Call The Alzheimer's Association can help you learn more about Alzheimer's and other dementias, and help you find local support services. You can also call the SSA at Find Your Chapter. Take the Brain Tour. Learn More. Types of Dementia. Share or Print this page. Read more: Cuidado. Read more: Creutzfeldt-Jakob Disease. Don't just hope for a cure. All he told me was that it was negative. She thought a picture of her was our grandmother, however, I showed her an old picture of our mother and she knew who it was right away!
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Out of these, the cookies that are categorized as necessary are stored on your browser as they are essential for the working of basic functionalities of the website. Finally, studies not corroborated by pathological data are necessarily tautological to some extent. For example, since the presence of behavioral disorders constitutes a diagnostic criterion for FTD, 3 only FTD patients with behavioral disorders are selected for inclusion, and this could artificially increase their true frequency.
At the same time, symptoms not specifically mentioned in the diagnostic criteria adopted are misidentified, and their occurrence is thus underestimated. The assessment of behavioral disturbances also suffers from other limitations compared with the assessment of cognitive disorders. Symptom detection and quantification are not based on direct observation of patients and mostly rely on caregivers' reports, and the influence caregivers' variables may have on symptom description and quantification is not always adequately taken into account.
Many behavioral disorders have been reported in AD patients, ranging from mood changes to psychoses and to modification in social conduct. Occasionally, noncognitive disorders may characterize the onset. Second, methodological reasons may also contribute to heterogeneity.
Only in the last decade have symptom detection and quantification been evaluated by means of structured or semistructured scales, validated in large groups of patients.
This has allowed for more objective descriptions of symptoms, as well as attempts to compare different reports. Nevertheless, the prevalence rate seems to be still largely influenced by the clinical diagnostic criteria used for evaluation. For example, if the temporal variant of FTD is erroneously included in AD dementia groups differential diagnosis may not be easy at earlier stages manifestations of this type of dementia might, indeed, be considered proper to AD.
There is some agreement in considering major depression and, in general, the affective disorders, as common symptoms either at the onset 28 and throughout the entire clinical course of AD. The emergence of psychotic symptoms is currently considered to predict faster cognitive and functional decline 48 - 53 as well as increased risk of mortality, 54 even if some studies lead to different conclusions.
Currently, there are descriptions of other noncognitive symptoms, primarily pathological conduct, which merge into a large variety of syndromes. As previously mentioned, most research on noncognitive disorders in FTD consists of comparative studies between the two most frequent forms of dementia, AD and FTD.
Only in more recent years have comparisons been made with vascular dementia, 64 , 65 DLB, or Parkinson's disease. From the time of the first reports on FTD, 68 alteration of social conduct, reduced insight, personality changes, and apathy have been described as core features of the disease and have been included in the diagnostic criteria.
Not only severity, but also symptom patterns, seem to differentiate the two dementias. From the onset, pathological processes may be distributed asymmetrically in the frontal region, 83 determining variability in the clinical manifestation.
Behavioral disorders do not seem significantly different in the frontal vs temporal variant semantic dementia 10 , 71 , 84 or PPA, 11 even if they tend to manifest earlier in the frontal variant. For example, apathy 74 , 84 and stereotypes 74 are described as being more frequent in the frontal compared with the temporal variant, while sleep disorders 84 and a complex disorder such as the Kluver-Bucy syndrome, dominated by oral exploratory behavior, hyperphagia, and hypersexuality, 80 are more likely to manifest in the temporal variant.
Studies on FTD do not generally take into consideration the issue regarding left vs right asymmetry of atrophy distribution. Indirect evidence about the characteristics of the behavioral syndrome in asymmetric-left atrophy can be obtained by observing patients with SD and PPA in which linguistic disorders suggest left-sided involvement.
Similarly, a few papers are also available on FTD patients in whom cognitive symptoms suggest a prevalent right pathology. In general, although the pattern of cognitive impairment is largely consistent with the distribution of atrophy, 69 , 85 mostly when the diagnosis of PPA or semantic dementia temporal variant is made, 10 the influence of left-right asymmetry is less predictable in the behavioral domain.
