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Pseudodementia (otherwise known as “depression-related cognitive dysfunction”) is a condition where mental cognition can be temporarily decreased. Pseudodementia is a phenotype approximated by a wide variety of underlying disorders.[1] Data indicate that some of the disorders that can convert to a pseudodementia-like presentation include depression (mood), schizophrenia, mania, dissociative disorders, Ganser syndrome, conversion reaction, and psychoactive drugs.[2] Although the frequency distribution of disorders presenting as pseudodementia remains unclear, what is clear is that depressive pseudodementia, synonymously referred to as depressive dementia[3] or major depression with depressive dementia, represents a major subclass of the overarching category of pseudodementia.[4] It has long been observed that in the differential diagnosis between dementia and pseudodementia, depressive pseudodementia appears to be the single most difficult disorder to distinguish from nosologically established "organic" categories of dementia,[5] especially degenerative dementia of the Alzheimer type.[6] Depressive pseudodementia is a syndrome seen in older people in which they exhibit symptoms consistent with dementia but the cause is actually depression.

Pseudodementia vs. DementiaEdit

Pseudodementia symptoms can appear similar to dementia. Due to the similar side effects to dementia, this can result in a misdiagnosis of depression, or the adverse effects of medications being taken.[7] This form of dementia is not the original form and does not result from the same cognitive changes. Once the depression is properly treated or the medication therapy is changed, the cognitive impairment can be effectively reversed. Generally, dementia involves a steady and irreversible cognitive decline but in some cases there may be different outcomes.[7] In addition, diminished mental capacity and social withdrawal are commonly identified as symptoms in the elderly but oftentimes is due to symptoms of depression.[8] As a result, elderly patients are often misdiagnosed especially when healthcare professionals do not make an accurate assessment.

Older people with predominantly cognitive symptoms such as loss of memory, and vagueness, as well as prominent slowing of movement and reduced or slowed speech, were sometimes misdiagnosed as having dementia when further investigation showed they were suffering from a major depressive episode.[9] This was an important distinction as the former was untreatable and progressive and the latter treatable with antidepressant therapy, electroconvulsive therapy, or both.[10] In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology.[11]


If effective medical treatment for depression is given, this can aid in the distinction between pseudodementia and dementia. Antidepressants have been found to assist in the elimination of cognitive dysfunction associated with depression, whereas cognitive dysfunction associated with true dementia continues along a steady gradient.  In cases where antidepressant therapy is not well tolerated, patients can consider electroconvulsive therapy as a possible alternative.[7] However, studies have revealed that patients who displayed cognitive dysfunction related to depression eventually developed dementia later on in their lives.

The development of treatments for dementia has not been as fast as those for depression. Thus far, cholinesterase inhibitors are the most popular drug used to slow the progression of the disease and improves cognitive function for a period of time.[12]


Leslie Gordon Kiloh was educated at Battersea Grammar School and studied medicine at London University and King's College Hospital. During World War II he served in the Middle East and was wounded in Athens when his group came under sniper fire while rescuing a superior.

After the war he worked in a psychiatric position at the Netherne Hospital in Surrey and, working with Samuel Nevin, completed his DPM. He then left the army and returned to King's where he was based in the neurological unit working with such leading British neurologists as McDonald Critchley (1900-1997) and Samuel Nevin (1905-1979).

Samuel Nevin studied medicine at Queen's University, Belfast, graduating first-class honours in 1927. Leslie Gordon Kiloh and Samuel Nevin defined it as an isolated lesion of the anterior interosseous nerve in 1952. Its old name was KilohNevin syndrome

Doubts about the classification and features of the syndrome,[13] and the misleading nature of the name, led to proposals that the term be dropped.[14] However, proponents argue that although it is not a defined singular concept with a precise set of symptoms, it is a practical and useful term which has held up well in clinical practice, and also highlights those who may have a treatable condition.[15]

Presentation and DifferentialEdit

The history of disturbance in pseudodementia is often short and abrupt onset, while dementia is more often insidious. Clinically, people with pseudodementia differ from those with true dementia when their memory is tested. They will often answer that they don't know the answer to a question, and their attention and concentration are often intact. They may appear upset or distressed, and those with true dementia will often give wrong answers, have poor attention and concentration, and appear indifferent or unconcerned. The symptoms of depression oftentimes mimic dementia even though it may be co-occurring[16]

The implementation and application of existing collaborative care models, such as DICE, can aid in avoiding misdiagnosis. Comorbidities (such as vascular, infectious, traumatic, autoimmune, idiopathic, or even becoming malnourished) have the potential to mimic symptoms of dementia.[17] For instance, studies have also shown a relationship between depression and its cognitive effects on everyday functioning and distortions of memory.[18]

