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Biomedical subjects

P Scheltens

Publications and source records attributed to P Scheltens.

At least 163 records · Page 9Linked to original sources
PubMed1991

Serial quantitative MR assessment of optic neuritis in a case of neuromyelitis optica, using Gadolinium- "enhanced" STIR imaging.

A patient is presented with neuromyelitis optica. MR imaging, using a short inversion time inversion recovery (STIR) technique, clearly depicted the lesion in the left optic nerve. Subsequent serial STIR imaging, with and without Gadolinium-DTPA, allowed quantitative assessment of changes parallel to improved optic nerve function. STIR imaging is a sensitive technique to demonstrate optic nerve lesions, and enables quantitative assessment to be made of the effect of (steroid) medication.

Adult↗
PubMed1991

Quantitative MRI changes in gadolinium-DTPA enhancement after high-dose intravenous methylprednisolone in multiple sclerosis.

In 12 patients with definite multiple sclerosis who received a total of 21 courses of high-dose (1 gram daily for 10 consecutive days) intravenous methylprednisolone, we performed MRI of the brain with and without gadolinium-DTPA before and after treatment. On the initial MRI, there was a total of 98 enhancing lesions, 93 of which were also represented on the unenhanced images. After treatment, 13 patients improved clinically, and 78 of the lesions lost enhancement but remained visible on the unenhanced images. There were six new enhancing lesions on the second MRI. Thus, the blood-brain-barrier integrity improved after high-dose IV methylprednisolone, which correlated well with the clinical improvement. The lesions remaining visible on the unenhanced images indicate an incomplete histologic recovery at the time of the second scan, and also demonstrate that unenhanced MRI alone is not sufficient to monitor disease activity in the short term in multiple sclerosis.

Adult↗
PubMed1990

A Dutch family with autosomal dominant pure spastic paraparesis (Strümpell's disease).

Families with "pure" hereditary spastic paraparesis of late onset have rarely been reported. Since the original article by Strümpell in 1880, many "complicated" forms of the disorder have been reported, and the question as to whether a "pure" form exists still arises from time to time. We present a Dutch family with "pure" hereditary spastic paraparesis, involving 15 affected members in three generations. The mode of inheritance was autosomal dominant, with onset of clinical signs in the fourth or fifth decade. Severity of the disease was mild; only a few of them became chairbound in the end. There were no sensory symptoms. Mild sphincter disturbances were mentioned by six patients. A review of the reports on Dutch families is given and arguments in favour of the existence of "pure" hereditary spastic paraparesis are discussed.

Adult↗
PubMed1990

A case of progressive aphasia without dementia: "temporal" Pick's disease?

We report a patient who suffered from progressive aphasia for nine years, before developing mild behavioural disturbances. Sequential computed tomography (CT) scanning and magnetic resonance (MRI) imaging showed progressive bilateral temporal atrophy. The case is thought to be a temporal form of Pick's disease, in which isolated progressive aphasia was the only symptom over many years.

Aphasia↗
PubMed1989

Anterolateral lumbar meningocele presenting as an ovarian cyst, in a patient with neurofibromatosis.

A case of an anterolateral lumbar meningocele in a patient with neurofibromatosis is presented. As anterolateral lumbar meningocele may present itself only by non-specific symptoms like low back pain or abdominal pain, such symptoms require prompt diagnostic work up in patients with neurofibromatosis. The significance of MR imaging in early recognition of this rare anomaly is emphasized.

Adult↗
PubMedDate not supplied

Vascular dementia: the role of cerebral infarcts.

Although vascular dementia (VaD) is the second most frequent cause of dementia after Alzheimer disease (AD), the concept remains controversial in terms of delineation. The objective of this review is to investigate, from available literature, the role of cerebral infarcts in the pathogenesis of VaD and to identify areas of interest that need further evaluation and research. The incidence of new onset dementia is increased after stroke. Stroke subtypes, total volume of cerebral infarction and functional tissue loss, and location of the lesions are probably the major determinants of VaD. Any cause of stroke can lead to VaD. In some circumstances the causal relation between stroke and dementia is clear: (1) in young patients who are unlikely to have associated Alzheimer pathology; (2) when the cognitive functioning was normal before stroke, impaired immediately after, and does not worsen over time; (3) when the lesions are located in strategic areas; and (4) when a well-defined vasculopathy known to cause dementia is proven. However, several issues remain unsolved in VaD: lack of specificity of the diagnostic criteria; influence of white matter changes and associated Alzheimer pathology; influence of preexisting cognitive status; possibility of having VaD without stroke and the clinical relevance of silent infarcts to VaD; and best therapeutic strategy to be used to prevent VaD and to prevent stroke in patients with VaD. These questions form the basis for proposals for future research.

Cerebral Infarction↗
PubMedDate not supplied

Diagnostic criteria for vascular dementia.

