A Critical Review: Dementia in Middle Age

McMenemey, W. H.

doi:10.1136/jnnp.4.1.48

Cited by 14 publications

(2 citation statements)

References 78 publications

(14 reference statements)

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“…Traditionally, presenile cases of dementia are distinguished from senile cases because of the suspected heterogeneity of these diseases. The majority of 20th century clinical neuropathologists believed that the two forms of dementia were not a single form of senile dementia and that these diseases were heterogeneous in nature and origin . In addition, clinicians who cared for demented patients for years—from disease onset through the progressing symptoms, clinical course, and terminal stage—believed the cases to be diverse and were unable to conclude that these cases belong to one uniform disease entity …”

Section: Discussionmentioning

confidence: 99%

Alzheimer's disease or Alzheimer's syndrome?: a longitudinal computed tomography neuroradiological follow‐up study of 56 cases diagnosed clinically as Alzheimer's disease

et al. 2015

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Cases of so-called Alzheimer's disease, as observed through continued clinical follow-up and serial CT examinations, appear so diverse in symptomatology and radiological pathomorphology that it is difficult to consider them a single nosological entity. The pathology of Alzheimer's disease has to be reconsidered in accordance with the variety observed in the sequential development of neuroradiological findings. The pathology must be reconstructed in terms of topographical dimensions and chronological developments. The diagnosis of Alzheimer's disease appears to be not so simple based on any conventional diagnostic operational standards.

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Section: Discussionmentioning

confidence: 99%

Alzheimer's disease or Alzheimer's syndrome?: a longitudinal computed tomography neuroradiological follow‐up study of 56 cases diagnosed clinically as Alzheimer's disease

et al. 2015

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“…William McMenemey (1941), later director of the pathology laboratory at the National Hospitals for Nervous Diseases, Maida Vale, wrote that the 'so-called CJD' was a doubtful entity which should be regarded as a syndrome rather than a disease. He wrote: 'It remains at present a convenient dumping ground for several instances of atypical presenile dementias which run a rapid course and have for their histology a parenchymatous degeneration of the brain with some glial hyperplasia' (p. 60).…”

Section: Objections To Jakob's Viewsmentioning

confidence: 98%

Origins of the Creutzfeldt and Jakob Concept

Duckett¹,

Stern²

1999

Journal of the History of the Neurosciences

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A review of the publications of Hans Creutzfeldt and Alfons Jakob pertaining to the concept which bears their name (CJD) reveals that they described a neuropathological syndrome and were opposed to its classification as a neurological disease. The evidence on which Creutzfeldt and Jakob based their view is reevaluated, and studies by other workers are cited in which a range of environmental and genetic factors generated the CJ syndrome, challenging the proposition that CJD is a disease with a single cause.

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Creutzfeldt-Jakob Disease

May¹,

Itabashi²,

DeJong³

1968

Arch Neurol

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Background: The prevalence and characteristics of sleep-wake disturbances in sporadic Creutzfeldt-Jakob disease (sCJD) are poorly understood. Methods: Seven consecutive patients with definite sCJD underwent a systematic assessment of sleep-wake disturbances, including clinical history, video-polysomnography, and actigraphy. Extent and distribution of neurodegeneration was estimated by brain autopsy in six patients. Western blot analyses enabling classification and quantification of the protease-resistant isoform of the prion protein, PrP Sc , in thalamus and occipital cortex was available in four patients. Results: Sleep-wake symptoms were observed in all patients, and were prominent in four of them. All patients had severe sleep EEG abnormalities with loss of sleep spindles, very low sleep efficiency, and virtual absence of REM sleep. The correlation between different methods to assess sleep-wake functions (history, polysomnography, actigraphy, videography) was generally poor. Brain autopsy revealed prominent changes in cortical areas, but only mild changes in the thalamus. No mutation of the PRNP gene was found. Conclusions: This study demonstrates in sporadic Creutzfeldt-Jakob disease, first, the existence of sleep-wake disturbances similar to those reported in fatal familial insomnia in the absence of prominent and isolated thalamic neuronal loss, and second, the need of a multimodal approach for the unambiguous assessment of sleep-wake functions in these patients.

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A Critical Review: Dementia in Middle Age

Cited by 14 publications

References 78 publications

Alzheimer's disease or Alzheimer's syndrome?: a longitudinal computed tomography neuroradiological follow‐up study of 56 cases diagnosed clinically as Alzheimer's disease

Alzheimer's disease or Alzheimer's syndrome?: a longitudinal computed tomography neuroradiological follow‐up study of 56 cases diagnosed clinically as Alzheimer's disease

Origins of the Creutzfeldt and Jakob Concept

Creutzfeldt-Jakob Disease

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