Pseudodementia

Last updated

Psuedodementia
Other namesDepression-related cognitive dysfunction, depressive cognitive disorder, pseudosenility, [1] reversible dementia [2]
Specialty Psychiatry
Symptoms Sadness, anxiety, somatic symptoms
CausesDepression, schizophrenia, psychosis, and other psychiatric conditions that can impair cognitive functions
Risk factors Depression, mania
TreatmentTreatment of the causative factor such as antidepressants

Pseudodementia (otherwise known as depression-related cognitive dysfunction or depressive cognitive disorder) is a condition that leads to cognitive and functional impairment imitating dementia that is secondary to psychiatric disorders, especially depression. Pseudodementia can develop in a wide range of neuropsychiatric disease such as depression, schizophrenia and other psychosis, mania, dissociative disorders, and conversion disorders. The presentations of pseudodementia may mimic organic dementia, but are essentially reversible on treatment and doesn't lead to actual brain degeneration. However, it has been found that some of the cognitive symptoms associated with pseudodementia can persist as residual symptoms and even transform into true neurodegenerative dementia in some cases. [3]

Contents

Psychiatric conditions, mainly depression, is the strongest risk factor of pseudodementia rather than age. Even though most of the existing studies focused on older age groups, younger adults can develop pseudodementia if they have depression. While aging does affect the cognition and brain function and making it hard to distinguish depressive cognitive disorder from actual dementia, there are differential diagnostic screenings available. [4] It is crucial to confirm the correct diagnosis since depressive cognitive disorder is reversible with proper treatments.

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. Since the symptoms of pseudodementia is highly similar to dementia, it is critical complete differential diagnosis to completely exclude dementia. People with pseudodementia are typically very distressed about the cognitive impairment they experience. Currently, the treatment of pseudodementia is mainly focused on treating depression, cognitive impairment, and dementia. And we have seen improvements in cognitive dysfunction with antidepressants such as SSRI (Selective serotonin Reuptake Inhibitors), SNRI (Serotonin-norepinephrine Reuptake Inhibitors), TCAs (Tricyclic Antidepressants), Zolmitriptan, Vortioxetine, and Cholinesterase Inhibitors.

History

Carl Wernicke is often believed to have been the source of the term pseudodementia (in his native German, pseudodemenz). Despite this belief being held by many of his students, Wernicke never actually used the word in any of his written works. It is possible that this misconception comes from Wernicke's discussions on Ganser's syndrome. [5] Instead, the first written instance of pseudodementia was by one of Wernicke's students, Georg Stertz. [6] However the term itself was not linked to the modern understanding of it until 1961 by psychiatrist Leslie Gordon Kiloh, who noticed patients with cognitive symptoms consistent with dementia who improved with treatment. Kiloh believed that the term should be used to describe a person's presentation, rather than an outright diagnosis. Modern research, however, has shown evidence for the term being used in such a way. [6] Reversible causes of true dementia must be excluded. [7] His term was mainly descriptive. [8] The clinical phenomenon, however, has been well-known since the late 19th century as melancholic dementia. [9]

Doubts about the classification and features of the syndrome, [10] and the misleading nature of the name, led to proposals that the term be dropped. [11] 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 that has held up well in clinical practice, and also highlights those who may have a treatable condition. [12]

Presentation

The history of disturbance in pseudodementia is often short and abrupt onset, while dementia is more often insidious. In addition, there is often minor, or an absence of, any abnormal brain patterns seen via imaging which indicate an organic component to the cognitive decline, such as what one would see in dementia. [13] The key symptoms of pseudodementia include: speech impairments, memory deficits, attention problems, emotional control issues, organization difficulties, and decision making. [14] 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. By contrast, those presenting with organic dementia will often have "near-miss" answers rather than stating that they do not know the answer. This can make diagnosis difficult and result in misdiagnosis as a patient might have organic dementia but answer questions in a way that suggests pseudodementia, or vice versa. [15] In addition, people presenting with pseudodementia often lack the gradual mental decline seen in true dementia. They instead tend to remain at the same level of reduced cognitive function throughout. [13] However, for some, pseudodementia can eventually progress to organic dementia and lead to lowered cognitive function. [16] Because of this, some recommend that elderly patients that present with pseudodementia should receive a full screening for dementia, as well as closely monitor cognitive faculties in order to catch the progression to organic dementia early. [17] 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. [18]

