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Pseudosenility also reversible dementia is a condition where older people are in a state of memory loss, confusion, or disorientation that may have a cause other than the ordinary aging process.[1] Generally, the term "reversible dementia" is used to describe most cases.[2] A more specific term "Pseudodementia" is referring to "behavioral changes that resembler those of the progressive degenerative dementias, but which are attributable to so-called functional causes".[3]

The New York Times reports that illnesses such as the flu and hydrocephalus, as well as side-effects to common medications, can produce symptoms in the elderly that are difficult to distinguish from ordinary dementia caused by aging. However, if the real cause of the effects is caught early enough, the effects can be reversed.[4][5] According to studies cited in Cunha (1990), approximate 10% to 30% of patients who have exhibited symptoms of dementia might have a treatable or reversible pathologic process to some extent.[6]


It should be noticed that describing the causation of reversible dementia is extremely difficult due to the complicated biopsychological systems and the hard-to-define collection of factors associated with cognitive decline. Roughly, the etiological factors that contribute to cognitive decline could be assigned into four categories: chemical, environmental, physical, and psychiatric. Chemical intoxication might be attributed to anesthesia, alcohol, heavy metal and commonly used medications. Jenike (1988) has recorded a certain amount of medications which may induce cognitive change in elder people.[7] The list is provided below.

Antihypertensive agents Neuroleptics 'Benzodiazepines Antiseizure medications Antihisatamines Anticholinergic agents Antiarrythmic agents Steroids
methyldopa Haloperidol (Haldol) Diazepam (Valium) Barbiturates Cimetidine (Tagamet) Atropine Procainamide
Beserpine Chlorpromazine (Thorazine) Flurazepam (Dalmane) Carbamazepine (Tegretol) Beztropine Disopyramide
Clonidine Thioridazine (Mellaril) Clorazepate (Tranxene) Phenytoin (Dilantin) Diphenhydramine Quinidine
Diuretics Fluphenazine (Prolixin) Prazepam (Centrax) Phenobarbital Trihexyphenidyl
Beta-blockers, especially propranolol (Inderal) Perphenazine (Trilafon) Alprazolam (Xanax)
Loxapine (Loxitane) Halazepam (Paxipam)
Molindone (Moban) Triazolam (Halcion)
Tiothixene (Navane) Temazepam (Restoril)
Trifluoperazine (Stelazine) Oxazepam (Serax)
Lorazepam (Ativan)


Environmental sources include overstimulation, radical changes in lifestyle, and sensory impairment. Physical disorders which are mostly induced by the aging process, consist of thyroid and other endocrine-system deprivation; metabolic disturbance, and vitamin deficiency. Psychiatric disorders, such as chronic schizophrenia and depression could also produce cognitive decline.[9]

In summary, the etiological factors of reversible dementia are various, subtle and frequently interactive. Therefore, in-depth medical and psychosocial evaluations are vital for accurate diagnosis and treatment design. It is important for families and patients to understand the difficulties in determining an correct diagnosis and be prepared for probable frustration and confusion during evaluation and assessment process.[2]

Differentiating Pseudodementia from Dementia[edit]

As certain of pseudodementia remains potentially treatable, it is essential that they are distinguished from primarily dementia of the Alzheimer's type (DAT), and multi-infarct dementia (MID). For instance, pseudodementia associated with depression (DD) has been found as the most frequently appearing, while as many as 10% to 20% patients are misdiagnosed as primary degenerative dementia (PDD) or vice versa.[10] A significant overlapping in cognitive and neuropsychological dysfunction in DD and PDD patients seemed to increase the difficulty in diagnosis. However, differences in the severity of impairment and quality of patients' responses could be observed, and DD patients exhibited a greater depressive symptomatology. Additionally, a test of antisaccadic movements may be used to differentiate DD from PDD patients. as PDD patients significantly display poorer performance on this test.[2] A general comparison between aspects of DD and PDD is shown below.

