THE TRAGEDY OF GUARDIANSHIP FRAUD
Reversible Cognitive Disorder - Pseudodementia
A primary reason that accurate diagnosis is so important among people exhibiting cognitive problems is that some causes of cognitive impairment are reversible. Consider the costs - physically, emotionally, and financially - of diagnosing someone with irreversible dementia when, in fact, the problem could have been reversed. Reversible conditions creating cognitive problems include pseudodementia, medical conditions, and delirium.
Pseudodementia is a situation where a person who has depression also has cognitive impairment that looks like dementia. Depression is a mental disorder that includes a depressed mood that lasts at least two weeks accompanied by the loss of interest or pleasure in nearly all activities, feelings of guilt or suicidality, social withdrawal, and sleep and appetite disturbances. Depression can also create cognitive symptoms such as difficulty thinking clearly, problems concentrating, and difficulty making decisions. For more detailed information about the symptoms of depression, please click here to visit our associated topic center. Pseudodementia is not permanent; once a person's depression is successfully treated, his or her cognitive symptoms will go away as well.
Estimates suggest that between 2% and 32% of older individuals who experience cognitive problems actually have pseudodementia. However, this number may not be completely accurate, because it is often tricky to distinguish between depression and dementia in older adults. A thorough clinical interview can reveal important clues about the proper diagnosis. For instance, while people with depression may complain of having memory problems and appear upset about them, they will usually perform well on objective neuropsychological tests of memory administered in a clinician's office. On the other hand, individuals with dementia will often deny having any problems with memory or minimize their importance, and display impairment on neuropsychological tests.
The Geriatric Depression Scale (GDS) (described in an earlier section is often used to help differentiate between pseudodementia and other forms of dementia. Results from the GDS are combined other information about a person's history and current functioning to help with diagnosis. For example, people with pseudodementia typically do not have a history of mood swings (unless they have Bipolar Disorder, an illness characterized by repetitive swings in mood and energy levels) and are likely to score high (high = more depressed) on the GDS. In contrast, people with dementia usually show a range of emotions, sometimes responding to situations with an inappropriate emotion (e.g., laughing while others are sad).
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Pseudodementia is a syndrome seen in older people in which they exhibit symptoms consistent with dementia but the cause is a pre-existing psychiatric illness rather than a degenerative one. The name is derived from the combining form of the "Ancient Greek:" "ψευδής" (pseudēs, "false, lying"), prepended to "dementia". Pseudodementia has been partially linked in a small amount to "Bipolar disorder"-Type I, linked in a case of a 21 year-old female patient. The patient was shown to have "Vitamin B12" (possibly the "Vitamin B" "group") and Folate or "Folic acid" deficiencies; which were thought to be partially responsible. Especially, due to the underlying affects that can be attributed to "Bipolar spectrum" disorder(s). This also helps to solidify the idea of pseudodementia being caused by underlying psychiatric illnesses.
Older people with predominant 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". This was an important distinction as the former was untreatable and progressive and the latter treatable with "Antidepressant" therapy or "Electroconvulsive_therapy" or both.
[-] History and controversy of term
The term was first coined in 1961 by psychiatrist Leslie Kiloh, who noticed patients with cognitive symptoms consistent with dementia who improved with treatment. His term was mainly descriptive. The clinical phenomenon, however, was well-known since the late 19th century.span style='font-size:12.0pt;font-family:"Times New Roman"'>
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 which has held up well in clinical practice, and also highlights those who may have a treatable condition.
[-] Presentation and differential
The history of disturbance in pseudodementia is often short and abrupt onset, while dementia is more often insidious. 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, and they may appear upset or distressed. Those with true dementia will often give wrong answers, have poor attention and concentration, and appear indifferent or unconcerned.
Investigations such as SPECT imaging of the brain show reduced blood flow in areas of the brain in people with Alzheimer's disease, compared with a more normal blood flow in those with pseudodementia.
