, and individuals affected are unable to act or make decisions independently, with severity ranging from subtle to overwhelming.
Quick Facts
- First described
- 1838
- Prevalence in alzheimer's disease
- 25-50%
- Prevalence in mild alzheimer's
- 14%
- Prevalence in severe alzheimer's
- 61%
Facts from the source article.
Symptoms and signs
Clinical features most commonly associated with abulia include difficulty in initiating and sustaining purposeful movements, lack of spontaneous movement, reduced spontaneous speech, increased response-time to queries, passivity, reduced emotional responsiveness and spontaneity, reduced social interactions, and reduced interest in usual pastimes. In patients with progressive dementia, it may affect feeding, with individuals continuing to chew or hold food in their mouths for hours without swallowing, especially after eating part of a meal when appetite is low. The condition 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. It is considered more recently as a reduction in action, emotion, and cognition.
Causes
Abulia is most often the result of frontal lesions, not cerebellar or brainstem lesions. Evidence suggests it may be a dopamine-related dysfunction, as the mesolimbic and mesocortical dopamine systems are key to motivation and responsiveness to reward. It can result from brain injuries causing personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere. Injuries to the frontal lobe or basal ganglia can interfere with initiating speech, movement, and social interaction. A case study of two patients with acute confusional state and abulia found that an infarct in the capsular genu led to cognitive and behavioral alterations persisting one year after stroke, likely due to disruption of thalamo-cortical projection fibers. This supports the idea that abulia may exist independently of depression. It should be differentiated from apraxia, where impairment in comprehending movements needed for a motor task occurs without paralysis.
Diagnosis
Diagnosis can be difficult because abulia falls between apathy and akinetic mutism on the spectrum of diminished motivation; misdiagnosis may lead to inappropriate treatment. The best approach is clinical observation of the patient combined with questioning of close relatives to compare current behavior with past behavior. Imaging studies using CT or MRI scans help localize brain lesions, a main cause. Conditions associated with abulia include normal pressure hydrocephalus, major depressive disorder, persistent depressive disorder, attention deficit hyperactivity disorder, schizophrenia, frontotemporal dementia, Parkinson's disease, Huntington's disease, Pick's disease, progressive supranuclear palsy, traumatic brain injury, and stroke. A lack of motivation occurs in 25–50% of Alzheimer's disease patients, but abulia is not merely a symptom of depression, as over half of Alzheimer's patients with abulia do not have depression. Abulia is most prevalent in severe dementia, likely from reduced metabolic activity in prefrontal brain regions.
Treatment
Most current treatments are pharmacological, including antidepressants, though these are not always successful. The first step is a preliminary evaluation of the patient's general medical condition and addressing easily fixable problems such as seizures, headaches, or sensory loss, as improved physical status may enhance motivation. Pharmacological treatment involves five steps: optimize medical status; diagnose and treat other conditions associated with diminished motivation (e.g., apathetic hyperthyroidism, Parkinson's disease); eliminate or reduce psychotropics that aggravate motivational loss (e.g., SSRIs, dopamine antagonists); treat depression when both diminished motivation and depression are present; and increase motivation using stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.
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