Causes

Pseudodementia refers to "behavioral changes that resemble those of the progressive degenerative dementias, but which are attributable to so-called functional causes". [19] The main cause of pseudodementia is depression. Any age group can develop pseudodementia. In depression, processing centers in the brain responsible for cognitive function and memory are affected, including the prefrontal cortex, amygdala, and hippocampus. Reduced function of the hippocampus results in impaired recognition and recall of memories, a symptom commonly associated with dementia. [20] While not as common, other mental health disorders and comorbidities can also cause symptoms that mimic dementia, and thus must be considered when making a diagnosis. [21]

Diagnosis

Differential diagnosis

While there is currently no cure for dementia, other psychiatric disorders that may result in dementia-like symptoms are able to be treated. Thus, it is essential to complete differential diagnosis, where other possibilities are appropriately ruled out to avoid misdiagnosis and inappropriate treatment plans. [21]

The implementation and application of existing collaborative care models, such as DICE (describe, investigate, create, evaluate), can aid in avoiding misdiagnosis. DICE is a method utilized by healthcare workers to evaluate and manage behavioral and psychological symptoms associated with dementia. [22] Comorbidities (such as vascular, infectious, traumatic, autoimmune, idiopathic, or even becoming malnourished) have the potential to mimic symptoms of dementia and thus must be evaluated for, typically through taking a complete patient history and physical exam. [23] [24] For instance, studies have also shown a relationship between depression and its cognitive effects on everyday functioning and distortions of memory. [25]

Since pseudodementia does not cause deterioration of the brain, brain scans can be used to visualize potential deterioration associated with dementia. 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), the most common type of dementia, compared with a more normal blood flow in those with pseudodementia. Reduced blood flow leads to an inadequate oxygen supply that reaches the brain, causing irreversible cell damage and cell death. [26] [27] In addition, MRI results show medial temporal lobe atrophy, which causes impaired recall of facts and events (declarative memory), in individuals with AD. [28]

Pseudodementia vs. dementia

Pseudodementia symptoms can appear similar to dementia. Due to the similar signs and symptoms, it can result in a misdiagnosis of depression, as well as adverse effects from inaccurately prescribed medications.Generally, dementia involves a steady and irreversible cognitive decline while pseudodementia-induced symptoms are reversible. Thus, once the depression is properly treated or the medication therapy has been modified, depression-induced cognitive impairment can be effectively reversed. [29] Commonly within older adults, diminished mental capacity and social withdrawal are identified as dementia symptoms without considering and ruling out depression. [30] As a result, older adult patients are often misdiagnosed due to insufficient testing.

Cognitive symptoms such as memory loss, slowed movement, or reduced/ slowed speech, are sometimes initially misdiagnosed as dementia, however, further investigation determined that these patients were suffering from a major depressive episode. [31] This is an important distinction as the former is untreatable, whereas the latter is treatable using antidepressant therapy, electroconvulsive therapy, or both. [32] In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology. [7]

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] Other researchers have suggested additional criteria to differentiate pseudodementia from dementia, based on their studies. However, the sample size for these studies are relatively small so the validity of the studies are limited. [33] A systematic review conducted in 2018 reviewed 18 longitudinal studies about pseudodementia. Among the 284 patients that were studied, 33% of the patients developed irreversible dementia while 53% of the patients no longer met the criteria for dementia during follow-up. [34] 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]

