Pseudodemencia pdf

Cognitive changes in the elderly blur the distinction between normal aging and early signs of PDD. Cognitive impairment frequently accompanies depression and can be severe enough to cause confusion between dementia and depression. Signs of some neurologic diseases associated with progressive decline e. This classification summarizes the cognitive deficits in depressive disorders. However, it lacked specificity for the cognitive deficits. Further, along this review, we will focus more on specific cognitive domains, and will do it as a comparison with the cognitive deficits in dementing disorders.

We will limit present discussion to memory, executive functions and speech and language deficits among the other cognitive deficits. Memory has been the most assessed function for evaluation of cognitive differences between depression and dementia. It is now commonly accepted that depression presents with a number of deficits in the domains of episodic memory and learning.

This finding has been consistent across most studies and appears to involve both explicit verbal and visual memory functions and is similarly affected in patients suffering from both melancholic endogenous and non-melancholic non-endogenous depression types.

It is well known that temporal lobe lesions result in impairments in episodic memory. This fact along with the finding that reductions in hippocampal volume are demonstrated in patients with major depression[ 28 ] may point towards temporal lobe deficit as the culprit for these deficits. However, incidental memory for symbols on DS and information processing capacity slope function of the ST were not affected by the depressive status. Till now, we have focused on memory deficits in depression patients in comparison to normal individuals.

However, there have been many other studies, which show that memory deficits in depression are considerably mild when seen in comparison to dementia. Early work by Whitehead addressed the issue of verbal learning and memory deficits in depression by comparing elderly depressed and patients with mild dementia. They posited that variation in response strategies was the core reason for the memory-related differences observed in these groups of patients.

They found that the accuracy of depressed patients on a recognition memory task was significantly better than that in dementia of Parkinson's disease patients. They found superior delayed recall performance of depressed elderly relative to patients with DAT. In addition to AD, other subcortical neurodegenerative disorders also have been reported with impairments in cognitive processing including Friedreichs Ataxia[ 39 ] and Parkinson's disease[ 41 ].

A consistent outcome of his studies was a qualitatively worse performance of PDD patients as compared to depressed patients. Hart et al. In their study, the depressed patients, AD patients, and normal subjects were differentially exposed to the to-be-remembered information. Patients were presented line drawings for 2, 4, and 8 s for normal, depressed, and Alzheimer's patients, respectively , in view of the fact that the levels of learning impairments groups were suffering was different.

Their results indicated that AD patients showed a much more rapid rate of forgetting as compared to depressed and normal individuals who forgot information at the same rate.

However, there was relatively equivalent general intellect, verbal fluency, and concentration ability. Some early studies have assessed recall-memory functions using several different standardized neuropsychological tools.

However, the OME was far better at distinguishing between groups. In view of these findings of memory impairments in depression, the question of etiopathogenesis becomes all the more important. This encoding deficit can be seen in the context of different information processing stages of memory. In a small sample study, Weingartner et al. Their findings suggested that depressed patients failed to engage in encoding strategies that would maximize the likelihood of subsequent recall which however, improved in performance when material was presented in a predecided organized fashion.

To summarize, depression presents with several memory-function deficits most common being those related to tasks of recall or remembering. However, the sample sizes of these studies have been relatively small generally subjects per group , and the methodologies vary widely, which have been the main limitations of these studies.

Additionally, these memory deficits inspite of being significantly worse than normal individuals, are comparably better than those associated with dementia Regarding the basic neurobiology of these deficits, most researchers have suggest that such differences represent general cognitive inefficiency and attention problems rather than a fundamental lack of ability due to structural deficits.

This can be seen in the differences between depression and dementia patients as well as in the temporariness of these deficits in the clinical picture of depression, which will be dealt in next sections.

Executive function deficits are prevalent in depressive disorders and recently they have been found to produce clinically significant effects, which may in fact be a significant mediator of the functional impairments found in such patients.

Task switching or the set-shifting abilities have been the most commonly found impairments among executive functions in depressed patients. Studies in past decade examining impairment in executive tasks have produced somewhat consistent findings of impairments in set shifting tasks in depressed patients. Same finding has been reflected even in younger patients suffering from moderate depression by Purcell et al.

Similar findings of set shifting ability deficits have been observed in several other studies. This impairment corresponds to the inability to prevent the corresponding to the interference effect of the Stroop test as described by Golden[ 18 ]. There have also been attempts to evaluate the executive functions on various subgroups of depression.

