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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.

StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-.

Depressive Cognitive Disorders

Sandeep Sekhon; Raman Marwaha.

Author Information and Affiliations

Authors

Sandeep Sekhon1; Raman Marwaha2.

Affiliations
1 Delhi University/Maulana Azad Medical College, New Delhi, India
2 Case Western Reserve Un/MetroHealth MC

Last Update: July 4, 2022.

Continuing Education Activity

Depressive cognitive disorders, also called pseudodementia (a term founded by Kiloh in the year
1961), is defined as the cognitive and functional impairment imitating neurodegenerative
disorders caused secondary to neuropsychiatric symptoms. Depression with cognitive
impairment was given less significance in the past. Though the current practice has given
heightening attention to these disorders, as it has been found that the cognitive symptoms
associated with depression persist, as residual symptoms (in addition to mood symptoms), and in
some cases transform into true neurocognitive dementia over time, these cognitive distortions
considerably affect the functioning and increase the risk of recurrence of a depressive disorder in
the patients. This activity will review the role of the interprofessional team in the diagnosis and
treatment of this condition.

Objectives:

Identify the etiology of pseudodementia medical conditions and emergencies.

Review the evaluation of pseudodementia.

Outline the management options available for pseudodementia.

Describe how interprofessional teams can improve communication and care of patients
with pseudodementia.

Access free multiple choice questions on this topic.

Introduction
Depressive cognitive disorders, also called pseudodementia (a term founded by Kiloh in the year
1961), is defined as the cognitive and functional impairment imitating neurodegenerative
disorders caused secondary to neuropsychiatric symptoms.[1] Depression with cognitive
impairment was given less significance in the past. Though the current practice has given
heightening attention to these disorders, as it has been found that the cognitive symptoms
associated with depression persist, as residual symptoms (in addition to mood symptoms), and in
some cases transform into true neurocognitive dementia over time, these cognitive distortions
affect the functioning considerably and increase the risk of recurrence of a depressive disorder in

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the patients.

Since the 1980s, depressive cognitive disorders have been incorporated as part of the reversible
and treatable forms of dementia, and in the 1990s, it became more noticeable that depression
with cognitive distortion can be the prodromal phase of neurodegenerative dementia that is
irreversible. Recent research studies found that a depressive disorder is correlated with a
heightened risk and acts as a strong predictor of developing true dementia. Depression with
cognitive impairment nearly always implies incipient dementia and should prompt the
professional to begin a relevant diagnostic workup.[2] Based on these findings, the term
pseudodementia has been strongly criticized and is considered inappropriate and misleading.

According to the diagnostic and statistical manual of mental disorders, fifth edition (DSM-5),
cognitive impairment like difficulty thinking, concentrating, and decision making are categorized
as core symptoms of depression, but a description of reversible dementia secondary to
neuropsychiatric disorders is not yet considered as a formal diagnosis in the classification
system.[3] In the elderly population, two distinct forms of mixed mood and cognitive disruptions
are found. They can present with a preliminary mood disorder associated with cognitive
disruption, or they can present with a preliminary dementing disorder that is associated with
depression. Numerous overlapping characteristics make it difficult to distinguish the two. The
connection between depressive disorder and neurodegenerative dementia is complicated and
intricate. Cognitive impairment has been found to be persistent even after the depressive phase
has remitted.[4] The entire picture becomes more challenging when the depression is part of a
bipolar disorder.[5]

Mania in the elderly also has atypical presentation as compared to younger patients. They are
often misdiagnosed as having dementia (Manic Pseudodementia) secondary to the pressured
speech, and hyperkinesis is seen in manic elderly patients.[6]

Although in current practice, the term pseudodementia has been considered redundant and
misleading, its concept inaugurated a useful principle that every physician should think of
depression as an etiology in a patient presenting with symptoms of neurodegenerative dementia
and vice versa before formulating the final diagnosis.[7]

