The Mental Status Examination in Patients With Suspected Dementia

Grossman, Murray; Irwin, David J.

doi:10.1212/con.0000000000000298

Cited by 21 publications

(25 citation statements)

References 51 publications

(34 reference statements)

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“…The diagnostic approach for evaluating standard dementia has been presented in the article “The Mental Status Examination in Patients With Suspected Dementia” by Murray Grossman, MD, FAAN, and David J. Irwin, MD, 1 in this issue of Continuum . For evaluating patients with RPDs, many of the same principles apply, but because of the rapidity of decline, and as many causes of RPD are treatable, it is essential to have a systematic, comprehensive approach to the diagnostic plan.…”

Section: Diagnostic Approach To Rapidly Progressive Dementiasmentioning

confidence: 99%

“…44 Three radiologic features suggested against Jakob-Creutzfeldt disease in this case: (1) such quick resolution of the restricted diffusion without volume loss; (2) the striatal involvement was uniformly bright, whereas in Jakob-Creutzfeldt disease there is usually an anterior to posterior decreasing gradient; and (3) isolated striatal involvement without any cortical ribboning is uncommon in Jakob-Creutzfeldt disease (approximately 2% of cases). 1 Symptoms such as dysarthria, bradykinesia, dystonia, and akinetic mutism mimic sporadic Jakob-Creutzfeldt disease, but clinical and radiologic improvement are different from those seen in sporadic Jakob-Creutzfeldt disease. A detailed description of this case is published.…”

Section: Figure 7-1mentioning

confidence: 99%

“…The general approach to a patient with dementia is discussed in the article “The Mental Status Examination in Patients With Suspected Dementia” by Murray Grossman, MD, FAAN, and David J. Irwin, MD, 1 in this issue of Continuum , but the diagnosis of rapidly progressive dementias (RPDs) entails a different diagnostic approach. Although there is no clear definition for the time frame of an RPD, the author typically uses the term to refer to conditions that progress from onset of first symptom to dementia (decline in more than one cognitive domain with functional impairment) in less than 1 to 2 years, although most occur over weeks to months.…”

Section: Introductionmentioning

confidence: 99%

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Rapidly Progressive Dementia

Geschwind¹

2016

CONTINUUM: Lifelong Learning in Neurology

132

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Purpose of Review This article presents a practical and informative approach to the evaluation of a patient with a rapidly progressive dementia (RPD). Recent Findings Prion diseases are the prototypical causes of RPD, but reversible causes of RPD might mimic prion disease and should always be considered in a differential diagnosis. Aside from prion diseases, the most common causes of RPD are atypical presentations of other neurodegenerative disorders, curable disorders including autoimmune encephalopathies, as well as some infections, and neoplasms. Numerous recent case reports suggest dural arterial venous fistulas sometimes cause RPDs. Summary RPDs, in which patients typically develop dementia over weeks to months, require an alternative differential than the slowly progressive dementias that occur over a few years. Because of their rapid decline, patients with RPDs necessitate urgent evaluation and often require an extensive workup, typically with multiple tests being sent or performed concurrently. Jakob-Creutzfeldt disease, perhaps the prototypical RPD, is often the first diagnosis many neurologists consider when treating a patient with rapid cognitive decline. Many conditions other than prion disease, however, including numerous reversible or curable conditions, can present as an RPD. This chapter discusses some of the major etiologies for RPDs and offers an algorithm for diagnosis.

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Section: Diagnostic Approach To Rapidly Progressive Dementiasmentioning

confidence: 99%

Section: Figure 7-1mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Rapidly Progressive Dementia

Geschwind¹

2016

CONTINUUM: Lifelong Learning in Neurology

132

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“…Visuospatial abilities can be assessed by asking the patient to draw two interlocking pentagons (or other geometric figures like a cube, a circle, two overlapping rectangles) or performing the clock face-drawing test. The Rey-Osterreith Complex Figure test can also be used 53,54 . In fact, CBD patients may present with other cognitive and motor deficits, such as apraxia, executive dysfunction and dystonia, which may negatively affect the neuropsychological exam of visuospatial abilities.…”

Section: Visuospatial Abilitiesmentioning

confidence: 99%

“…Single-word processing can be assessed with confrontation naming and is usually impaired in the nonfluent/agrammatic variant of primary progressive aphasia. Comprehension can be assessed by providing written and verbal command, asking the patient to write a sentence and repeat words and sentences and, finally, asking the patient to read some words or a sentence 53 . Of note, a more generalized pattern of atrophy involving the inferior frontal and temporal lobes was related to CBS patients presenting with marked dementia and aphasia 50 .…”

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confidence: 99%

Cognitive dysfunction in corticobasal degeneration

Oliveira

Barcellos

Teive

et al. 2017

Arq. Neuro-Psiquiatr.