Investigations such as PET and SPECT imaging of the brain show reduced blood flow in areas of the brain in people with Alzheimer's disease, compared with a more normal blood flow in those with pseudodementia.[19]


  1. ^ Emery, VOB (1999). "The relation between memory and language in the dementia spectrum of depression, Alzheimer syndrome, and normal aging". In Hamilton, Heidi (ed.). Language and Communication in Old Age: Multidisciplinary Perspectives. Issues in Aging. 9. New York: Garland Pub. pp. 25–63. ISBN 978-0-8153-2356-3. OCLC 906769876.
  2. ^ Emery, V. Olga B; Case Western Reserve Geriatric Education Center (1988). Pseudodementia: A Theoretical and Empirical Discussion. Interdisciplinary monograph series. 4. Cleveland, Ohio: Western Reserve Geriatric Education Center.
  3. ^ Emery, V. Olga B.; Oxman, Thomas E. (2003). "A 'prepermanent intermediate-stage dementia' in a long-term disease course of permanent dementia?". Dementia: Presentations, Differential Diagnosis, and Nosology. Johns Hopkins University Press. pp. 361–397. ISBN 978-0-8018-7156-6.
  4. ^ Emery VOB, Oxman TE (1992). "Update on the dementia spectrum of depression". American Journal of Psychiatry. 149: 305–317. doi:10.1176/ajp.149.3.305.
  5. ^ Emery, V. O.; Oxman, T. E. (1997). "Depressive dementia: A 'transitional dementia'?". Clinical Neuroscience. 4 (1): 23–30. ISSN 1065-6766. PMID 9056119.
  6. ^ Emery VOB (2011). "Alzheimer disease: Are we intervening too late?". Journal of Neural Transmission. 118: 1361–1378. doi:10.1007/s00702-011-0663-0.
  7. ^ a b c Thakur, Mugdha Ekanath. "Pseudodementia." Encyclopedia of Health & Aging, edited by Kyriakos S. Markides, SAGE Reference, 2007, pp. 477-478. Gale Virtual Reference Library. Accessed 5 July 2018. (subscription required)
  8. ^ Venes, Donald. Taber's Cyclopedic Medical Dictionary.Philadelphia: F.A. Davis Company, [2017] Print.
  9. ^ Caine, ED (1981). "Pseudodementia. Current concepts and future directions". Archives of General Psychiatry. 38 (12): 1359–64. doi:10.1001/archpsyc.1981.01780370061008. PMID 7316680.
  10. ^ Bulbena A, Berrios GE (1986). "Pseudodementia: Facts and figures". The British Journal of Psychiatry. 148 (1): 87–94. doi:10.1192/bjp.148.1.87. PMID 3955324.
  11. ^ Warrell, David; Timothy, Cox; John, Firth. "Neuropsychiatric disorders". doi:10.1093/med/9780199204854.003.2604. Cite journal requires |journal= (help)
  12. ^ Swartout-Corbeil, Deanna M., and Rebecca J. Frey. "Dementia." The Gale Encyclopedia of Nursing and Allied Health, edited by Brigham Narins, 3rd ed., vol. 2, Gale, 2013, pp. 966-976. Gale Virtual Reference Library. Accessed 20 Aug. 2018. (subscription required)
  13. ^ McAllister, TW (May 1983). "Overview: Pseudodementia". American Journal of Psychiatry. 140 (5): 528–33. doi:10.1176/ajp.140.5.528. PMID 6342420.
  14. ^ Poon, Leonard W (1991). "Toward an understanding of cognitive functioning in geriatric depression". International Psychogeriatrics. 4 (4): 241–66. doi:10.1017/S1041610292001297.
  15. ^ Sachdev, Perminder; Reutens, Sharon (2003). "The Nondepressive Pseudodementias". In V. Olga B. Emery; Thomas E. Oxman (eds.). Dementia: Presentations, Differential Diagnosis, and Nosology. JHU Press. p. 418. ISBN 0-8018-7156-5.
  16. ^ Wells, CE (May 1979). "Pseudodementia". American Journal of Psychiatry. 136 (7): 895–900. doi:10.1176/ajp.136.7.895. PMID 453349.
  17. ^ Kverno, Karan S. and Roseann Velez. “Comorbid Dementia and Depression: The Case for Integrated Care.” Journal for Nurse Practitioners Volume 14, Issue 3, March 2018, Pages 196-201.
  18. ^ Sjunaite, Karolina, Claudia Lanza, and Matthias W. Riepe. “Everyday false memories in older persons with depressive disorder.” Psychiatry Research 261 (2018): 456-463.
  19. ^ Parker, Gordon; Dusan Hadzi-Pavlovic; Kerrie Eyers (1996). Melancholia: A disorder of movement and mood: A phenomenological and neurobiological review. Cambridge: Cambridge University Press. pp. 273–74. ISBN 0-521-47275-X.