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 asdepression, schizophrenia and other psychosis, mania, dissociative disorder and conversion disorder. 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]

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.

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.^[4] His term was mainly descriptive.^[5] The clinical phenomenon, however, has been well-known since the late 19th century as melancholic dementia.^[6]

Doubts about the classification and features of the syndrome,^[7] and the misleading nature of the name, led to proposals that the term be dropped.^[8] 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.^[9]

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.^[10] The key symptoms of pseudodementia include: speech impairments, memory deficits, attention problems, emotional control issues, organization difficulties, and decision making.^[11] 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. In addition, patients 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.^[10] 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.^[12]

Pseudodementia refers to "behavioral changes that resemble those of the progressive degenerative dementias, but which are attributable to so-called functional causes".^[13] The main cause of pseudodementia is depression. 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, which is a symptom commonly associated with dementia. ^[14] While not as common, other mental health disorders and comorbidities can also cause symptoms that mimic dementia.^[15]

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.^[15]

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.^[16] 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.^{[17] [18]} For instance, studies have also shown a relationship between depression and its cognitive effects on everyday functioning and distortions of memory.^[19]

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. ^{[20] [21]} In addition, MRI results show medial temporal lobe atrophy, which causes impaired recall of facts and events (declarative memory), in individuals with AD.^[22]

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.^[23] 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 modified, the cognitive impairment can be effectively reversed. Generally, dementia involves a steady and irreversible cognitive decline while pseudodementia-induced symptoms are reversible.^[23] Diminished mental capacity and social withdrawal are commonly identified as dementia symptoms within the elderly population without ruling out depression.^[24] As a result, elderly patients are often misdiagnosed especially when healthcare professionals do not make an accurate assessment or suggest the correct testing.

Older adults 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.^[25] This was an important distinction as the former was untreatable and progressive and the latter treatable with antidepressant therapy, electroconvulsive therapy, or both.^[26] In contrast to major depression, dementia is a progressive neurodegenerative syndrome involving a pervasive impairment of higher cortical functions resulting from widespread brain pathology.^[4]

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.^[27] 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.^[28] 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]

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.^[23] 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, Vortioxetine, and cholinesterase inhibitors. ^[30]