Only a few studies have specifically compared the behavioral syndrome of patients with prevalent left or right hemispheric atrophy. Disinhibition, 69 , 84 but also anxiety, depression, and eating disorders 84 have been associated with right-asymmetric frontotemporal atrophy. Three cortical subcortical circuits are supposed to underlie cognition and behavior in the prefrontal lobe.
While the dorsolateral prefrontal circuit is postulated to be involved in cognitive activities proper, primarily planning and attention, the orbitofrontal and anterior cingulate dorsomedial circuits are likely involved in behavior. In particular, social cognition and empathy require the integrity of the orbitofrontal circuit, while motivation is accomplished by the anterior cingulate circuit.
It is plausible that degeneration involves these neural subsystems in disease evolution differently, giving rise to different cognitive-behavioral patterns. Indeed, this is confirmed by clinical evidence. For example, it is well known that the behavioral manifestations greatly precede the cognitive deficits in some patients, and this is to some extent consistent with the relative preservation, in early stages, of the dorsolateral circuit.
Functional studies conducted in fv-FTD are also consistent with this view. Metabolic involvement of separate brain clusters has recently been demonstrated. The relationship between cognitive and behavioral disorders is a central issue in all types of dementia. However, while studies on AD are mostly descriptive and focused on clinical aspects, recent studies on FTD are more speculative.
Although there is little evidence suggesting that the cognitive and behavioral manifestations in AD are independent of each other, 90 many studies report data in support of a relationship at least quantitative between the severity of cognitive and behavioral syndromes.
For example, the severity of the behavioral disorders is predicted by the severity of the cognitive deficit. Reduced ability on cognitive tasks sensitive to frontal lobe damage seems to be associated with a higher risk of psychotic symptoms in AD, 43 , 48 supporting the hypothesis that symptoms such as hallucinations and delusions could be produced by pathological frontal circuitry.
Generally, however, studies do not explicitly take into account the potential cause-effect relationship between the two types of manifestations. Indeed, it is likely that any limitation of cognitive resources could reduce a patient's ability to efficiently react to environmental stimulation in order to generate adequate behavioral responses. The memory disorder, to mention the most common example, typical of AD but also frequent in other types of dementia, might produce such severe functional limitation as to generate reactive depression in amnesic subjects with good insight.
The hypothesis of a direct relationship between cognition and behavior in FTD is now currently proposed in the neuropsychological literature.
Particular attention has been devoted to the theory of mind TofM. TofM is the ability to make inferences about others 5 mental states, thoughts, and feelings in order to predict and understand their behavior. A deficit in TofM, originally proposed to account for developmental disorders in social cognition of subjects affected by pathologies such as autism or Asperger's syndrome, 94 , 95 could also explain some aspects of the pathological behavior typical of patients with FTD.
The effects of frontal lobe damage on behavior, and in particular of damage in the orbital and ventral regions, have long been known. There is basic agreement in considering the amygdala 97 and the orbitofrontal cortex, 95 and also the medial prefrontal cortex 98 as the anatomical base for TofM see also ref A few reports have specifically taken into consideration the relationship between impaired TofM and behavioral disorders in patients with FTD.
They interpreted this finding as supporting the hypothesis that some aspects of the changes in interpersonal behavior typical of this pathology might be caused by impaired TofM. Correlation between TofM and NPI, as well as dissociation between TofM and executive functions see also ref 97 , suggests that TofM tasks should not be considered simply as a measure of the cognitive skill of the frontal lobe, namely of executive function.
Rather, they should be considered as reflecting the ability to understand mental states, crucial for generating normal interpersonal behavior. It has also been demonstrated that the reduced competence shown by FTD patients in understanding emotions empathy and social transgressions is not fully accounted for by the documented impairment in executive tasks, confirming the independence of social and cognitive abilities.
Metacognition refers to high-level processing that consists of planning, self-evaluation, and self-monitoring of cognitive activities. Deficits in self-regulatory behavior, deriving from a lack of metacognitive control on executive abilities, have been related to prefrontal lesions. Recently, this aspect was investigated in patients with FTD, and mostly patients with the frontal variant showed poor self-awareness and self-knowledge, not only in cognitive but also in emotional and social domains.