VariablePseudodementiaDementia
OnsetMore precise, usually in terms of days or weeksSubtle
CourseRapid, unevenSlow, worse at night
Past historyDepression or mania frequentlyUncertain relation
Family historyDepression or maniaPositive family history for dementia in approximately 50% DAT
MoodDepressed; little or no response to sad or funny situations; behavior and affect inconsistent with degree of cognitive deficitShallow or labile; normal or exaggerated response to sad or funny situations; consistent with degree of cognitive impairment
CooperationPoor; little effort to perform well; responds often with "I don't know"; apathetic, emphasizes failureGood; frustrated by inability to do well; response to queries approximate con fabricated or perseverated; emphasizes trivial accomplishment
MemoryHighlight 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). [35] Changeable on repeated testsStable on repeated tests
SymptomsIncreased psychologic symptoms: sadness, anxiety, somatic symptomsIncreased neurologic symptoms: dysphasia, dyspraxia, agnosia, incontinence
Computed Tomography (CT) and Electroencephalogram (EEG)Normal for ageAbnormal

Management

Pharmacological

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. [29] 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. Hence, the pharmacological treatments for pseudodementia do not directly treat the condition itself but directly treat dementia, depression, and cognitive impairment. These medications include SSRI (Selective Serotonin Reuptake Inhibitor), SNRI (Serotonin-norepinephrine Reuptake Inhibitors), TCAs (Tricyclic antidepressants), Zolmitriptan, and cholinesterase inhibitors. [36]

Non-pharmacological

When pharmacological treatments are ineffective, or in addition to pharmacological treatments, there are a number of non-pharmacological therapies that can be used in the treatment of depression. For some patients, cognitive behavior therapy (This is an effective form of therapy for a wide range of mental illnesses including depression, anxiety disorders, drug abuse problems, etc. that is based on the belief that psychological problems are rooted, in part, in one's own behavior and thought patterns. As such, by changing these patterns using new strategies learned in cognitive behavioral therapy, a patient can learn to better cope. [43] ) or interpersonal therapy (This is a form of therapy that has been used in an integrated manner to treat a wide range of psychiatric disorders. It is based on the belief that a patient's relationships in the past and/or present is directly linked to their mental challenges and by improving those relationships, a patient's mental health can be improved. [44] ) can be used to delve deeper into their symptoms, ways to manage them, and the root causes of a patient's depression. Patient's can chose to participate in these therapies in individual sessions or in a group setting. [4]

Future Research

Given the limitations and amount of current researches and studies about pseudodementia, there are still many questions left to answer. Future research regarding younger age groups is necessary to better characterize the risk factors, further criteria, and correlation of age and development of pseudodementia. Future study should also incorporate more modern technologies such as genetic sequencing, investigation of possible pseudodementia-related biomarkers, [45] and PET scans to better understand the underlying mechanism of pseudodementia. [46] In addition, future studies should incorporate larger sample size to increase the validity of the study results and any groups with higher risk of developing pseudodementia to extend the scope of the study. [47]

Related Research Articles

<span class="mw-page-title-main">Antidepressant</span> Class of medication used to treat depression and other conditions

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

An anxiolytic is a medication or other intervention that reduces anxiety. This effect is in contrast to anxiogenic agents which increase anxiety. Anxiolytic medications are used for the treatment of anxiety disorders and their related psychological and physical symptoms.

<span class="mw-page-title-main">Tricyclic antidepressant</span> Class of medications

Tricyclic antidepressants (TCAs) are a class of medications that are used primarily as antidepressants. TCAs were discovered in the early 1950s and were marketed later in the decade. They are named after their chemical structure, which contains three rings of atoms. Tetracyclic antidepressants (TeCAs), which contain four rings of atoms, are a closely related group of antidepressant compounds.

A psychiatric or psychotropic medication is a psychoactive drug taken to exert an effect on the chemical makeup of the brain and nervous system. Thus, these medications are used to treat mental illnesses. These medications are typically made of synthetic chemical compounds and are usually prescribed in psychiatric settings, potentially involuntarily during commitment. Since the mid-20th century, such medications have been leading treatments for a broad range of mental disorders and have decreased the need for long-term hospitalization, thereby lowering the cost of mental health care. The recidivism or rehospitalization of the mentally ill is at a high rate in many countries, and the reasons for the relapses are under research.

