Pseudodementia

Pseudodementia (fake dementia or fake cognitive pass up) occurs when a person is and then slowed down from depression or another psychiatric disease that they present as intellectually or cognitively impaired.

From: Forensic Psychiatry , 2016

Delirium and Dementia

Ron One thousand. Walls Medico , in Rosen's Emergency Medicine: Concepts and Clinical Practice , 2018

Groundwork

Dementia is not a unmarried disease entity but rather a highly variable clinical syndrome characterized by a gradually progressive deterioration of cognitive function. Prognosis depends on the underlying cause (Box 94.2). Dementia is classified every bit either irreversible (primary degenerative) or potentially reversible (secondary); information technology is further classified according to the caste of cognitive harm. Mild dementia implies some impairment of work and social activities; however, the capacity for independent living remains intact. With moderate dementia, independent living is hazardous, and some degree of supervision is necessary. With severe dementia, continual supervision and often custodial care are needed.

Primary degenerative dementias include Alzheimer'due south disease, dementia with Lewy bodies, subcortical dementias involving the basal ganglia and thalamus (eg, progressive supranuclear palsy, Huntington's chorea, Parkinson's disease), and dementia of the frontal lobe blazon, which includes Pick's disease. Dementia with Lewy bodies, clinically manifested by persistent, well-formed visual hallucinations and prominent extrapyramidal movements, has been found to be the tertiary virtually common blazon of dementia. With advanced aging, dementia may take mixed causes, with Alzheimer'south disease and vascular dementia oftentimes coexisting. A smaller percentage of dementias are attributable to causes, such as anoxic encephalopathy, hepatolenticular degeneration, tumors, and slow virus infections.

Potentially reversible dementias are caused by adverse drug reactions, endocrinopathies, metabolic abnormalities, intracranial processes, and depression. The clinical manifestation is either an acute delirium or an astute or gradual progressive cognitive impairment that reverses once the underlying etiology is addressed and resolved. Drug-induced dementia occurs primarily in elders and tin be acquired by various psychotropic drugs, antihypertensive medications, anticonvulsants, anticholinergics, and miscellaneous medications, such every bitl-dopa. Dementia too may be caused by heavy metals and other exogenous agents, such every bit carbon monoxide, carbon disulfide, and trichloroethylene.

Endocrinopathies and metabolic abnormalities that can cause secondary and potentially reversible dementia include hypothyroidism, hyperthyroidism, parathyroid disease, Addison's disease, Cushing'due south illness, and panhypopituitarism. Metabolic abnormalities such as nutritional deficiencies that cause dementia include thiamine deficiency (Wernicke's syndrome), niacin deficiency (pellagra), vitamin B12 deficiency, and folate deficiency.

Intracranial processes, infinite-occupying lesions, and hydrocephalus may as well cause dementia. Repetitive intracranial trauma resulting from contact sports tin can produce a chronic organic encephalon syndrome without evidence of hematoma or significant contusion (dementia pugilistica). Intracranial processes that may eventually lead to a chronic organic brain syndrome include infections with slow viruses, man immunodeficiency virus type 1 (HIV-1) infection, chronic meningitis (tubercular or fungal), encephalon abscess, and neurosyphilis. In addition to master HIV-1 CNS infection, toxoplasmosis, cryptococcal meningitis, malignant disease, and infections due to herpesvirus, cytomegalovirus, varicella-zoster virus, and papovavirus (progressive multifocal leukoencephalopathy) can cause progressive cognitive impairment in this compromised group of patients and must be excluded.

Organic disorders

Alan J Carson , ... Tom Chocolate-brown , in Companion to Psychiatric Studies (8th Edition), 2010

Definition

In 'pseudodementia', which is a functional psychiatric disorder or rarely a deliberate simulation, the clinical flick is similar to that of an organic dementia. However, at that place are differences which aid in differential diagnosis:

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Depressive pseudodementia is cognitive harm on the groundwork of a depressive illness, sometimes in the absence of typical symptoms of depression.

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Hysterical pseudodementia is cognitive impairment mimicking organic dementia which proves not to be due to organic pathology. 'Functional dementia' might exist a more than appropriate term for both depressive and hysterical pseudodementia.

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Simulated dementia is cognitive impairment that has been feigned deliberately in the pursuit of some grade of gain.

