Pseudodementia

Pseudodementia
Pseudodementia
Other names	Depression-related cognitive dysfunction, depressive cognitive disorder, pseudosenility, reversible dementia
Specialty	Psychiatry

Last updated April 13, 2024

Pseudodementia (otherwise known as depression-related cognitive dysfunction or depressive cognitive disorder) is a condition where mental cognition can be temporarily decreased. The term pseudodementia is applied to the range of functional psychiatric conditions such as depression, schizophrenia and other psychosis, mania, dissociative disorder and conversion disorder that may mimic organic dementia, but are essentially reversible on treatment. Pseudodementia typically involves three cognitive components: memory issues, deficits in executive functioning, and deficits in speech and language. Specific cognitive symptoms might include trouble recalling words or remembering things in general, decreased attentional control and concentration, difficulty completing tasks or making decisions, decreased speed and fluency of speech, and impaired processing speed. People with pseudodementia are typically very distressed about the cognitive impairment they experience. Two treatments found to be effective for the treatment of depression may also be beneficial in the treatment of pseudodementia: Cognitive behavioral therapy (CBT) which identifies behaviors that positively and negatively impact mood, and Interpersonal therapy which focuses on identifying ways in which interpersonal relationships contribute to depression.

Presentation

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.^[3]

Causes

Pseudodementia refers to "behavioral changes that resemble those of the progressive degenerative dementias, but which are attributable to so-called functional causes".^[4] The main cause is depression.

Diagnosis

Differential diagnosis

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.^[5] For instance, studies have also shown a relationship between depression and its cognitive effects on everyday functioning and distortions of memory.^[6]

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 (AD) compared with a more normal blood flow in those with pseudodementia, and the MRI shows medial temporal lobe atrophy in people with AD.^[7]

Pseudodementia vs. dementia

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.^[8] 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.^[8] In addition, diminished mental capacity and social withdrawal are commonly identified as symptoms in the elderly but oftentimes is due to symptoms of depression.^[9] 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.^[10] This was an important distinction as the former was untreatable and progressive and the latter treatable with antidepressant therapy, electroconvulsive therapy, or both.^[11] In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology.^[12]

A significant overlap in cognitive and neuropsychological dysfunction in Dementia and pseudodementia patients increases the difficulty in diagnosis. Differences in the severity of impairment and quality of patients' responses can be observed, and a test of antisaccadic movements may be used to differentiate the two, as pseudodementia patients have poorer performance on this test.^[2] Individuals with pseudodementia 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]

A comparison between dementia and pseudodementia is shown below.^[2]

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).^[13]	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

Treatments

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.^[8] 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 Alzheimer's disease (most frequent dementia) and improves cognitive function for a period of time.^[14]

History

The term was first coined in 1961 by psychiatrist Leslie Kiloh, who noticed patients with cognitive symptoms consistent with dementia who improved with treatment. Reversible causes of true dementia must be excluded.^[12] His term was mainly descriptive.^[15] The clinical phenomenon, however, was well-known since the late 19th century as melancholic dementia.^[16]

Doubts about the classification and features of the syndrome,^[17] and the misleading nature of the name, led to proposals that the term be dropped.^[18] 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.^[19]

Related Research Articles

Antidepressants are a class of medications used to treat major depressive disorder, anxiety disorders, chronic pain, and addiction.

Major depressive disorder (MDD), also known as clinical depression, is a mental disorder characterized by at least two weeks of pervasive low mood, low self-esteem, and loss of interest or pleasure in normally enjoyable activities. Introduced by a group of US clinicians in the mid-1970s, the term was adopted by the American Psychiatric Association for this symptom cluster under mood disorders in the 1980 version of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III), and has become widely used since.

Dementia is a syndrome associated with many neurodegenerative diseases, which is characterized by a general decline in cognitive abilities that impacts a person's ability to perform everyday activities. This typically involves problems with memory, thinking, behavior, and motor control. Aside from memory impairment and a disruption in thought patterns, the most common symptoms include emotional problems, difficulties with language, and decreased motivation. The symptoms may be described as occurring in a continuum over several stages. Dementia ultimately has a significant effect on the individual, caregivers, and on social relationships in general. A diagnosis of dementia requires the observation of a change from a person's usual mental functioning and a greater cognitive decline than what is caused by normal aging.

Cognitive disorders (CDs), also known as neurocognitive disorders (NCDs), are a category of mental health disorders that primarily affect cognitive abilities including learning, memory, perception, and problem-solving. Neurocognitive disorders include delirium, mild neurocognitive disorders, and major neurocognitive disorder. They are defined by deficits in cognitive ability that are acquired, typically represent decline, and may have an underlying brain pathology. The DSM-5 defines six key domains of cognitive function: executive function, learning and memory, perceptual-motor function, language, complex attention, and social cognition.