<span class="mw-page-title-main">Sertraline</span> Antidepressant (SSRI class) medication

Sertraline, sold under the brand name Zoloft among others, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class. The effectiveness of sertraline for depression is similar to that of other antidepressants, and the differences are mostly confined to side effects. Sertraline is better tolerated than the older tricyclic antidepressants. Sertraline is effective for panic disorder, social anxiety disorder, generalized anxiety disorder (GAD), and obsessive–compulsive disorder (OCD). Although approved for post-traumatic stress disorder (PTSD), sertraline leads to only modest improvement in this condition. Sertraline also alleviates the symptoms of premenstrual dysphoric disorder (PMDD) and can be used in sub-therapeutic doses or intermittently for its treatment.

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

Venlafaxine, sold under the brand name Effexor among others, is an antidepressant medication of the serotonin–norepinephrine reuptake inhibitor (SNRI) class. It is used to treat major depressive disorder, generalized anxiety disorder, panic disorder, and social anxiety disorder. Studies have shown that venlafaxine improves post-traumatic stress disorder (PTSD). It may also be used for chronic pain. It is taken orally. It is also available as the salt venlafaxine besylate in an extended-release formulation.

Premenstrual dysphoric disorder (PMDD) is a mood disorder characterized by emotional, cognitive, and physical symptoms. PMDD causes significant distress or impairment in menstruating women during the luteal phase of the menstrual cycle. The symptoms occur in the luteal phase, improve within a few days after the onset of menses, and are minimal or absent in the week after menses. PMDD has a profound impact on a woman’s quality of life and dramatically increases the risk of suicidal ideation and even suicide attempts. Many women of reproductive age experience discomfort or mild mood changes prior to menstruation. However, 5–8% experience severe premenstrual syndrome causing significant distress or functional impairment. Within this population of reproductive age, some will meet the criteria for PMDD.

<span class="mw-page-title-main">Serotonin–norepinephrine reuptake inhibitor</span> Class of antidepressant medication

Serotonin–norepinephrine reuptake inhibitors (SNRIs) are a class of antidepressant medications used to treat major depressive disorder (MDD), anxiety disorders, social phobia, chronic neuropathic pain, fibromyalgia syndrome (FMS), and menopausal symptoms. Off-label uses include treatments for attention-deficit hyperactivity disorder (ADHD), obsessive–compulsive disorder (OCD), and migraine prevention. SNRIs are monoamine reuptake inhibitors; specifically, they inhibit the reuptake of serotonin and norepinephrine. These neurotransmitters are thought to play an important role in mood regulation. SNRIs can be contrasted with the selective serotonin reuptake inhibitors (SSRIs) and norepinephrine reuptake inhibitors (NRIs), which act upon single neurotransmitters.

Amotivational syndrome is a chronic psychiatric disorder characterized by signs that are linked to cognitive and emotional states such as detachment, blunted emotion and drives, executive functions like memory and attention, disinterest, passivity, apathy, and a general lack of motivation. This syndrome can be branched into two subtypes - marijuana amotivational syndrome, interchangeably known as cannabis induced amotivational syndrome which is caused by usage and/or dependency of the substance and is primarily associated with long-term effects of cannabis use, and SSRI-induced amotivational syndrome or SSRI-induced apathy caused by the intake of SSRI medication dosage. According to the Handbook of Clinical Psychopharmacology for Therapists, amotivational syndrome is listed as a possible side effect of SSRIs in the treatment of clinical depression. It is a disorder of diminished motivation.

Dysthymia, also known as persistent depressive disorder (PDD), is a mental and behavioral disorder, specifically a disorder primarily of mood, consisting of similar cognitive and physical problems as major depressive disorder, but with longer-lasting symptoms. The concept was used by Robert Spitzer as a replacement for the term "depressive personality" in the late 1970s.