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Clinical Neurophysiology and Electroencephalography

Theodore A. Stern MD , in Massachusetts Full general Infirmary Comprehensive Clinical Psychiatry , 2016

The EEG in Dementia and in Pseudodementia

With "normal aging", there may exist a decrease in the frequency of the posterior ascendant rhythm by upwardly to 1 Hz or 10% of the baseline EEG obtained at a younger age. A further driblet in the frequency of the posterior dominant rhythm may be a sign of a degenerative process, even if the background frequency remains in the alpha range. 50 Afterwards a dementing illnesses is established, lengthened EEG slowing is seen, with or without slowing of the posterior ascendant rhythm. Alzheimer'due south affliction (AD) often causes these non-specific findings on the EEG. At times, withal, slowing may be maximal in temporal and parietal regions. The EEG in Advertisement may also show attenuation of the beta rhythm. 51 These changes ordinarily parallel the clinical grade of the disease, merely are not specific enough to allow for EEG-based case detection. 52 In multi-infarct vascular demen­tia, focal or multi-focal slowing may exist seen. Focal temporal theta is a signature of microvascular illness. In cases where there is deep sub-cortical vascular pathology, widespread cortical pathology, or where there is mixed vascular/AD pathology, diffuse rather than focal slowing may be seen. Fronto-temporal dementias touch frontal lobes and/or the temporal lobes, often asymmetrically. EEG findings may suggest that a frontal variant of dementia if the EEG shows frontally localized slowing, but the EEG is often normal or shows lengthened slowing in this entity. 53,54 Finally, obtaining an EEG may be helpful when differentiating dementia from depression-related cognitive impairment (usually referred to as pseudodementia), in which the EEG tin be either normal or very mildly slowed. In patients with early on dementia with balmy cognitive complaints, the EEG may be normal or bear witness balmy abnormalities (such every bit slowing in the posterior ascendant rhythm). However, a normal EEG in a patient with an avant-garde dementing illness with severe cerebral deficits is atypical and should raise doubts nigh the diagnosis. In contrast, the bulk of patients with dementia have abnormal EEGs; in up to one-third of patients, there may be moderate or severe abnormalities. 55

Organic psychiatry and epilepsy

Pádraig Wright , Marina Zvartau-Hind , in Core Psychiatry (Third Edition), 2012

Pseudodementia

Pseudodementia may exist defined as dementia diagnosed in patients who accept psychiatric disorders that are associated with apparent cognitive reject. Low in elderly patients is particularly associated with such cerebral decline, but it may also exist nowadays in patients with schizophrenia or with dissociative disorders. A diagnosis of pseudodementia is suggested by the following findings:

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A family history of depression or schizophrenia

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A personal history of depression, schizophrenia or dissociative disorder

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Other depressive, schizophrenic or dissociative symptoms are present

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Depressive, schizophrenic or dissociative symptoms precede cognitive harm

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Acute onset of cerebral harm

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Retention of normal cognitive function in some domains (patients may be able to learn new information, for example)

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Cognitive impairment may be reversed by attempt or past taking more time than is usual to complete a task

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Cognitive impairment may be reversed past treatment of the underlying depression, schizophrenia or dissociative disorder.

A trial of treatment – usually antidepressant medication or electroconvulsive therapy – is appropriate if there is any doubt about the diagnosis of dementia.

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Geriatrics

Mary P. Harward MD, FACP , in Medical Secrets , 2019

49 How does one differentiate pseudodementia and dementia?

Initially by assessing the patient for symptoms of depression. Major depression is commonly associated with cognitive difficulties (pseudodementia), and many patients in the early stages of dementia get depressed. The differentiation of pseudodementia from true dementia tin be a clinical claiming. Clues that depression is the cause of cognitive difficulties include decline over weeks to months rather than years and whether the patient has overt business organisation for the memory loss. Referral for complete neuropsychological testing can exist helpful in elucidating the diagnosis in many cases. Treatment with antidepressants will significantly improve cerebral part in patients with pseudodementia, whereas truly demented patients may see improvements in overall function but will go along to accept cerebral impairment.

Dementia

Rachelle Doody MD, PhD , in Neurology Secrets (Fifth Edition), 2010

4 What features are characteristic of pseudodementia associated with depression?

Patients with pseudodementia may or may not have a history of depressive or vegetative symptoms. They tend to accept apartment impact, to requite up easily when mental status is examined, or to say that they cannot perform a chore without fifty-fifty trying it. They oft respond surprisingly well when given extra time and encouragement, only they may deny their success. Results of mental condition examination are inconsistent; for example, they may fail a simple task simply perform a similar, more hard one correctly. Or they may have variable strengths and weaknesses over repeated testing sessions.

