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J V Bowler

Publications and source records attributed to J V Bowler.

29 records · Page 2Linked to original sources
PubMed1993

Vascular dementia.

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Cerebrovascular Disorders↗
PubMed1992

High resolution SPECT, small deep infarcts and diaschisis.

Eighteen cases of lacunar infarction are presented. Six of these cases had a purely motor clinical deficit. All the cases were studied by serial high resolution SPECT (single photon emission computerized tomography) using 99Tcm HMPAO. The degree and extent of the changes in cerebral perfusion consistent with diaschisis were noted and these compared with the severity of the clinical deficit at presentation and over time. No significant correlation between diaschisis and the clinical state was found at any stage. The nature, aetiology and importance of diaschisis are discussed and it is suggested that caution should be exercised in attributing clinical features to diaschisis simply because it may be present.

Aged↗
PubMed1990

Syringomyelia and syringobulbia following tuberculous meningitis.

Tuberculous meningitis may rarely be followed by the development of a syrinx even after apparently successful chemotherapy. There are only six previously reported cases of this unusual complication; these are reviewed. A case is described of syringomyelia which developed 1 year after TBM. One year later magnetic resonance imaging demonstrated not only the spontaneous resolution of the syringomyelia but also the appearance of a new cavity within the brain stem. This surprising sequence of events illustrates the need for extensive studies of the natural history of syrinxes of differing aetiologies.

Adult↗
PubMedDate not supplied

Profiles of cognitive decline in Alzheimer disease.

Most recent studies have used only two observations to estimate the rate of cognitive decline in patients with Alzheimer disease (AD); few have data taken from more than a 2-year period; and none report on autopsy-verified cases. Repeated observations over the complete course of the disease are necessary to quantitatively evaluate hypotheses such as the triphasic linear model of Brooks et al. (1993). The goal of this study is to compare the triphasic linear and quadratic models of decline in a group of 12 AD patients confirmed at autopsy with a group of age- and sex-matched normal control subjects. Both groups were taken from the University of Western Ontario Dementia Study, and the Extended Scale for Dementia was used as the outcome measure. The squared multiple correlation as a measure of goodness of fit suggested the superiority of the more parsimonious quadratic model over the triphasic linear model. Quantitative models more accurately reflect the profiles of change in AD and may prove more sensitive in measuring the effects of drugs on these patterns.

Aged↗
PubMedDate not supplied

The cognitive syndrome of vascular dementia: implications for clinical trials.

Dementia is common among patients with cerebrovascular disease, particularly in a setting of one or more clinically evident strokes. Prior cohort and case studies have suggested that the cognitive syndrome of vascular dementia is characterized by predominant executive dysfunction, in contrast to the deficits in memory and language function that are typical of patients with Alzheimer disease. The course of cognitive decline may also differ between those dementia subtypes, with many, but not all, patients with vascular dementia exhibiting a stepwise course of decline caused by recurrent stroke and most patients with Alzheimer disease exhibiting a gradually progressive course of decline. The findings of prior studies of the cognitive syndrome of vascular dementia must be interpreted with caution, however, because of (1) possible inaccuracies in the determination of the dementia subtype and the loss of precision that might result from pooling heterogeneous subgroups of patients with vascular dementia, (2) difficulties inherent in identifying a pattern of strengths and weaknesses in patients who are required to have memory impairment and other deficits to meet operationalized criteria for dementia, and (3) the use of limited test batteries whose psychometric properties are incompletely understood. Specific questions that should be addressed by future studies are discussed.

Clinical Trials as Topic↗
PubMedDate not supplied

Conceptual background to vascular cognitive impairment.

The current criteria for vascular dementia use a paradigm that first diagnoses dementia on the basis of Alzheimer-type criteria and then superimposes upon this vascular events and risk factors to convert a diagnosis of Alzheimer disease to one of vascular dementia. There are two fundamental flaws with this approach. First, the neuropsychological features of Alzheimer disease are not the same as those for vascular dementia and so use of the current criteria will fail to diagnose many cases, particularly those in whom memory loss is not prominent. Second, progression of vascular dementia should be modifiable by adjustment of risk factors and, possibly, by the use of neuroprotective agents. Given this, it is absurd to wait until patients are frankly demented. It is far more appropriate to detect patients at risk of developing cognitive loss as soon as possible. This could be in the earliest symptomatic stage (vascular cognitive impairment) or even prior to this (brain-at-risk) stage. New criteria, based on evidence rather than on supposition, that focus on early disease are urgently needed.

Alzheimer Disease↗
PubMedDate not supplied

Imaging of static brain lesions in vascular dementia: implications for clinical trials.

Vascular dementia (VaD) relates to different vascular mechanisms and changes in the brain and has different causes and clinical manifestations, reflecting complex interactions between vascular etiologies, changes in the brain, host factors, and cognition. Critical elements to the concept and diagnosis of VaD are defining the vascular causes, the vascular etiologies, and changes in the brain. Verifying the relation between brain lesions and cognition (i.e., the extent to which brain changes cause, compound, or coexist with cognitive impairment) and establishing the types, extent, side, site, and tempo of brain lesions that relate to incident cognitive impairment are major diagnostic challenges. Previous work on interactions between brain lesion and cognition in to cerebrovascular disease (CVD) have shown variation in the definitions and measures of cognitive impairment, in the techniques and methods used to reveal different brain changes, and in the selection of patient populations. Furthermore, small sample sizes and the absence of multivariate statistics have been design limitations. Accordingly, the different sets of criteria used and methods applied identify different numbers and clusters of subjects and different distribution of brain changes. Furthermore, this heterogeneity is reflected in variation in natural history such as the rate of progression of decline in different cognitive domains over time. All these factors have hampered optimal designs of clinical drug trials. A summary of generalizations regarding lesion and cognition interaction in VaD can be made. (1) Not a single feature, but a combination of infarct features--extent and type of white matter lesions (WMLs), degree and site of atrophy, and host factor characteristics--constitues correlates of VaD. (2) Infarct features favoring VaD include bilaterality, multiplicity (>1), location in the dominant hemisphere, and location in the limbic structures (fronto- and mediolimbic). (3) WML features favoring VaD are extensive WMLs (extensive periventricular WMLs and confluent to extensive WMLs in the deep WM). (4) It is doubtful that only a single small lesion could provide imaging evidence for a diagnosis of VaD. (5) Absence of CVD lesions on computed tomography or magnetic resonance imaging is strong evidence against a diagnosis of VaD. In forthcoming protocols on CVD-associated cognitive impairment, the following brain imaging features should be specified: detailed characterization of brain changes; use of possible predefined subtypes based on brain imaging; use of rating of vascular burden; defining the type and extent of WMLs favoring a diagnosis of VaD; defining the extent of medial temporal lobe atrophy disfavoring a diagnosis of VaD; and technical harmonization of methods of scanning and analysis.

Brain↗