Atypical depression is defined in the DSM-IV as depression that shares many of the typical symptoms of major depressive disorder or dysthymia but is characterized by improved mood in response to positive events. In contrast to those with atypical depression, people with melancholic depression generally do not experience an improved mood in response to normally pleasurable events. Atypical depression also often features significant weight gain or an increased appetite, hypersomnia, a heavy sensation in the limbs, and interpersonal rejection sensitivity that results in significant social or occupational impairment.

<span class="mw-page-title-main">Moclobemide</span> Antidepressant

Moclobemide, sold under the brand names Amira, Aurorix, Clobemix, Depnil and Manerix among others, is a reversible inhibitor of monoamine oxidase A (RIMA) drug primarily used to treat depression and social anxiety. It is not approved for use in the United States, but is approved in other Western countries such as Canada, the UK and Australia. It is produced by affiliates of the Hoffmann–La Roche pharmaceutical company. Initially, Aurorix was also marketed by Roche in South Africa, but was withdrawn after its patent rights expired and Cipla Medpro's Depnil and Pharma Dynamic's Clorix became available at half the cost.

Treatment-resistant depression (TRD) is a term used in psychiatry to describe people with major depressive disorder (MDD) who do not respond adequately to a course of appropriate antidepressant medication within a certain time. Definitions of treatment-resistant depression vary, and they do not include a resistance to psychotherapy. Inadequate response has most commonly been defined as less than 50% reduction in depressive symptoms following treatment with at least one antidepressant medication, although definitions vary widely. Some other factors that may contribute to inadequate treatment are: a history of repeated or severe adverse childhood experiences, early discontinuation of treatment, insufficient dosage of medication, patient noncompliance, misdiagnosis, cognitive impairment, low income and other socio-economic variables, and concurrent medical conditions, including comorbid psychiatric disorders. Cases of treatment-resistant depression may also be referred to by which medications people with treatment-resistant depression are resistant to. In treatment-resistant depression adding further treatments such as psychotherapy, lithium, or aripiprazole is weakly supported as of 2019.

Organic brain syndrome, also known as organic brain disease, organic brain damage, organic brain disorder, organic mental syndrome, or organic mental disorder, refers to any syndrome or disorder of mental function whose cause is alleged to be known as organic (physiologic) rather than purely of the mind. These names are older and nearly obsolete general terms from psychiatry, referring to many physical disorders that cause impaired mental function. They are meant to exclude psychiatric disorders. Originally, the term was created to distinguish physical causes of mental impairment from psychiatric disorders, but during the era when this distinction was drawn, not enough was known about brain science for this cause-based classification to be more than educated guesswork labeled with misplaced certainty, which is why it has been deemphasized in current medicine. While mental or behavioural abnormalities related to the dysfunction can be permanent, treating the disease early may prevent permanent damage in addition to fully restoring mental functions. An organic cause to brain dysfunction is suspected when there is no indication of a clearly defined psychiatric or "inorganic" cause, such as a mood disorder.

A major depressive episode (MDE) is a period characterized by symptoms of major depressive disorder. Those affected primarily exhibit a depressive mood for at least two weeks or more, and a loss of interest or pleasure in everyday activities. Other symptoms can include feelings of emptiness, hopelessness, anxiety, worthlessness, guilt, irritability, changes in appetite, difficulties in concentration, difficulties remembering details, making decisions, and thoughts of suicide. Insomnia or hypersomnia and aches, pains, or digestive problems that are resistant to treatment may also be present.

The emphasis of the treatment of bipolar disorder is on effective management of the long-term course of the illness, which can involve treatment of emergent symptoms. Treatment methods include pharmacological and psychological techniques.

Alcohol-related dementia (ARD) is a form of dementia caused by long-term, excessive consumption of alcohol, resulting in neurological damage and impaired cognitive function.

Bipolar II disorder (BP-II) is a mood disorder on the bipolar spectrum, characterized by at least one episode of hypomania and at least one episode of major depression. Diagnosis for BP-II requires that the individual must never have experienced a full manic episode. Otherwise, one manic episode meets the criteria for bipolar I disorder (BP-I).

Post-acute withdrawal syndrome (PAWS) is a hypothesized set of persistent impairments that occur after withdrawal from alcohol, opiates, benzodiazepines, antidepressants, and other substances. Infants born to mothers who used substances of dependence during pregnancy may also experience a PAWS. While PAWS has been frequently reported by those withdrawing from opiate and alcohol dependence, the research has limitations. Protracted benzodiazepine withdrawal has been observed to occur in some individuals prescribed benzodiazepines.

Management of depression is the treatment of depression that may involve a number of different therapies: medications, behavior therapy, psychotherapy, and medical devices.