Over the years, pseudodementia has remained valuable in promoting discussion of numerous
treatable neuropsychiatric symptoms, but in recent times its use is strongly condemned in clinical
practice. Despite the fact that it helps clinicians to think about treatable and reversible causes of
dementing illness, it has major limitations. It implies that the patient has either an organic
disorder or a functional impairment, but most of the patients have components of both. It is a
descriptive term and should not be used as a diagnostic category. ’cognitive impairment’ has
been proposed to be used instead of pseudodementia.[8]

Etiology
The long-term persistence of inflammatory processes leads to cognitive deficits in depression.[9]
It is presented in two different forms— ‘depressive cognitive disorders’ or the ‘Wernicke
pseudodementia.’ The latter is considered a more severe form.

Depression is the dominating cause of memory loss in the elderly population. Numerous factors
contribute to the development of depressive cognitive disorders:

Neurotransmitter hypothesis— The serotonin hypothesis formulates the basis of the

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treatment of major depressive disorder and the accompanying memory impairment. The
serotonin 5-HT-1B receptor is proposed as a likely factor in the etiology of depressive
disorders. The dysfunction of 5-HT-1B receptors is detected in the brains of depressive
patients.[10]

Neurological pathways— Memory and learning process is linked with an intricate circuitry
that involves the amygdala and its associations with the structures in the frontal and
temporal lobes: The medial temporal gyrus, prefrontal, and the anterior cingulate cortex.
Major depressive disorder mainly affects these brain structures (specifically the amygdala
and hippocampus), leading to deficits in memory and the verbal learning process.[11]

Neuroendocrine factors— Researchers have found that hypercortisolemia attributed to

depressive disorder is related to the degeneration of neurons in the hippocampus leading to
cognitive impairment.

Genetic factors— C9ORF72 repeats on chromosome 9 are found in patients suffering from
depressive cognitive disorders. This has been earlier correlated with neurodegenerative
dementia. This finding confirms the genetic association of depressive cognitive disorders.
[12]

Psychosocial and environmental factors— the interplay of various factors such as abuse
(mental and physical) in the past, poor social support, loss of a job, negative life events,
and substance abuse leads to increased stress and depression by altering the hypothalamic-
pituitary axis, which eventually causes cognitive impairment.[13]

Epidemiology
The prevalence of a major depressive disorder in the elderly population varies between 30
and 45%. Out of these, 10 to 12% of the patients get admitted to an acute care setting, and 12%
to 14% get admitted to a nursing home.[14] The cognitive impairment has been documented to
be 85 to 94% of the time during an acute depressive episode and 39% to 44% of the time after
recovery of the depressive episode.[3] On the other hand, neurodegenerative dementia is
accompanied by depression in 15 to 23% of cases. Research shows 20% to 30% of executive
function deficits in depressed individuals.[15]

Pathophysiology
The pathophysiology of depressive cognitive disorders is originated from the underlying
neuropsychiatric disorder. Due to the overlapping signs and symptoms of depression and
dementia, it becomes difficult to discern the exact pathology of cognitive impairment. Numerous
cognitive deficits are found in late-onset depression. Among those, memory impairment
(anterograde and retrograde) is extensively analyzed for the evaluation of cognitive distinctions
in depressive disorder and dementia. Major depressive disorder depicts a multitude of deficits in
the spheres of episodic memory, including explicit vocal and visual memory domains. The
implicit memory functions are preserved. This memory impairment is secondary to the temporal
lobe abnormality seen in a depressive disorder. Circadian rhythm disruption seen in depression
has been theorized to contribute to cognitive decline.