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.

Antidepressant discontinuation syndrome, also called antidepressant withdrawal syndrome, is a condition that can occur following the interruption, reduction, or discontinuation of antidepressant medication following its continuous use of at least a month. The symptoms may include flu-like symptoms, trouble sleeping, nausea, poor balance, sensory changes, akathisia, intrusive thoughts, depersonalization and derealization, mania, anxiety, and depression. The problem usually begins within three days and may last for several weeks or months. Psychosis may rarely occur.

Treatment-resistant depression (TRD) is major depressive disorder in which an affected person does not respond adequately to at least two different antidepressant medications at an adequate dose and for an adequate duration. Inadequate response has most commonly been defined as less than 25% reduction in depressive symptoms following treatment with an antidepressant. Many clinicians and researchers question the construct validity and clinical utility of treatment-resistant depression as currently conceptualized.

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.

<span class="mw-page-title-main">Psychological intervention</span>

In applied psychology, interventions are actions performed to bring about change in people. A wide range of intervention strategies exist and they are directed towards various types of issues. Most generally, it means any activities used to modify behavior, emotional state, or feelings. Psychological interventions have many different applications and the most common use is for the treatment of mental disorders, most commonly using psychotherapy. The ultimate goal behind these interventions is not only to alleviate symptoms but also to target the root cause of mental disorders.

A serotonin–norepinephrine–dopamine reuptake inhibitor (SNDRI), also known as a triple reuptake inhibitor (TRI), is a type of drug that acts as a combined reuptake inhibitor of the monoamine neurotransmitters serotonin, norepinephrine, and dopamine. It does this by concomitantly inhibiting the serotonin transporter (SERT), norepinephrine transporter (NET), and dopamine transporter (DAT), respectively. Inhibition of the reuptake of these neurotransmitters increases their extracellular concentrations and, therefore, results in an increase in serotonergic, adrenergic, and dopaminergic neurotransmission. The naturally-occurring and potent SNDRI cocaine is widely used recreationally and often illegally for the euphoric effects it produces.

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

Vilazodone, sold under the brand name Viibryd among others, is a medication used to treat major depressive disorder. It is classified as a serotonin modulator and is taken by mouth.

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.

<span class="mw-page-title-main">Selective serotonin reuptake inhibitor</span> Class of antidepressant medication

Selective serotonin reuptake inhibitors (SSRIs) are a class of drugs that are typically used as antidepressants in the treatment of major depressive disorder, anxiety disorders, and other psychological conditions.