FTD and AD are both characterized by a wide range of behavioral disorders. The neural correlates of noncognitive manifestations are more identifiable in FTD, and refer to specific cortical subcortical circuits in the prefrontal regions. For these reasons, studies on FTD can make an important contribution to defining the neural basis of human behavior, and also offer a model for studying behavioral disorders in other forms of dementia.
From the clinical point of view, the possibility of identifying specific patterns of cognitive-behavioral symptoms would be very relevant in the differential diagnoses of dementia, mostly in the absence of reliable biological markers. Newly proposed investigations in the social cognition domain such as TofM, but also metacognition 87 or decision-making, may offer further opportunities for interpreting the nature of the behavioral manifestations and their relationship to cognitive disorders.
The correlation some authors have found between tasks exploring social cognition, primarily TofM, and standardized measures of behavioral impairment, has a potentially useful clinical application. Until now, detection and quantification of behavioral changes have relied almost exclusively on caregivers' reports in structured questionnaires aimed toward defining specific symptoms or syndromes.
Quantifying the severity of the social cognition disorder could provide a direct measure of the severity of the behavioral manifestation in dementia. This perspective should encourage the development of specific test batteries for investigating this area. National Center for Biotechnology Information , U. Journal List Dialogues Clin Neurosci v.
Dialogues Clin Neurosci. Author information Copyright and License information Disclaimer. This article has been cited by other articles in PMC. Abstract Behavioral manifestations may dominate the clinical picture of the frontal variant of frontotemporal dementia fv-FTD for a long time before the appearance of true cognitive deficits.
Keywords: frontotemporal dementia , Alzheimer's disease , behavioral disorder , theory of mind , social cognition. Indeed, the histopathological features of the frontal dementias are not distinctive, and a continuum towards other neurological conditions, such as the tauopathies or motor neuron diseases, has now been documented, 5 , 6 suggesting extensive pathological and etiological heterogeneity In spite of this, there is quite a large consensus that the clinical presentations of FTD should be restricted to three main subtypes principally reflecting the distribution of neuronal loss, ie, of atrophy, in the brain: i the behavioral or frontal variant fv-FTD due to prevalent prefrontal damage, dominated by behavioral symptoms and dysexecutive disorders; ii primary progressive aphasia PPA , 7 characterized by a progressive nonfluent linguistic impairment associated with left perisylvian atrophy; 8 and iii semantic dementia SD , in which a progressive agnosia for words and objects follows left anterior temporal lobe degeneration.
Noncognitive disorders in AD and FTD: a brief review AD Many behavioral disorders have been reported in AD patients, ranging from mood changes to psychoses and to modification in social conduct. Frontal vs temporal variant and right vs left atrophy in FTD From the onset, pathological processes may be distributed asymmetrically in the frontal region, 83 determining variability in the clinical manifestation. Impairment of different cortical subcortical prefrontal circuits: different cognitive-behavioral syndromes?
Relationship between cognitive and noncognitive symptoms in dementia The relationship between cognitive and behavioral disorders is a central issue in all types of dementia. Theory of mind and behavior in FTD The hypothesis of a direct relationship between cognition and behavior in FTD is now currently proposed in the neuropsychological literature.
Metacognition and behavior in FTD Metacognition refers to high-level processing that consists of planning, self-evaluation, and self-monitoring of cognitive activities. Neary D. Dementia of frontal lobe type. Neurologic Clinics. Bang J, et al. Non-Alzheimer's dementia 1: Frontotemporal dementia. The Lancet. Frontotemporal dementia information page. National Institute of Neurological Disorders and Stroke.
Diagnosing frontotemporal dementia. The Association for Frontotemporal Dementia. What causes frontotemporal disorders? National Institute on Aging. Lee SE, et al. Frontotemporal dementia: Treatment. Young JJ, et al. Frontotemporal dementia: Latest evidence and clinical implications.
Therapeutic Advances in Psychopharmacology. Gerlach LB, et al. Managing behavioral and psychological symptoms of dementia.
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