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Memory

James B. Brewer , ... Allyson C. Rosen , in Textbook of Clinical Neurology (3rd Edition), 2007

Pseudodementia

The term pseudodementia refers generically to treatable disorders that mimic dementia. The most common is depression. Depression and dementia can both lead to reduced motivation, impaired concentration, and mental slowing. Consequently, both diseases can lead to widespread cerebral and retentivity dysfunctions. Formal testing has shown that purely depressed patients perform meliorate on declarative memory tests than genuinely demented patients, but this departure may be difficult to decide in item patients. Because depression, with or without the co‐occurrence of dementia, is treatable, it should exist considered in any diagnostic evaluation. Some instruments, such as the Geriatric Depression Scale, may be useful in diagnosing depression in elderly individuals.

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Dementia

R.J. Perry , B.L. Miller , in Encyclopedia of the Neurological Sciences, 2003

Differentiating Dementia from Pseudodementia

The term pseudodementia is used to describe the condition in which depression causes cognitive deficits that masquerade as dementia. Patients will often nowadays with difficulties in memory and concentration and deny depressive symptoms. A previous history of low tin can exist helpful, as tin can the presence of vegetative symptoms, such as sleep or ambition disturbance, and lack of activeness or enthusiasm for previously enjoyed pastimes. The memory disturbance in depressive pseudodementia is traditionally one in which learning is impaired but recall of learned information is relatively preserved, in contrast to early Alzheimer's disease, in which recall is also severely afflicted. Performance is oft patchy and inconsistent and improves with encouragement. Patients with cerebral damage secondary to depression may have word-finding difficulty on fluency tasks just do not take impairments in naming or produce paraphasias. A reasonable approach to patients with depressive symptoms and memory impairment in whom even formal neuropsychological testing cannot differentiate depression alone from depression in Alzheimer's disease is to requite a trial of antidepressant therapy for several months before repeating the neuropsychological testing.

An issue of continued contend is whether depression can lead to Alzheimer's disease. Several contradictory studies have assessed whether low that occurs in the years preceding Alzheimer's disease tin can be a prodrome to the disease or whether depressive episodes occurring many years before the onset of Alzheimer'due south disease act every bit a hazard factor. A possible neuroendocrine mechanism for the link lies in the increased exposure of the brain to glucocorticoids every bit a result of the increased activeness of the hypothalamic–pituitary axis in depression. Such an increment in glucocorticoids has been shown to lower the threshold for age-associated degeneration of the hippocampus, the initial locus of pathology in Alzheimer's illness.

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Old-age psychiatry

Neill H Anderson , Kirstie Woodburn , in Companion to Psychiatric Studies (8th Edition), 2010

Cognitive impairment associated with depression

The term pseudodementia has been used historically to describe the reversible cognitive impairment that may accompany depression, just it has lacked precise and consistent definition. The neuropsychological contour of older depressed patients varies according to the age at which depression start occurs, suggesting the involvement of unlike biological mechanisms (Herrmann et al 2007). Tardily-onset depression is accompanied past impairment of executive operation and processing speed and is associated with frontal and temporal white affair hyperintensities on MRI (O'Brien et al 2006), with deep rather than periventricular lesions being most implicated. Past contrast, in those with early-onset low episodic and semantic memory is more typically affected, and neuroimaging reveals testify of hippocampal atrophy (McKinnon et al 2009). It is thought that hippocampal harm is mediated via neurophysiological stress – peradventure cortisol hypersecretion – simply there is no credible correlation with raised cortisol levels. Contempo studies refute the merits that the neurocognitive changes associated with tardily-life depression are temporary and remit after recovery. Bhalla et al (2006) found that 94% of those with depression who were cognitively impaired at baseline remained so a year afterward, despite being no longer depressed. Moreover, this study and others suggest that depressive symptoms without apparent cognitive impairment predict the later development of cognitive pass up and dementia, especially in those with persistent and more astringent depressive symptoms.

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Iodine, Thyroid Diseases and Neuromuscular Dysfunction

Huy A. Tran , in Comprehensive Handbook of Iodine, 2009

Higher Middle Considerations

Hypothyroidism can result in depression, pseudodementia and, in severe cases, myxedema coma. Conversely, it can also lead to inappropriate euphoria, low and frank psychosis ( Lichtenstein, 1980). Other higher centre problems include sensorineural deafness, and the mechanism is thought to be due to the deposition of glycosamino glycan and bone hypertrophy, but this can be hard to confirm. Severe hypothyroidism can result in astringent mental retardation (cretinism) in children. Grandmal seizure is not uncommon. Information technology is thought to be due to the failure to excrete water, resulting in severe hyponatremia and occurs in about 25% of cases (Myers and Hays, 1975).

Effigy 72.vii summarizes all the potential neuromuscular conditions associated with hypo- and hyperthyroidism in relation to iodine excess.

Figure 72.7. Comparison and contrast of numerous neuromuscular conditions associated with iodine-induced hyper- and hypo­thyroidism. These occur at both peripheral and primal nervous systems.

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