References

  1. ↑ Libow LS (March 1973). "Pseudo-senility: acute and reversible organic brain syndromes". Journal of the American Geriatrics Society. 21 (3): 112–120. doi:10.1111/j.1532-5415.1973.tb00855.x. PMID   4702407. S2CID   23256265.
  2. 1 2 3 4 Nixon SJ (1996). "Secondary dementias: reversible dementias and pseudomentia". In Adams RL, Parsons OA, Culbertson JL, Nixon SJ (eds.). Neuropsychology for Clinical Practice: etiology, assessment, and treatment of common neurological disorder. Washington, DC: American Psychological Association. pp. 107–130. doi:10.1037/10198-003. ISBN   1-55798-298-8.
  3. ↑ Sekhon S, Marwaha R (2024), "Depressive Cognitive Disorders", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   32644682 , retrieved 2024-07-31
  4. 1 2 Mouta S, Fonseca Vaz I, Pires M, Ramos S, Figueiredo D (2023-08-22). "What do we know about pseudodementia?". General Psychiatry. 36 (4): e100939. doi:10.1136/gpsych-2022-100939. ISSN   2517-729X. PMC   10445398 . PMID   37622032.
  5. ↑ Vinet-Couchevellou M, Sauvagnat F (April 2015). "Pseudodémence, de quoi parle-t-on ? Partie I: à la recherche de la pseudodémence de Wernicke". L'Encéphale (in French). 41 (2): 130–136. doi:10.1016/j.encep.2013.10.005. PMID   24513017.
  6. 1 2 Vinet-Couchevellou M, Sauvagnat F (June 2015). "Pseudodémence, de quoi parle-t-on ? Partie II: de Stertz à Alzheimer: une maladie psychogène après traumatisme". L'Encéphale (in French). 41: S37–S43. doi:10.1016/j.encep.2014.08.015. PMID   25439856.
  7. 1 2 Warrell D, Timothy C, John F (2010). "Neuropsychiatric disorders". Oxford Textbook of Medicine. pp. 5268–5283. doi:10.1093/med/9780199204854.003.2604. ISBN   9780199204854.
  8. ↑ Kiloh LG (1961). "Pseudo-dementia". Acta Psychiatrica Scandinavica. 37 (4): 336–351. doi:10.1111/j.1600-0447.1961.tb07367.x. PMID   14455934. S2CID   221390518.
  9. ↑ Berrios GE (May 1985). ""Depressive pseudodementia" or "Melancholic dementia": a 19th century view". Journal of Neurology, Neurosurgery, and Psychiatry. 48 (5): 393–400. doi:10.1136/jnnp.48.5.393. PMC   1028324 . PMID   3889224.
  10. ↑ McAllister TW (May 1983). "Overview: pseudodementia". The American Journal of Psychiatry. 140 (5): 528–533. doi:10.1176/ajp.140.5.528. PMID   6342420.
  11. ↑ Poon LW (1991). "Toward an understanding of cognitive functioning in geriatric depression". International Psychogeriatrics. 4 (4): 241–266. doi:10.1017/S1041610292001297. PMID   1288665.
  12. ↑ Sachdev P, Reutens S (2003). "The Nondepressive Pseudodementias". In Emery VO, Oxman TE (eds.). Dementia: Presentations, Differential Diagnosis, and Nosology . JHU Press. p.  418. ISBN   0-8018-7156-5.
  13. 1 2 Sachdev PS, Smith JS, Angus-Lepan H, Rodriguez P (March 1990). "Pseudodementia twelve years on". Journal of Neurology, Neurosurgery, and Psychiatry. 53 (3): 254–259. doi:10.1136/jnnp.53.3.254. PMC   1014139 . PMID   2324757.
  14. ↑ Mouta S, Fonseca Vaz I, Pires M, Ramos S, Figueiredo D (2023-08-22). "What do we know about pseudodementia?". General Psychiatry. 36 (4): e100939. doi:10.1136/gpsych-2022-100939. PMC   10445398 . PMID   37622032.
  15. ↑ Good MI (1981-06-01). "Pseudodementia and physical findings masking significant psychopathology". American Journal of Psychiatry. 138 (6): 811–814. doi:10.1176/ajp.138.6.811. ISSN   0002-953X. PMID   7246813.
  16. ↑ Yu Y, Wang S (August 2021). "Evolution from pseudodementia to dementia: is depressive symptom an optional extra?". International Psychogeriatrics. 33 (8): 751–754. doi:10.1017/S1041610220003890. ISSN   1041-6102. PMID   34423754.
