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 clinical depression. Pseudodementia can develop in a wide range of neuropsychiatric disease such as depression, schizophrenia and other psychoses, 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. Psychiatric conditions, mainly depression, are 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. 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 for 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. Treatments with antidepressants such as SSRIs (selective serotonin reuptake inhibitors), SNRIs (serotonin-norepinephrine reuptake inhibitors), TCAs (tricyclic antidepressants), Zolmitriptan, Vortioxetine, and Cholinesterase inhibitors can lead to improvements in cognitive dysfunction. Dopaminergic psychostimulants such as dextroamphetamine, methylphenidate, and to a lesser extent modafinil, may also produce robust improvements in cognition in the short-term. Among the stimulant class, dextroamphetamine produces the greatest improvements in symptoms, but is more neurotoxic at higher-than-therapeutic doses.
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. Instead, the first written instance of pseudodementia was by one of Wernicke's students, Georg Stertz. 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. Reversible causes of true dementia must be excluded. His term was mainly descriptive. The clinical phenomenon, however, has been well-known since the late 19th century as melancholic dementia. Doubts about the classification and features of the syndrome, and the misleading nature of the name, led to proposals that the term be dropped. 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.
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. The key symptoms of pseudodementia include: speech impairments, memory deficits, attention problems, emotional control issues, organization difficulties, and difficulties in decision making. 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. 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. However, for some, pseudodementia can eventually progress to organic dementia and lead to lowered cognitive function. 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. 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.
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