Patients with neurodegenerative dementia exhibit a considerably more fast rate of forgetting as
differed to depressed and normal people who forget data at a similar rate. Depressed individuals
with memory impairment also tend to show less random variation in their responses. A clear-cut

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‘unified theory’ for the cognitive impairment in depression has not been formulated, but research
points to an encoding problem seen in these patients. A depressive disorder is associated with
negative automatic thought (NAT) and rumination, which encroach into the consciousness
affecting cognition.[16] Lack of natural instincts linked with motivation, impetus, action,
concentration, and arousal seems to be associated with the presence of effort mandating
cognitive impairment in depressive disorders.[15]

History and Physical

The assessment of depressive symptoms in dementia is confounded by numerous factors:
overlapping symptoms, the issue of symptom continuation, communication problems in severe
dementia, and reliability of caretaker opinions. A detailed history and a thorough mental status
examination are required for adequate diagnosis.

Overlapping symptoms in history are decreased interest in pleasurable activities, altered sleep,
decreased/increased appetite, increased/decreased psychomotor activity, difficulty concentrating,
and decreased energy. The likelihood of a superimposed depression in neurocognitive dementia
should be contemplated when the patient's symptoms, such as sleep alterations due to loss of
diurnal rhythm or lack of motivation, become more serious over a short span of time. In severe
dementia, a history of depressive symptoms may be hard to find secondary to aphasia. In such
cases, the collection of history from the caregiver as well as detailed observation during the
examination is required to formulate a diagnosis. Besides, sometimes patients with dementia
have anosognosia (refusal of disability), which further complicates the reporting of symptoms
suggestive of depression.

Collecting history from the caregiver can benefit, as well as complicate the diagnosis as they are
themselves vulnerable to increased degrees of responsibility and sadness. The occurrence of
depression in dementia has been strongly associated with the caretaker's burden and their own
depression.

Clues in history that helps to diagnose depression are—

Acute or subacute changes in symptoms

Symptoms of hopelessness, helplessness, guilt, death wishes, and suicidal ideation. A

detailed history should be taken to rule out active suicidal ideations, intent, or plans in any
patient who expresses death wishes.

In severe dementia, signs such as frequent moan, saddening appearance, sudden changes in
psychomotor activity (agitation or retardation)

Episodes of frequent screaming with depressive content, refusal to eat

Past history and family history of depression

Prominent complaints of memory loss and related feelings of distress, recent and long-
term memory equally affected with a complete absence of language disturbance.

In addition to history, a detailed mental status examination, neurocognitive tests, and laboratory
tests are required to rule out other medical causes. Observing the patient's behavior during
examination is very critical and important. Depressed people lack adequate motivation to finish
the task, take additional time to accomplish the task, and document frequent attention or

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concentration problems. They are usually apathetic and easily diverted. Patients with depression
often document memory difficulties and associated distress repeatedly. On the other hand,
patients with dementia seem to be less distressed and familiar with the magnitude of their own
cognitive deficiencies.

On further questioning during the mental status examination: Patients with depression either do
not respond or will reply," I don't know," to questions pertaining to orientation, attention,
concentration, memory, calculation, abstraction, and judgment.

Evaluation
In addition to history and mental status examination, laboratory testing to rule out other medical
causes of cognitive deficits such as HIV, syphilis, vitamin B12, and folate deficiency, and
paraneoplastic syndromes, etc., should be ordered.

Neuropsychological tests— Repeatable Battery for the Assessment of Neuropsychological Status

(RBANS), Wechsler Memory scale (WMS), clock drawing test, and Trail Making test are
commonly used.[9] RBANS is a test that measures immediate and delayed memory, attention,
language, and visuospatial skills. It was formulated for two primary applications: as a test for the
diagnosis and description of dementia and as a tool for finding neurocognitive deficiencies in a
mixture of disorders. WMS measures patients' performance on seven domains testing the
auditory, visual, visual working, immediate, and delayed memory.[17]

Neuroimaging studies— Magnetic Resonance Imaging (MRI), Positron Emission Tomography

(PET), Single Photon Emission Computed Tomography (SPECT) are ordered to look for
particular brain abnormalities seen in dementia.[5]