  17. ↑ Sáez-Fonseca JA, Lee L, Walker Z (2007-08-01). "Long-term outcome of depressive pseudodementia in the elderly". Journal of Affective Disorders. 101 (1): 123–129. doi:10.1016/j.jad.2006.11.004. ISSN   0165-0327. PMID   17184844.
  18. ↑ Wells CE (July 1979). "Pseudodementia". The American Journal of Psychiatry. 136 (7): 895–900. doi:10.1176/ajp.136.7.895. PMID   453349.
  19. ↑ Jones R, Tranel D, Benton A, Paulsen J (January 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.
  20. ↑ Trifu SC, Trifu AC, Aluaş E, Tătaru MA, Costea RV (2020). "Brain changes in depression". Romanian Journal of Morphology and Embryology. 61 (2): 361–370. doi:10.47162/RJME.61.2.06. ISSN   1220-0522. PMC   7864313 . PMID   33544788.
  21. 1 2 Brodaty H, Connors MH (January 2020). "Pseudodementia, pseudo-pseudodementia, and pseudodepression". Alzheimer's & Dementia. 12 (1): e12027. doi:10.1002/dad2.12027. PMC   7167375 . PMID   32318620.
  22. ↑ Albrecht T, Schroeder M, LeCaire T, Endicott S, Marschall K, Felten K, et al. (2022-11-01). "Training dementia care professionals to help caregivers improve the management of behavioral and psychological symptoms of dementia using the DICE Approach: A pilot study". Geriatric Nursing. 48: 74–79. doi:10.1016/j.gerinurse.2022.08.016. ISSN   0197-4572. PMID   36155312.
  23. ↑ Kverno KS, Velez R (March 2018). "Comorbid dementia and depression: the case for integrated care". The Journal for Nurse Practitioners. 14 (3): 196–201. doi:10.1016/j.nurpra.2017.12.032.
  24. ↑ Scott KR, Barrett AM (April 2007). "Dementia syndromes: evaluation and treatment". Expert Review of Neurotherapeutics. 7 (4): 407–422. doi:10.1586/14737175.7.4.407. ISSN   1473-7175. PMC   2536654 . PMID   17425495.
  25. ↑ Sejunaite K, Lanza C, Riepe MW (March 2018). "Everyday false memories in older persons with depressive disorder". Psychiatry Research. 261: 456–463. doi:10.1016/j.psychres.2018.01.030. PMID   29407717.
  26. ↑ "What Happens to the Brain in Alzheimer's Disease?". National Institute on Aging. 2024-01-19. Retrieved 2024-07-31.
  27. ↑ Bracko O, Cruz Hernández JC, Park L, Nishimura N, Schaffer CB (July 2021). "Causes and consequences of baseline cerebral blood flow reductions in Alzheimer's disease". Journal of Cerebral Blood Flow & Metabolism. 41 (7): 1501–1516. doi:10.1177/0271678X20982383. ISSN   0271-678X. PMC   8221770 . PMID   33444096.
  28. ↑ Parker G, Hadzi-Pavlovic D, Eyers K (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.
  29. 1 2 Thakur ME (2007). "Pseudodementia" . In Markides KS (ed.). Encyclopedia of Health & Aging. Gale Virtual Reference Library. SAGE Reference. pp. 477–478. Retrieved 5 July 2018.
  30. ↑ Venes D (2017). Taber's Cyclopedic Medical Dictionary. Philadelphia: F.A. Davis Company.
  31. ↑ Caine ED (December 1981). "Pseudodementia. Current concepts and future directions". Archives of General Psychiatry. 38 (12): 1359–1364. doi:10.1001/archpsyc.1981.01780370061008. PMID   7316680.
  32. ↑ Bulbena A, Berrios GE (January 1986). "Pseudodementia: facts and figures". The British Journal of Psychiatry. 148 (1): 87–94. doi:10.1192/bjp.148.1.87. PMID   3955324.
  33. ↑ Yousef G, Ryan WJ, Lambert T, Pitt B, Kellett J (June 1998). "A preliminary report: a new scale to identify the pseudodementia syndrome". International Journal of Geriatric Psychiatry. 13 (6): 389–399. doi:10.1002/(sici)1099-1166(199806)13:6<389::aid-gps782>3.0.co;2-c. ISSN   0885-6230. PMID   9658274.
