649 research outputs found

    Hachinski's ischemic score and the diagnosis of vascular dementia: a review

    No full text
    The Hachinski ischemic score (HIS) scale is a simple clinical tool proposed and currently used for differentiating types of dementia (primary degenerative, vascular or multi-infarct, mixed type). Criteria for rating the items of the HIS were never given, or inter-observer reliability in applying it has never been tested. However, the studies which estimated the validity of this scale in predicting the true diagnosis (clinical/CT or neuropathological definition) demonstrated acceptable sensitivity and specificity in defining degenerative or vascular dementia. This scale seems unable to define mixed type dementia or subtypes of vascular dementia. Our review supports the use of the HIS in epidemiological studies on dementia

    The first Italian report on "Binswanger's disease"

    No full text
    The eponym "Binswanger's disease" is frequently used to indicate a form of vascular dementia characterized by white matter rarefaction and lacunar infarcts; however, it is difficult to find any consistency between this picture and the single case reported by Binswanger in 1894, which was vaguely defined both clinically and pathologically, and was probably a case of neurosyphilis. The first Italian report of a case of "Binswanger's disease" was published in 1958 by Donegani and Grattarola, who described a patient with a history of manic episodes followed by progressive mental deterioration. Pathological examination revealed changes mainly located in the hemispheric white matter, and the authors defined the patient as being affected by Binswanger's encephalopathy. Re-evaluation of this report indicates that the term "Binswanger's disease" has been applied to cases with non-specific clinical and pathological characteristics in the past. In this paper, we briefly compare Binswanger's original and the 1958 Italian case report, and discuss the current use of the term "Binswanger's disease"

    Transient global amnesia: a review emphasizing pathogenic aspects

    No full text
    The transitory memory disturbance known as transient global amnesia (TGA) remains an enigma from a pathogenic point of view. In spite of its typical benign prognosis, TGA is a frightening experience for patients and their relatives. Moreover, a TGA episode usually leads to extensive investigation of patients in search of organic alterations that might be responsible for the event. Finally, TGA generates queries about therapeutic choices. In this review, we critically re-evaluate the evidence in support of and against the three main pathogenic hypotheses (i.e. ischemia, seizure discharge, and migraine), and we conclude that none of these appears completely convincing. Given the good prognosis and the lack of association with organic and instrumental abnormalities, we advance the hypothesis that TGA may be related to psychological disturbances causing transient alteration in brain metabolism and, consequently, amnesia. Our conclusion has relevant consequences in the evaluation of patients with TGA

    White matter changes: the clinical consequences in the aging population

    No full text
    Neuroimaging changes in the cerebral subcortical white matter (WMC) are recognized with the highest frequency in elderly subjects, particularly in those with vascular risk factors. WMC have been consistently reported to be associated with global or selective cognitive deficits, depression, motor and gait impairment. All these deficits are main contributors to disability in the elderly. Moreover, subjects with WMC have an increased risk of cardiovascular events and death from vascular causes. Functional status in subjects with WMC is variable, from normal to severely (physically or cognitively) disable. The association of WMC with age and with some of the clinical manifestations of aging suggests that WMC could be one of the age-related processes involved in the transition to disability in the elderly. Large cohorts of patients with WMC of different severity and detailed follow-up observation may help elucidating this issue. If WMC are shown to have an impact on disability in the aged population, efforts could be made to prevent WMC and WMC-related motor and cognitive deficits, and to identify measures aimed to halt or slow their progression

    Cognitive decline and dementia related to cerebrovascular diseases : some evidence and concepts

    No full text
    Background: Cerebrovascular diseases (CVDs) are considered the second most common cause of cognitive decline in the elderly after neurodegeneration of the Alzheimer's type. Despite impressive epidemiological data, the actual burden of CVDs in terms of cognitive decline is still incompletely appreciated by physicians and health regulators. Methods: In this brief position paper, we review some evidence related to the topic and its clinical relevance, and we present some concepts that we consider of crucial importance for the correct recognition of the problem. Results and Conclusions: We conclude that: (1) different approaches to the topic exist (clinical, neuroimaging-based, pathological) and the inconsistent use of one or another, together with lack of definitions, has limited the appreciation of the contribution of CVDs to cognitive decline; (2) cognitive impairment related to CVDs is very frequent and constitutes a topic with high epidemiological impact; (3) cognitive impairment associated with CVDs is heterogeneous in clinical and pathogenic terms; (4) vascular lesions often interact with other type lesions, the most important of which are today considered those of the Alzheimer's type, in determining cognitive impairment; (5) for some vascular lesions, namely white matter lesions and lacunar infarcts, strong evidence suggests their role as determinants of cognitive decline; (6) cognitive impairment is only part of the consequences of CVDs as it is almost invariably accompanied by gait disturbances, depressive symptoms, and sphincteric control dysfunction, all factors contributing to loss of independence

    Cytokines and cell adhesion molecules in cerebral ischemia: experimental bases and therapeutic perspectives

    No full text
    The possibility of reopening an occluded cerebral artery by means of thrombolysis has renewed interest in a number of the several mechanisms that are active during acute cerebral ischemia. Over recent years, it has become apparent that leukocytes play a central role not only during the healing stage of brain infarction but also during the early phases of cerebral ischemia, when it is postulated that these cells produce harmful effects, particularly in the presence of reperfusion. This review is based on the critical analysis of more than 150 publications dealing with the role of leukocytes and some inflammatory mediators (cytokines, chemokines, and adhesion molecules) in cerebral ischemia. Animal studies indicate that leukocyte involvement is promoted by a variety of inflammatory molecules produced immediately after the onset of cerebral ischemia. Considerable experimental evidence suggests that these mediators play a key role in the progression from ischemia to irreversible injury (ie, cellular death and necrosis). However, the precise role of each molecule alone remains to be further elucidated as well as in relation to the complex network existing among different mediators. Progress in our understanding of the inflammatory mechanisms operating in cerebral ischemia has enabled the testing of new compounds with promising results in animals; in contrast, one recent controlled trial of an anti-leukocyte molecule in acute stroke patients showed negative results. This discrepancy may derive in part from our incomplete understanding of the complexity of the inflammatory mechanisms involved in cerebral ischemia. Our analysis suggests that until sufficient knowledge of the underlying disease mechanisms is acquired, more care should be taken when testing new and potentially efficacious drugs in stroke patients
    corecore