Rating Scales— The most commonly used scale for screening depression in dementia is the
Cornell Scale for Depression in Dementia (CSDD). The CSDD is a 19-item instrument
assimilating data from both patient and caretaker. It evaluates mood-related signs (Anxiety,
sadness, anhedonia, irritability), behavioral disturbance (Agitation, retardation loss of interest),
physical signs (Appetite and weight loss), cyclic functions (diurnal variation in symptoms), and
ideational disturbance (Suicide, poor self-esteem, etc.). Scores greater than ten are associated
with a probable diagnosis of a major depressive episode. Scores of more than 18 indicate a
definite major depressive disorder.[18]

Treatment / Management
Pharmacological Treament

Selective Serotonin Reuptake Inhibitor (SSRI)— Recent data approves serotonin reuptake
inhibitors (SSRIs) as the first-line treatment for depression in dementia as cholinergic side
effects (including cognitive impairment) have been less prominent with SSRIs. Adverse
effects commonly seen in the elderly are decreased sodium levels, akathisia, markedly
decreased appetite, and bradycardia. Other side effects include gastrointestinal discomfort
(nausea, vomiting, loose stools), anxiety, and sleep abnormalities.

Serotonin-norepinephrine reuptake inhibitors (SNRI)— These act as the next-line of

treatment after SSRIs. It comprises venlafaxine, desvenlafaxine, and duloxetine. This class
of drug is believed to be safe in older people. The commonly seen adverse effects are
nausea, dizziness, insomnia, and constipation. [14]

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Tricyclic antidepressants (TCAs)— These drugs should be avoided in patients with

cognitive impairment as these increase susceptibility to anticholinergic effects, including
cognitive deficits, by blockage of muscarinic receptors.

Zolmitriptan— It is a 5-HT-1B agonist found to be effective in the treatment for depression

and associated cognitive impairment. It acts by modifying the serotonergic receptors. The
adverse effects commonly seen in the elderly are numbness, tingling, and drowsiness. [10]

Vortioxetine— It has a multimodal mechanism of action: agonist at 5-HT1A receptors, 5-

HT1B partial agonist, and 5-HT3 receptor antagonist. Recent data confirm its effectiveness
in the treatment of depression with cognitive deficits. Adverse effects are similar to
SSRIs. [3]

Cholinesterase Inhibitors (Donepezil, galantamine, rivastigmine)— These medications

have been found to ameliorate subsyndromal depression in patients with dementia. These
have a positive effect on the behavioral symptoms of dementia in addition to the effect on
improving cognition.[19]

Non-Pharmacological Treament

Electroconvulsive therapy (ECT)— It is safe and beneficial in depression and other

disorders leading to cognitive deficits. ECT limits cognitive injury related to a major
depressive disorder associated with dementia in the elderly. In depressed patients with
dementia, it showed substantial refinements in both mood and cognition. Though it causes
confusion as a side effect, it could be decreased by reducing the frequency of
administering ECT to one to two times weekly.[20]

Interpersonal/Behavioral Approaches— Both strategies are associated with considerable

improvement in depressive symptoms in patients and their family members. Therapy of
the caretaker is a critical factor in the treatment of the patient with depression associated
with cognitive impairment.

Healthy habits

1. Diet: Researchers have ascertained that people who follow a 'healthy' diet routine are less
likely to be depressed.

2. Regular workout: Meditation and yoga are guarding against depressing disorders. A
plausible reason seems to be the impact of everyday work out on brain-derived
neurotrophic factor (BDNF).

3. Omega-3 fatty acids: It regulates the serotonergic and dopaminergic neurotransmitters,

leading to mood regulation. It also has an anti-inflammatory effect.

Differential Diagnosis

Major depressive disorder— Cognitive deficits, including memory impairment, are one of
the core diagnostic symptoms in patients with depression.[21]

Dementia— Neurodegenerative dementia is presented with the disruption of numerous

cortical functions along with behavioral manifestations as the primary symptom. A

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thorough examination and cognitive testing should be performed before formulating the
diagnosis.

