Encyclopedia of Clinical Neuropsychology

Living Edition
| Editors: Jeffrey Kreutzer, John DeLuca, Bruce Caplan


  • Irene PiryatinskyEmail author
Living reference work entry
DOI: https://doi.org/10.1007/978-3-319-56782-2_1874-2



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.

See Also

Further Reading

  1. Berrios, G. E., & Grli, M. (1995). Abulia and impulsiveness revisited: A conceptual history. Acta Psychiatrica Scandinavica, 92(3), 161–167.CrossRefPubMedGoogle 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.CrossRefPubMedGoogle 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.PubMedPubMedCentralGoogle Scholar
  6. Kumral, E., Evyapan, D., & Balkir, K. (1999). Acute caudate vascular lesions. Stroke, 30, 100–108.CrossRefPubMedGoogle 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.CrossRefPubMedGoogle 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.CrossRefPubMedGoogle 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.CrossRefPubMedPubMedCentralGoogle Scholar

Copyright information

© Springer International Publishing AG 2017

Authors and Affiliations

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