The term vascular dementia implies the presence of a clinical syndrome (dementia) caused by, or at least assumed to be caused by, a specific disorder (cerebrovascular disease). In this review, the various sets of criteria used to define vascular dementia are outlined. The various sets of criteria are judged whether they contain criteria for both dementia and vascular disease as well as for the relationship between the two. We conclude that only the criteria of the State of California Alzheimer's Disease Diagnostic and Treatment Centers and of NINDS-AIREN provide sufficient operational criteria for dementia suitable for use in patients with vascular disease as well as for the diagnosis of cerebrovascular disease and for the establishment of a relationship between dementia and vascular disease. The latter criteria include also specific recommendations to the use of CT and MRI. However, the interpretation of the neuroimaging findings in the context of mixed vascular and degenerative dementia demands further study. Given the heterogeneous pathophysiology and pathology of vascular dementia and the modest reliability of the criteria, it seems plausible that the diagnosis of vascular dementia will become more reliable when specific diagnostic tests for the various degenerative diseases, from which vascular dementia has to be differentiated, become available.

Aging↗
PubMedDate not supplied

Diagnosing Alzheimer's disease in community-dwelling elderly: a comparison of EEG and MRI.

In a study on the course of cognitive impairment in people over 65 years of age, 58 randomly selected community dwelling elderly underwent EEG and MRI studies. The EEG was visually and quantitatively (qEEG) assessed. Nine out of 58 subjects appeared to have Alzheimer dementia (AD) according to CAMDEX criteria. In this group medial temporal lobe atrophy on MRI, as an objective criterium for AD, showed a total accuracy of 72%, visually assessed EEG 81% and qEEG 81-84%. There was an incomplete overlap in subjects regarding MRI and EEG abnormalities, implying that both methods may be complementary.

Aged↗
PubMedDate not supplied

Role of white matter lesions in cognitive impairment of vascular origin.

White matter changes are detected with high frequency by neuroimaging techniques in aged subjects with cerebrovascular risk factors or diseases and in cognitively impaired patients. Their direct role in causing cognitive deterioration has not been established, although their frequency is higher in demented subjects than in normal controls, and they are associated with specific cognitive deficits, particularly those related to impairment of frontal lobe functions. The aim of this paper is to critically review the existing knowledge about the role of white matter lesions in cognitive impairment of vascular origin. After reviewing the scarce evidence and the numerous clues suggesting a possible role of white matter lesions in causing mental decline, proposals are advanced about elements that could be a basis for revised criteria for vascular dementia for clinical trials. Finally, some items requiring future joint investigations in the fields of age-related white matter lesions are identified.

Cerebrovascular Disorders↗
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↗
PubMedDate not supplied

Functional MR imaging in Alzheimer's disease during memory encoding.

BACKGROUND AND PURPOSE: We applied functional MR imaging with a learning task in healthy elderly volunteers and in patients with Alzheimer's disease to study brain activation during memory performance. The purpose was to determine the feasibility of functional MR imaging during a learning task in healthy elderly volunteers and in patients with Alzheimer's disease and to test our hypothesis that brain activation is decreased in the medial temporal lobe (MTL) memory system in patients with Alzheimer's disease compared with control volunteers. METHODS: In 12 patients with mild to moderate forms of Alzheimer's disease and 10 elderly control volunteers, activation of the MTL memory system was studied. We used two learning tasks that required the encoding of new information into memory. After the functional MR imaging experiment, participants were tested for recognition of the encoded objects. RESULTS: In the elderly control volunteers, activation during memory encoding was observed in medial and lateral temporal lobe structures (fusiform, parietal and occipital parts, and hippocampal formation) and in the frontal cortex, as reported previously in studies of young control volunteers. Focusing on the MTL, we observed that activation was significantly decreased in patients with Alzheimer's disease compared with control volunteers in the left hippocampus and parahippocampal gyrus bilaterally during the first encoding task but not during the second (P < .05, uncorrected). CONCLUSION: Functional MR imaging with a learning task seems feasible in elderly volunteers and in patients with Alzheimer's disease. The measured functional signal decrease in MTL areas warrants further exploration of the (early) diagnostic usefulness of functional MR imaging in cases of Alzheimer's disease and other dementias.

Aged↗
PubMedDate not supplied

Gadopentetate dimeglumine enhancement of multiple sclerosis lesions on long TR spin-echo images at 0.6 T.

The authors sought to determine if Gd-DTPA enhancement of multiple sclerosis (MS) hampers lesion detection on long TR spin-echo images (TE 60 msec) at 0.6 T. They measured the signal intensity (SI) of 41 lesions (10 patients) and normal-appearing gray (NAGM) and white matter (NAWM) before and after administration of contrast. The change in SI of nonenhancing lesions and NAGM and NAWM was small (less than or equal to 1.5%), and of enhancing lesions (5.3%) moderate. The contrast of nonenhancing lesions to NAGM and NAWM changed insignificantly, but the contrast of enhancing lesions to NAGM and NAWM increased significantly. The authors conclude that long TR images can be obtained after Gd-DTPA without hampering lesion conspicuity in research MR protocols in multiple sclerosis.

Adult↗