Some particularly interesting studies were conducted by Austin et al.. Other than these set-shifting problems, several other executive function deficits have been observed. Bomstein, et al. Gray, et al. They found that depressed patients were generally less impaired, as measured by the Halstead impairment index, than PDD and neurological groups. They were able to differentiate between the groups on all the 10 clinical scales of the form employed.

Patients with depression who were misclassified as having PDD tended to have more extreme degrees of depressive symptomatology and lower educational levels. In a most recent study, Egerhazi et al. They found that during the acute episode, delayed matching to sample, paired associate learning, spatial recognition memory, rapid visual processing and visuospatial planning were impaired.

In remission, improvements in the domains of visual learning ability, spatial recognition memory, psychomotor speed, and executive function were observed. Processing speed impairment is another important executive function deficit observed in depression. In a recent study by Brown et al.

A more clinical outcome of this processing speed impairment is psychomotor slowing, which is almost universally found in the depressed patients, irrespective of the number of episodes.

However, there also have been exceptions to these near-universal findings. Elliott et al. On the basis of these findings, they put forth the notion that differences between normal and depressed patients are sufficiently subtle to not significantly influence scores on standard cognitive screening instruments.

Small number of studies has specifically examined speech-language function in elderly depressed patients. While most of the tasks used to measure cognitive abilities in above-mentioned studies have obvious receptive and expressive language components, it is important to highlight some studies which have looked at specific language skills.

For instance, in the study by Emery and Breslau[ 67 ] it was observed that depressed patients performed better than AD patients on measures of naming, repetition, general reading skill, syntax, and auditory verbal comprehension. At the same time, normal individuals tended to show better language performance than depressed patients overall, though these differences were considerably less obvious than those noted between depressed and AD patients. Another commonly used measure of language function has been the Boston Naming Test.

As we highlighted in the previous sections, it is difficult to tease out true cases of pseudo-dementia given the overlaps between the clinical findings in dementia and depression with regards to both depressive symptoms and cognitive impairments.

Saez-fonseca[ 71 ] found in their year follow up study that Forty-four elderly patients of both sexes mean age When the depression subsided, cognitive function also reverted to premorbid level.

Patients were regularly interviewed and retested at six months intervals for four to 18 years average 8. Some patients experienced, during the follow-up period, a recurrence of the depression for which they were again successfully treated. For testing the progression of these cognitive deficits with time, several different study designs have been used. Some studies have used the more direct method of comparing cross-sectionally the performance of subjects who have recovered from depression with that of matched controls.

Paradiso et al. Additionally, these cognitive deficits were not related to medication status which suggested the independence of these deficits from treatment related variables. In the same line, Marcos et al. Although these studies provide a cross-sectional perspective regarding poor neuropsychological performance of depressed patients in comparison to normal controls, definitive findings can only be provided by testing the cognitive status before and after recovery so that any baseline cognitive deficits are eliminated.

Criteria for diagnosing reversible dementia caused by depression: Some reasons for the divergent findings on pseudo dementia prognosis in the literature are proposed. Severe denencia pseudo dementia with and without dementia. The relationship between senile dementia Alzheimer type and depression. How to cite this article. Lecturas recomendadas The Forgetting. To me that equals medals of honor. A neuropsychological case study. El deterioro de la capacidad intelectual puede ser consecuencia de distintas enfermedades y trastornos en las personas de edad avanzada.

This website uses cookies to improve your experience while you navigate through the website. A, Sougey B. Pero sabemos que los problemas graves de la memoria no son parte natural del envejecimiento y que por tanto no debemos pasarlos por alto.

To me that equals medals of honor. I have been mentioned in my last two long-term jobs as the loving caregiver in the obituaries. Reacciones a los medicamentos. Br J Psychiatry Muchas familias cuidan en el propio hogar a los pacientes de demencia. El primer paso consiste en determinar si la persona padece de un problema cognitivo, y su nivel de gravedad.

I have been a live-in caregiver for 20 years. Some reasons for the divergent findings on pseudo dementia prognosis in the literature are proposed. Can J Psychiatry The prognosis of depression in old age. These cookies will be stored in your browser only with your consent. You also have the option to opt-out of these cookies. But opting out of some of these cookies may have an effect on your browsing experience. Necessary cookies are absolutely essential for the website to function properly.

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