Pseudosenility
 | This article needs more reliable medical references for verification or relies too heavily on primary sources. (February 2012) |  |
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][2] A more specific term "pseudodementia" refers to "behavioral changes that resemble those of the progressive degenerative dementias, but which are attributable to so-called functional causes".[3]
Causes
Factors that contribute to cognitive decline can 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 listed medications which may induce cognitive change in elder people.[4]
| 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.[4]
The causes of reversible dementia are various, subtle and frequently interactive. In-depth medical and psychosocial evaluations are vital for accurate diagnosis and treatment design.[2]
Diagnosis
Differentiating pseudodementia from dementia
Since pseudodementia is potentially treatable, it is essential that it is 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.[6] 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).[7] | 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 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]
References
- ^ Libow, LS (1973-03-21). "Pseudo-senility: acute and reversible organic brain syndromes". J Am Geriatr Soc. 21 (3). American Geriatric Society: 112–20. doi:10.1111/j.1532-5415.1973.tb00855.x. PMID 4702407.
- ^ a b c d e 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
- ^ 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. doi:10.1037/0894-4105.6.1.13. ISSN 1931-1559.
{{cite journal}}: CS1 maint: multiple names: authors list (link) - ^ a b Thompson, T.L. (1987) Dementia. in R.E. Hales & S.C. Yudofsky (Eds), Textbook of neuropsychiatry (pp.107-124). Washington, DC: American Psychiatric Press
- ^ 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
- ^ desRosiers, G. (1992). "Primary or depressive dementia: psychometric assessment". Clinical Psychology Review. 12 (3): 307–343. doi:10.1016/0272-7358(92)90140-4.
- ^ 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 Psychiatric Research. 12 (3): 189–198. doi:10.1016/0022-3956(75)90026-6. PMID 1202204.
{{cite journal}}: CS1 maint: multiple names: authors list (link)
Further reading
- Michel JM, Sellal F (June 2011). "["Reversible" dementia in 2011]". Geriatr Psychol Neuropsychiatr Vieil (Review) (in French). 9 (2): 211–25. doi:10.1684/pnv.2011.0274. PMID 21690030.
- Oliveira LM, Nitrini R, Román GC (2019). "Normal-pressure hydrocephalus: A critical review". Dement Neuropsychol (Review). 13 (2): 133–143. doi:10.1590/1980-57642018dn13-020001. PMC 6601311. PMID 31285787.
- Sahyouni R, Goshtasbi K, Mahmoodi A, Tran DK, Chen JW (December 2017). "Chronic Subdural Hematoma: A Perspective on Subdural Membranes and Dementia". World Neurosurg (Review). 108: 954–958. doi:10.1016/j.wneu.2017.09.063. PMC 5705282. PMID 28935547.
- Sekhon S, Marwaha R (2020). "Depressive Cognitive Disorders (Pseudodementia)". Stat Pearls. PMID 32644682.
{{cite journal}}: Cite has empty unknown parameter:|1=(help) - Wesley SF, Ferguson D (April 2019). "Autoimmune Encephalitides and Rapidly Progressive Dementias". Semin Neurol (Review). 39 (2): 283–292. doi:10.1055/s-0039-1678583. PMID 30925620.