Abulia

Definition

Abulia (aboulia) is a “syndrome of hypofunction,” characterized by lack of initiative, spontaneity and drive (aspontaneity), apathy, slowness of thought (bradyphrenia), and blunting of emotional responses and response to external stimuli.

Pathology and Clinical features

It may be confused with the psychomotor retardation of depression and is sometimes labeled as “pseudodepression.” More plausibly, abulia has been thought of as a minor or partial form of akinetic mutism. There may also be some clinical overlap with catatonia. Abulia may result from frontal lobe damage, most particularly that involving the frontal convexity, and has also been reported with focal lesions of the caudate nucleus, thalamus, and midbrain. Abulia is not a separate condition; rather, it is a symptom associated with various forms of brain injury. It may occur in association with a variety of conditions, including stroke, brain tumor, traumatic brain damage, bleeding into the brain, and exposure to toxic substances.

As with akinetic mutism, it is likely that lesions anywhere in the “centromedial core” of the brain, from frontal lobes to brainstem, may produce this picture.

Pathologically, abulia may be observed in: Infarcts in anterior cerebral artery territory and ruptured anterior communicating artery aneurysms, causing basal forebrain damage. Closed head injury Parkinson’s disease; sometimes as a forerunner of a frontal lobe dementia Other causes of frontal lobe disease: tumor, abscess Metabolic, electrolyte disorders: hypoxia, hypoglycemia, hepatic encephalopathy Treatment is of the underlying cause where possible. There is anecdotal evidence that the dopamine agonist bromocriptine may help.

Treatment

There are no specific treatments for abulia. The underlying condition should be treated such as administering antidepressants or electroconvulsive therapy to depressed patients or antipsychotic medications to schizophrenic patients. Patients who have suffered brain injury due to stroke, bleeding, or trauma will benefit from rehabilitation programs that provide stimulation and attempt to re-teach skills. Research has looked at the possibility of treating abulia with medications that boost the activity of dopamine throughout the brain, but this is far from becoming a standard treatment

References

• Abdelgabar A, Bhowmick BK. Clinical features and current management of abulia. Progress in Neurology and Psychiatry 2001; 5(4): 14,15,17
• Bhatia KP, Marsden CD. The behavioral and motor consequences of focal lesions of the basal ganglia in man. Brain 1994; 117: 859-876 *Fisher CM. Abulia. In: Bogousslavsky J, Caplan L (eds.). Stroke syndromes. Cambridge: CUP, 1995: 182-187
• Friedman, Joseph H. “Mood, Emotion, and Thought.” In Textbook of Clinical Neurology, edited by Christopher G. Goetz. Philadelphia:W. B. Saunders Company, 2003.
• Al-Adawi, Samir. “Abulia: The Pathology of ‘Will’ and Dopaminergic Dysfunction in Brain-Injured Patients.” Medical Sciences 1 (1999): 27–40.
• Nishie, M. “Posterior Encephalopathy Subsequent to Cyclosporin A Presenting as Irreversible Abulia.” Internal Medicine 42, no. 8 (1 August 2003): 750–755.
• Pantoni, L. “Abulia and Cognitive Impairment in Two Patients with Capsular Genu Infarct.” Acta Neurologica Scandinavia 104, no. 3 (1 September 2001): 185–190.
• Vijayaraghavan. “Abulia: A Delphi Survey of British Neurologists and Psychiatrists.” Movement Disorders 17, no. 5 (September 2002): 1052–1057.
• The Gale Encyclopedia of Neurological Disorders

See also: Akinetic mutism ; Apathy ; Bradyphrenia ; Catatonia ; Frontal lobe syndromes ; Psychomotor retardation

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