Images of dementia versus pseudodementia
As the population ages, the incidence of dementia in the U.S. will become an even more common problem and take up an even larger percentage of the health care budget. With the advent of new medications that slow the course of some dementing processes, diagnostic tools that help in the early differential diagnosis of dementia is essential. The SPECT pattern for Alzheimer’s Disease is typically bilateral hypoperfusion in the parietal and temporal regions of the brain with frontal lobe hypoperfusion occurring later in the illness. Multi-infarct dementia is characterized by multiple areas of decreased perfusion. HIV dementia is typically seen by decreased patchy uptake across the cortex. Frontal lobe dementias (as the name indicates) are often characterized by very poor frontal lobe perfusion. Psuedodementia (another condition, such as depression, that clinically appears like dementia) will not have a typical dementia pattern and may be more like a depression pattern.
Here are several examples of how SPECT can be useful in the evaluation and treatment of dementia-like presentations.
When Frank, a wealthy, well-educated man, entered his seventies, he began to grow forgetful. At first it was over small things, but as time went on the lapses of memory progressed to the point where he often forgot essential facts of his life: where he lived, his wife’s name and even his own name. His wife and children, not understanding the change in behavior, were aggravated with his absent-mindedness and often angry at him for it. Frank’s SPECT study showed a marked suppression across the entire brain, but especially in the frontal lobes, the parietal lobes and temporal lobes. This was a classic Alzheimer’s disease pattern. By showing the family these images and pointing out the physiological cause of Frank’s forgetfulness, in living images, I helped them understand that he was not trying to be annoying, but had a serious medical problem.
Consequently, instead of blaming him for his memory lapses, they began to show compassion towards him, and they developed strategies to deal more effectively with the problems of living with a person who has Alzheimer’s Disease. In addition, I placed Frank on new experimental treatments for Alzheimer’s Disease that seemed to slow the progression of the illness.
Here is a scan of a 92 year old man with Alzheimer’s Disease who had become forgetful, frequently lost away from home, forgot how to do simple things such as dress himself and began getting aggressive with his wife. Notice the extensive frontal lobe involvement.
Before treatment notice good overall activity, with increased limbic system activity (center arrow), after treatment with Wellbutrin the limbic system normalizes.
I first met Margaret when she was 68 years old. Her appearance was ragged and unkempt. She lived alone and her family was worried because she appeared to have symptoms of serious dementia. They finally admitted her to the psychiatric hospital where I worked after she nearly burned the house down by leaving a stove burner on. When I consulted with the family I also found out that Margaret often forgot the names of her own children and frequently got lost when driving her car. Her driving habits deteriorated to the point where the Department of Motor Vehicles (DMV) had to take away her license after four minor accidents in a six month period. At the time when Margaret’s family saw me, some members had had enough and were ready to put her into a supervised living situation. Some family members, however, were against the idea and wanted her hospitalized for further evaluation.
While at first glance it may have appeared that Margaret was suffering from Alzheimer’s Disease, the results of her SPECT study showed full activity in her frontal, parietal and temporal lobes. If she had Alzheimer’s Disease, there should have been evidence of decreased blood flow in those areas. Instead, the only abnormal activity shown on Margaret’s SPECT was in the limbic system at the center of the brain where the activity was increased. Often, this is a finding in people suffering from depression. Sometimes in the elderly it can be difficult to distinguish between Alzheimer’s Disease and depression because the symptoms can be similar. Yet with pseudodementia (depression masquerading as dementia), a person may appear demented, yet not be at all. This is an important distinction to make because a diagnosis of Alzheimer’s Disease would lead to prescribing a set of coping strategies to the family and possibly new experimental medications, whereas a diagnosis of some form of depression would lead to prescribing an aggressive treatment of antidepressant medication for the patient along with psychother-apy.
Here is another example.
Before treatment notice poor prefrontal cortex activity and increased limbic system activity, after treatment with imipramine the limbic system normalizes and the prefrontal cortex improves significantly.
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