Late-onset bipolar disorder—Symptoms of bipolar disorder that may present as symptoms

of a dementia process— decrease the need for sleep, easy distractibility, irritability,
decreased energy, and decreased interest in pleasurable activities.[5]

Delirium— secondary to drugs (withdrawal of alcohol, barbiturates, steroids), metabolic

disturbance (hypo/hyperthyroidism, fluid-electrolyte imbalance), and infection (urinary
tract infection, lung infection, meningitis, encephalitis).[17]

Structural abnormalities (tumor, subdural hematoma, normal pressure hydrocephalus)—

The onset of symptoms would be abrupt or acute, the patient would complain of headache
in case of a tumor. On examination, shuffling gait will be found in the case of normal
pressure hydrocephalus or Parkinson disease.

Prognosis
The prognosis of depressive cognitive disorders is controversial, with surveys documenting
transformation to irreversible neurodegenerative dementia and additional reviews documenting
no transformation. In the past, it came to be more obvious that depression correlated with
cognitive deficits can be the prodromal phase of dementia. In this respect, current data reports
depression to be related to a twofold heightened risk of transforming to irreversible
dementia. Researchers have found that over an interval of 4 to 5 years, more than 70% of cases
originally diagnosed with depression with cognitive impairment transformed into dementia, and
18% of these cases were originally found to have no changes in cognition.

Complications
Depressive cognitive disorders are related to a considerable amount of disability. It complicates
management, exacerbates functional problems, and governs other adverse consequences.[22] It is
associated with interference with life and activities due to prolonged hospitalization. Cases with
coexisting depressive disorder and dementia seem to utilize health care and the nursing home
facility at a considerably increased amount than cases with either disorder alone. Caretaker
responsibility is heightened many folds when they have to care for patients who have both
dementia and a depressive disorder. The additional important complication of depressive
cognitive disorder is suicidal ideation. The percentage rises in aged separated or divorced white
men. Social withdrawal and associated medical illness further enhance the risk. Depression with
dementia furthermore increases the likelihood of medical co-morbidity in old age like
cardiovascular illnesses, diabetes, stroke, etc.

Deterrence and Patient Education

The heightening number of the elderly population gives rise to an increasing number of old-age
mentally ill. Disorders such as dementia and late-onset depression not merely cause difficulties
among their sufferers; they diminish the quality of life and inflict a heightened responsibility on
the caregiver. Depressive cognitive disorders, neurodegenerative dementia, and late-onset
depression contribute to all disability-adjusted life years (DALY) in the senior community.
Hence, aging possesses a profound impact on public and health programs. Thus, knowledge
about the symptoms and signs of the depressive cognitive disorder is essential for cases and

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caretakers, which would encourage them to seek timely assistance and avoid setting their lives at
risk.

Enhancing Healthcare Team Outcomes

Depressive cognitive disorder continually poses a diagnostic difficulty. These cases demonstrate
symptoms of a major depressive disorder associated with cognitive impairment. It may be due to
numerous causes with several etiologies. While the record may illustrate that the person has
pseudodementia, the reason is complicated to know without a comprehensive examination,
assessing cognition, and ordering laboratory tests.

For the early diagnosis and treatment of depressive cognitive disorders, collective
interprofessional activity is meaningful. For example, if an aged person complains of memory
problems along with behavioral disturbances, the clinician should contemplate the differential of
depressive cognitive disorders. An additional difficulty in old-age is polypharmacy and
medication interactions. The pharmacist should frequently monitor the drug dispensing and
discuss with the physician if there are any potentially lethal prescriptions. Eventually, a
psychiatric nurse and a social worker should be involved in the supervision of these cases as they
want assistance services, a stable living atmosphere, and appreciating caretakers. An
interprofessional squad strategy is crucial if one wishes to enhance outcomes and decrease
undesirable circumstances related to depressive cognitive disorders.

Review Questions

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Comment on this article.

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