  34. ↑ Connors MH, Quinto L, Brodaty H (April 2019). "Longitudinal outcomes of patients with pseudodementia: a systematic review". Psychological Medicine. 49 (5): 727–737. doi:10.1017/S0033291718002829. ISSN   1469-8978. PMID   30319082.
  35. ↑ Folstein MF, Folstein SE, McHugh PR (November 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.
  36. ↑ Sekhon S, Marwaha R (2020). "Depressive Cognitive Disorders (Pseudodementia)". Stat Pearls. Treasure Island (FL): StatPearls Publishing. PMID   32644682.
  37. ↑ Edinoff AN, Akuly HA, Hanna TA, Ochoa CO, Patti SJ, Ghaffar YA, et al. (2021-08-05). "Selective Serotonin Reuptake Inhibitors and Adverse Effects: A Narrative Review". Neurology International. 13 (3): 387–401. doi: 10.3390/neurolint13030038 . ISSN   2035-8385. PMC   8395812 . PMID   34449705.
  38. ↑ Strawn JR, Mills JA, Poweleit EA, Ramsey LB, Croarkin PE (July 2023). "Adverse Effects of Antidepressant Medications and their Management in Children and Adolescents". Pharmacotherapy: The Journal of Human Pharmacology and Drug Therapy. 43 (7): 675–690. doi:10.1002/phar.2767. ISSN   0277-0008. PMC   10378577 . PMID   36651686.
  39. ↑ Gillman PK (July 2007). "Tricyclic antidepressant pharmacology and therapeutic drug interactions updated". British Journal of Pharmacology. 151 (6): 737–748. doi:10.1038/sj.bjp.0707253. ISSN   0007-1188. PMC   2014120 . PMID   17471183.
  40. ↑ Bonilla-Jaime H, Sánchez-Salcedo JA, Estevez-Cabrera MM, Molina-Jiménez T, Cortes-Altamirano JL, Alfaro-Rodríguez A (February 2022). "Depression and Pain: Use of Antidepressants". Current Neuropharmacology. 20 (2): 384–402. doi:10.2174/1570159X19666210609161447. PMC   9413796 . PMID   34151765.
  41. ↑ Bird S, Derry S, Moore RA (2014-05-21). Cochrane Pain, Palliative and Supportive Care Group (ed.). "Zolmitriptan for acute migraine attacks in adults". Cochrane Database of Systematic Reviews (5): CD008616. doi:10.1002/14651858.CD008616.pub2. PMC   6485805 . PMID   24848613.
  42. ↑ Sharma K (2019-06-11). "Cholinesterase inhibitors as Alzheimer's therapeutics (Review)". Molecular Medicine Reports. 20 (2): 1479–1487. doi:10.3892/mmr.2019.10374. ISSN   1791-2997. PMC   6625431 . PMID   31257471.
  43. ↑ "Cognitive Behavioral Therapy (CBT)". American Psychological Association. 2017-07-31. Retrieved 2024-08-02.
  44. ↑ Rajhans P, Hans G, Kumar V, Chadda RK (2020-01-17). "Interpersonal Psychotherapy for Patients with Mental Disorders". Indian Journal of Psychiatry. 62 (Suppl 2): S201–S212. doi: 10.4103/psychiatry.IndianJPsychiatry_771_19 . ISSN   0019-5545. PMC   7001362 . PMID   32055063.
  45. ↑ Nascimento KK, Silva KP, Malloy-Diniz LF, Butters MA, Diniz BS (October 2015). "Plasma and cerebrospinal fluid amyloid-β levels in late-life depression: A systematic review and meta-analysis". Journal of Psychiatric Research. 69: 35–41. doi:10.1016/j.jpsychires.2015.07.024. ISSN   1879-1379. PMC   5102150 . PMID   26343592.
  46. ↑ Butters MA, Klunk WE, Mathis CA, Price JC, Ziolko SK, Hoge JA, et al. (2008). "Imaging Alzheimer pathology in late-life depression with PET and Pittsburgh Compound-B". Alzheimer Disease and Associated Disorders. 22 (3): 261–268. doi:10.1097/WAD.0b013e31816c92bf. ISSN   1546-4156. PMC   2636843 . PMID   18580591.
  47. ↑ Brodaty H, Connors MH (2020-04-19). "Pseudodementia, pseudo-pseudodementia, and pseudodepression". Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring. 12 (1): e12027. doi:10.1002/dad2.12027. ISSN   2352-8729. PMC   7167375 . PMID   32318620.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.