Encyclopedia of Clinical Neuropsychology

2018 Edition
| Editors: Jeffrey S. Kreutzer, John DeLuca, Bruce Caplan


  • Irene PiryatinskyEmail author
Reference work entry
DOI: https://doi.org/10.1007/978-3-319-57111-9_1874


Apathy; Athymia; Loss of psychic self-activation; Psychic akinesia

Also spelled Aboulia


The term is derived from the Greek “boul” (will). Abulia is manifested by lack of motivation; lack of spontaneity in speech and action; deficiency in initiation, inertia, mental, and motor slowness; poor attention; and easy distractibility. Inactivity comes from an inability to select a course of action, although a wish to participate may be present. Some research indicates that abulia occurs due to malfunction of the brain’s dopamine-dependent circuitry. In neurologic diseases, it is associated with bilateral lesions in the medial or orbital frontal lobes. The following criteria have been suggested for the diagnosis of abulia: (i) decreased spontaneity in activity and speech; (ii) prolonged latency in responding to queries, directions, and other stimuli; and (iii) reduced ability to persist with a task.

Further Reading

  1. Berrios, G. E., & Grli, M. (1995). Abulia and impulsiveness revisited: A conceptual history. Acta Psychiatrica Scandinavica, 92(3), 161–167.PubMedCrossRefGoogle Scholar
  2. Caplan, L. R., Schmahmann, J. D., Kase, C. S., Feldmann, E., Baquis, G., Greenberg, J. P., et al. (1990). Caudate infarcts. Archives of Neurology, 47(2), 133–143.PubMedCrossRefGoogle Scholar
  3. Drubach, D. A., Zeilig, G., Perez, J., Peralta, L., & Makley, M. (1995). Treatment of abulia with carbidopa/levadopa. Journal of Neuroengineering and Rehabilitation, 9, 151–155.Google Scholar
  4. Egnelborghs, S., Marien, M. A., Pickut, B. A., Verstraeten, M. A., & De Deyn, P. P. (2000). Loss of psychic self-activation after paramedian bithalamic infarction. Stroke, 31, 1762–1765.CrossRefGoogle Scholar
  5. Forstl, H., & Sahakian, B. A. (1991). A psychiatric presentation of abulia: Three cases of frontal lobe ischaemia and atrophy. Journal of the Royal Society of Medicine, 84, 89–91.PubMedPubMedCentralCrossRefGoogle Scholar
  6. Kumral, E., Evyapan, D., & Balkir, K. (1999). Acute caudate vascular lesions. Stroke, 30, 100–108.PubMedCrossRefGoogle Scholar
  7. Laplande, D., Attal, N., Sauron, B., de Billy, A., & Dubois, B. (1992). Lesions of the basal ganglia due to disulfiram neurotoxicity. Journal of Neurology, Neurosurgery, and Psychiatry, 55, 925–929.CrossRefGoogle Scholar
  8. Liddle, P. F. (1987). The symptoms of chronic schizophrenia. British Journal of Psychiatry, 151, 145–151.PubMedCrossRefPubMedCentralGoogle Scholar
  9. Litvan, I., Paulsen, J. S., Mega, M. S., & Cummings, J. L. (1998). Neuropsychiatric assessment of patients with hyperkinetic and hypokinetic movement disorders. Archives of Neurology, 55, 1313–1319.CrossRefGoogle Scholar
  10. Powell, J. H., Al-Adawi, S., Morgan, J., & Greenwood, R. J. (1996). Motivation deficits after brain injury: Effects of bromocriptine in 11 patients. Journal of Neurology, Neurosurgery, and Psychiatry, 60, 416–421.PubMedPubMedCentralCrossRefGoogle Scholar

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© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  1. 1.Butler Hospital and Alpert Medical School of Brown UniversityProvidenceUSA