In psychology and neuroscience, executive dysfunction, or executive function deficit, is a disruption to the efficacy of the executive functions, which is a group of cognitive processes that regulate, control, and manage other cognitive processes. Executive dysfunction can refer to both neurocognitive deficits and behavioural symptoms. It is implicated in numerous psychopathologies and mental disorders, as well as short-term and long-term changes in non-clinical executive control. Executive dysfunction is the mechanism underlying ADHD Paralysis, and in a broader context, it can encompass other cognitive difficulties like planning, organizing, initiating tasks and regulating emotions. It is a core characteristic of ADHD and can elucidate numerous other recognized symptoms.

Major depressive disorder, often simply referred to as depression, is a mental disorder characterized by prolonged unhappiness or irritability. It is accompanied by a constellation of somatic and cognitive signs and symptoms such as fatigue, apathy, sleep problems, loss of appetite, loss of engagement, low self-regard/worthlessness, difficulty concentrating or indecisiveness, or recurrent thoughts of death or suicide.

Depression is one of the most common psychiatric symptoms in Alzheimer's disease, occurring at all stages of the disease, but it often appears in a different form than other depressive disorders. In 2000, a workgroup of the U.S. National Institute of Mental Health created a set of provisional diagnostic criteria for depression of Alzheimer disease (dAD) as a separate diagnostic entity in its own right.

Late-life depression refers to depression occurring in older adults and has diverse presentations, including as a recurrence of early-onset depression, a new diagnosis of late-onset depression, and a mood disorder resulting from a separate medical condition, substance use, or medication regimen. Research regarding late-life depression often focuses on late-onset depression, which is defined as a major depressive episode occurring for the first time in an older person.

Melancholic depression, or depression with melancholic features, is a DSM-IV and DSM-5 specifier of depressive disorders. The specifier is used to distinguish clinically relevant subsets of causes and symptoms that have the potential to influence treatment.

Steroid dementia syndrome describes the signs and symptoms of hippocampal and prefrontal cortical dysfunction, such as deficits in memory, attention, and executive function, induced by glucocorticoids. Dementia-like symptoms have been found in some individuals who have been exposed to glucocorticoid medication, often dispensed in the form of asthma, arthritis, and anti-inflammatory steroid medications. The condition reverses, but not always completely, within months after steroid treatment is stopped.

References

↑ Libow LS (March 1973). "Pseudo-senility: acute and reversible organic brain syndromes". J Am Geriatr Soc. 21 (3): 112–20. doi:10.1111/j.1532-5415.1973.tb00855.x. PMID 4702407. S2CID 23256265.
1 2 3 4 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
↑ Wells, CE (May 1979). "Pseudodementia". American Journal of Psychiatry. 136 (7): 895–900. doi:10.1176/ajp.136.7.895. PMID 453349.
↑ 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)
↑ 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. https://doi.org/10.1016/j.nurpra.2017.12.032
↑ Sjunaite, Karolina, Claudia Lanza, and Matthias W. Riepe. “Everyday false memories in older persons with depressive disorder.” Psychiatry Research 261 (2018): 456-463. https://doi.org/10.1016/j.psychres.2018.01.030
↑ 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.
1 2 3 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)
↑ Venes, Donald. Taber's Cyclopedic Medical Dictionary.Philadelphia: F.A. Davis Company, [2017] Print.
↑ 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.
↑ 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.
1 2 Warrell, David; Timothy, Cox; John, Firth (2010). "Neuropsychiatric disorders". Oxford Textbook of Medicine. pp. 5268–5283. doi:10.1093/med/9780199204854.003.2604. ISBN 9780199204854.
↑ Folstein MF, Folstein SE, McHugh PR (November 1975). "'Mini-mental state'. A practical method for grading the cognitive state of patients for the clinician". J Psychiatr Res. 12 (3): 189–98. doi:10.1016/0022-3956(75)90026-6. PMID 1202204.
↑ 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)
↑ Kiloh, Leslie Gordon (1961). "Pseudodementia". Acta Psychiatr Scand . 37 (4): 336–51. doi:10.1111/j.1600-0447.1961.tb07367.x. PMID 14455934. S2CID 221390518.
↑ Berrios GE (May 1985). ""Depressive pseudodementia" or "Melancholic dementia": a 19th century view". J. Neurol. Neurosurg. Psychiatry. 48 (5): 393–400. doi:10.1136/jnnp.48.5.393. PMC 1028324 . PMID 3889224.
↑ McAllister, TW (May 1983). "Overview: Pseudodementia". American Journal of Psychiatry. 140 (5): 528–33. doi:10.1176/ajp.140.5.528. PMID 6342420.
↑ Poon, Leonard W (1991). "Toward an understanding of cognitive functioning in geriatric depression". International Psychogeriatrics. 4 (4): 241–66. doi:10.1017/S1041610292001297. PMID 1288665.
↑ 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.