Variable Pseudodementia Dementia
Onset More precise, usually in terms of days or weeks Subtle
Course Rapid, uneven Slow, worse at night
Past history Depression or mania frequently Uncertain relation
Family history Depression or mania Positive family history for dementia in approximately 50% DAT
Mood Depressed; little or no response to sad or funny situations; behavior and affect inconsistent with degree of cognitive deficit Shallow or labile; normal or exaggerated response to sad or funny situations; consistent with degree of cognitive impairment
Cooperation Poor; little effort to perform well; responds often with "I don't know"; apathetic, emphasizes failure Good; frustrated by inability to do well; response to queries approximate con fabricated or perseverated; emphasizes trivial accomplishment
Memory Highlight memory loss; greater impairment of personality features (e.g. confidence, drive, interests, and attention) Denies or minimizes impairments; greater impairment in cognitive features (recent memory and orientation to time and date)
Mini-Mental State Exam (MMSE).[11] Changeable on repeated tests Stable on repeated tests
Symptoms Increased psychologic symptoms:sadness, anxiety, somatic symptoms Increased neurologic symptoms: dysphasia, dyspraxia, agnosia, incontinence
Computed Tomography (CT) and Electroencephalogram (EEG) Normal for age Abnormal


In general, pseudodementia patients present a considerable cognitive deficits, including disorders in learning, memory and psychomotor performance. Substantial evidences from brain imaging such as CT scanning and positron emission tomography (PET) have also revealed abnormalities in brain structure and function.[2]


Since the term of "reversible" has been used, it simply implies a high possibility of recovery from the disease. Cunha (1990) examined the recovery process of 26 patients with reversible dementia. Unfortunately, only 2 patients have found as return to normal function indicated by the MMSE scores.[6] Poor results have also been reported in Copeland et al. (1992)'s studies, as 1 out of 21 DD patients had fully recovered.[12] Thus, attention should be arisen that the diagnosis of reversible or pseudodementia needs to be given with extreme care, and the recovery pattern for individual patient remains uncertain.[2]


  1. ^ Libow, LS (1973-03-21). "Pseudo-senility: acute and reversible organic brain syndromes". J Am Geriatr Soc. American Geriatric Society. 21: 112–20. PMID 4702407. doi:10.1111/j.1532-5415.1973.tb00855.x. 
  2. ^ a b c d e f Nixon, S.J. (1996) Secondary dementias: reversible dementias and pseudomentia in R.L. Adams, O.A. Parsons, J.L. Culbertson & S.J. Nixon (Eds.) Neuropsychology for Clinical Practice: etiology, assessment, and treatment of common neurological disorder. (pp. 107-130). Washington, DC: American Psychological Association
  3. ^ Jones, R.D., Tranel, D., Benton, A. & Paulsen, J (1992). "Differentiating dementia from "pseudodementia" early in the clinical course: utility of neuropsychological tests.". Neuropsychology. 6 (1): 13–21. ISSN 1931-1559. doi:10.1037/0894-4105.6.1.13. 
  4. ^ Henig, Robin Marantz (2009-03-11). "When It Isn't Really Senility". New York Times. Retrieved 20 February 2010. 
  5. ^ "Caregivers May Observe 'Pseudosenility'". Assisted Living Federation of America. 2009-03-17. Retrieved 20 February 2010. 
  6. ^ a b Cunha, U.G.V. (1990). "An investigation of dementia among elderly outpatients". Acta Psychiatrica Scandinavica. 82 (3): 261–263. ISSN 1600-0447. doi:10.1111/j.1600-0447.1990.tb03063.x. 
  7. ^ Thompson,T.L. (1987) Dementia. in R.E. Hales & S.C. Yudofsky (Eds), Textbook of neuropsychiatry (pp.107-124). Washington, DC: American Psychiatric Press
  8. ^ Jenike, M.A. (1988). Depression and other psychiatric disorders in M.S. Albert & M.Moss (Eds.) Geriatric Neuropsychology" (pp.115-144). New York, NY: Guilford Press
  9. ^ Thompson,T.L. (1987) Dementia. In R.E. Hales & S.C. Yudofsky (Eds.), Textbook of neuropsychiatry (pp. 107-124). Washington, DC: American Psychiatric Press
  10. ^ desRosiers, G. (1992). "Primary or depressive dementia: psychometric assessment". Clinical Psychology Review. 12 (3): 307–343. doi:10.1016/0272-7358(92)90140-4. 
  11. ^ Folstein, M.F., Folstein, S.E., & McHugh, P.R. (1975). ""Mini-Mental State": a practical method for grading the cognitive state of patients for the clinician.". Journal of Psychiatry Research. 12 (3): 189–198. PMID 1202204. doi:10.1016/0022-3956(75)90026-6. 
  12. ^ Copeland, J.R.M., Davidson, I.A., Dewey, M.E., Gilmore, C., Larkin, B.A., McWilliam, C., Saunders, P.A., Scott, A., Sharma, V., & Sullivan, C. (1992). "Alzheimer's disease, other dementias, depression and pseudodementia: prevalence, incidence and three-year outcome in Liverpool.". British Journal os Psychiatry. 161 (Aug): 230–239. ISSN 1472-1465. doi:10.1192/bjp.161.2.230.