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Corticobasal degeneration (CBD) is a rare and progressive neurodegenerative disease. It was originally described as a distinct clinicopathological entity in 1967 1 and later recognized as a polymorphous disease due to its complexity. In fact, the classical set of symptoms -namely asymmetric motor features associated with higher cortical function -were found to be associated with multiple histological presentations. Furthermore, the distinctive histopathological findings of cortical and striatal neuronal deposition of tau, and glial inclusions, were also linked to a wide variety of clinical phenotypes 2 . Hence, recent literature refers to corticobasal syndrome (CBS) as the constellation of symptoms described originally, limiting CBD to the distinctive histopathological findings .The different terminology with a seemingly paradoxical intrinsic overlap between these conditions makes diagnosis challenging. For instance, only 25% to 56.25% of patients with pathologically-confirmed CBD had previously presented with symptoms of CBS 4,5,6 . On the other hand, the proportion of patients diagnosed with CBS presenting with the histologic hallmarks of CBD is highly variable, ranging from 23.8% to 100% 4,5,6,7 . Considering the enormous difficulty in accurately diagnosing CBD during life, it is clear that current ABSTRACTCorticobasal degeneration (CBD) was originally described as a distinct clinicopathological entity in 1967. Since then, different phenotypic presentations have emerged as possible manifestations of CBD histopathological findings. In addition, pathophysiological findings and the molecular basis have been delineated and several aspects of its cognitive manifestations have been clarified. Thus, not only the spectrum of what is currently designated as CBD has expanded, but overlap with other degenerative and even secondary disorders has made clinical diagnostic certainty even more challenging in the absence of specific and readily-available markers. Cognitive deficits in CBD are now recognized as a frequent initial presentation and may appear up to eight years before the motor symptoms, depending on the phenotypic variant. Characteristic cognitive features of CBD involve language deficits, visuospatial and executive dysfunctions, apraxia, and behavioral disorders. Semantic and episodic memories are usually preserved, while language is often impaired in the early stages.Keywords: dementia; cognition; corticobasal degeneration. RESUMOA degeneração corticobasal (DCB) foi originalmente descrita como uma entidade clínico-patológica distinta em 1967. Desde então, nossa compreensão sobre DCB evoluiu substancialmente. Diferentes apresentações fenotípicas emergiram refletindo possíveis manifestações das anormalidades histopatológicos da DCB. Adicionalmente, dados fisiopatológicos e moleculares foram delineados e aspectos das manifestações cognitivas foram explorados. Assim, não só o espectro do que é atualmente designado DCB foi expandido, mas a sobreposição com outras doenças degenerativas e até mesmo secundárias to...

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Bias induced by ignoring double truncation inherent in autopsy‐confirmed survival studies of neurodegenerative diseases

Rennert

Xie

2019

Statistics in Medicine

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Neurodegenerative diseases require an autopsy for confirmation of diagnosis. When death is the event of interest, studies based on autopsy-confirmed diagnoses result in right truncated survival times, since individuals who live past the end of study date do not receive a pathological diagnosis and are therefore not included in the sample. Furthermore, many studies of neurodegenerative diseases recruit subjects only after the onset of the disease, which may result in left truncated survival times. Therefore double truncation, the simultaneous presence of left and right truncation, is inherent in many autopsy-confirmed survival studies of neurodegenerative diseases. The main focus of this paper is to inform about the inherent double truncation in these studies and demonstrate how to properly estimate and compare survival distribution functions in this setting. We do so by conducting a case study of subjects with autopsy-confirmed Alzheimer’s disease and frontotemporal lobar degeneration. This case study is supported by extensive simulation studies, which provide several new contributions to the literature on survival distribution estimation in the context of double truncation.

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The Mental Status Examination in Patients With Suspected Dementia

Cited by 21 publications

References 51 publications

Rapidly Progressive Dementia

Rapidly Progressive Dementia

Cognitive dysfunction in corticobasal degeneration

Bias induced by ignoring double truncation inherent in autopsy‐confirmed survival studies of neurodegenerative diseases

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