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Biomedical subjects

L Pantoni

Publications and source records attributed to L Pantoni.

At least 55 records · Page 3Linked to original sources
PubMed1997

Cognitive impairment and cellular/vascular changes in the cerebral white matter.

A possible relation between cerebral white-matter injury and dementia was intuitively attributed by Alzheimer to changes affecting the small penetrating vessels that supply the cerebral white matter. Several observations support the view that white-matter changes detectable by neuroimaging may contribute to cognitive deficits in the elderly. But many questions concerning this matter remain partially answered. In this communication we review: (1) Selected anatomic features of the blood vessels supplying the white matter; (2) possible pathogenetic mechanisms responsible for the white-matter changes; (3) observations on humans and animals suggesting a causal relationship between ischemia/hypoxemia and white-matter injury; (4) epidemiologic studies linking white-matter abnormalities with cognitive disorders. We conclude that abnormalities in the small vessels caused by aging and arterial hypertension, or other processes (cerebral amyloid angiopathy, CADASIL) together with systemic circulatory disturbances, such as abrupt variations in blood pressure values or cardiac diseases, may be the substrate of selective white-matter injury. The damage is structurally characterized by incomplete infarction or selective cellular injury.

Alzheimer Disease↗
PubMed1997

Emotional arousal and phobia in transient global amnesia.

OBJECTIVE: To evaluate the role of emotionally stressful or phobogenic events and phobic personality traits in transient global amnesia (TGA). DESIGN: Case-control study. SETTING: Tertiary care center. PATIENTS: Fifty-one case patients with TGA (mean +/- SD age, 62.7 +/- 6.7 years) compared with 51 control patients with transient ischemic attacks (mean +/- SD age, 63.8 +/- 6.7 years). MAIN OUTCOME MEASURES: Precipitant factors, life events, and phobic attitudes. RESULTS: Of the 25 TGA attacks that were triggered by a precipitant, 11 were possibly related to emotionally stressful or phobogenic situations. On a scale that measured phobic attitudes, the case patients with TGA scored significantly higher than the control patients with transient ischemic attacks (mean +/- SD total score, 15.21 +/- 11.0 vs 4.41 +/- 5.2; P < .001 by corrected analysis of variance for age, sex, and education). The amount of stressful live events in the year that preceded the attack did not differ between the case patients with TGA and the control patients with transient ischemic attacks. CONCLUSION: The results support the hypothesis that emotional arousal and phobia are involved in TGA.

Aged↗
PubMed1997

Vascular deaths in elderly neurological patients with leukoaraiosis.

OBJECTIVES: The prognostic significance of leukoaraiosis is still not completely elucidated. The objective was to examine survival and causes of death among elderly neurological patients with leukoaraiosis. METHODS: From 1 January 1994, vital status and causes of death were drawn from municipality lists and death certificates of 216 patients (mean age (SD) 70.6 (8.3) years) admitted to a geriatric unit who underwent cranial CT between 1 January 1984 and 31 December 1986 (mean observation period (SD) 8.4 (0.8) years). These patients had been enrolled for a study of clinical predictors of leukoaraiosis. Based on the presence of leukoaraiosis on CT, this group had been divided into two subgroups of patients, with and without leukoaraiosis. The difference in survival and causes of death between these groups formed the objective of the study. RESULTS: Survival time was shorter among the 90 patients with leukoaraiosis than among the 126 patients without (median survival time 4.07 v 7.78 years, log rank test P < 0.001). After controlling for age and other major death predictors, the risk of death remained significantly increased (relative risk (RR) = 1.64, 95% confidence interval (95% CI) 1.15-2.34) among patients with leukoaraiosis. Moreover, patients with leukoaraiosis had an almost threefold higher risk of dying from vascular causes than patients without (RR = 2.81, 95% CI 1.74-4.53). CONCLUSION: Leukoaraiosis is a predictor of vascular deaths in elderly neurological patients. Careful diagnostic evaluation and attention to preventive measures are required in patients with leukoaraiosis.

Aged↗
PubMed1997

Pathogenesis of leukoaraiosis: a review.

BACKGROUND: Changes in the cerebral hemispheric white matter, detectable with increasing frequency by modern neuroimaging methods, are associated with aging and conceivably may contribute to the development of specific cognitive deficits. The pathogenesis of these cerebral white matter abnormalities (sometimes described as leukoaraiosis) is unknown. This review evaluates the available evidence in support of the hypothesis that the etiology of leukoaraiosis is related to a specific type of cerebral ischemia and highlights mechanisms by which ischemic injury to the brain may induce selected structural alterations limited to the cerebral white matter. SUMMARY OF REVIEW: The review is based on the critical analysis of over 100 publications (most appearing in the last decade) dealing with the anatomy and physiology of the arterial circulation to the cerebral white matter and with the pathogenesis of leukoaraiosis. CONCLUSIONS: A significant number of clues support the hypothesis that some types of leukoaraiosis may be the result of ischemic injury to the brain. Structural changes affecting the small intraparenchymal cerebral arteries and arterioles that are associated with aging and with stroke risk factors, altered cerebral blood flow autoregulation, and the conditions created by the unique arterial blood supply of the hemispheric white matter each seem to contribute to the development of leukoaraiosis. To the best of our ability to interpret current information, the type of ischemic injury that is most likely responsible for these white matter changes involves transient repeated events characterized by moderate drops in regional cerebral blood flow that induce an incomplete form of infarction. This hypothesis could be tested in appropriate experimental models.

Brain Diseases↗
PubMed1997

Disappearance of motor tics after Wernicke's encephalopathy in a patient with Tourette's syndrome.

Tourette's syndrome (TS) is a disease characterized by multiple motor and vocal tics as well as behavioral abnormalities. The anatomic substrates of this syndrome are not defined. We report a 48-year-old man with TS in whom motor tics disappeared after the onset of a midbrain syndrome related to thiamine deficiency (Wernicke's encephalopathy). MRI study showed a lesion in the dorsal area of the midbrain. This case suggests that loops located in the midbrain tegmentum may influence the presence of motor tics in patients with TS.

Humans↗
PubMed1996

The first Italian report on "Binswanger's disease".

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".

Brain↗
PubMed1996

Vascular pathology in three cases of progressive cognitive deterioration.

The clinical condition known as vascular dementia remains poorly defined. Few studies have attempted a correlative link between the clinical syndrome and the structural abnormalities of the brain. Classically the clinical progression of the vascular dementing process is thought to be a multi-step process punctated by repeated episodes of ischemia, that are clinically expressed as strokes. In most instances it has been assumed that the substrate of vascular dementias consists of atherothrombotic infarcts. The objective of this report is to illustrate 3 cases of progressive (rather than stepwise) cognitive deterioration without clinical evidence of stroke, evolving over a period of several years, in which there were prominent vascular lesions. A complete autopsy and detailed neuropathologic examination demonstrated cerebral vascular lesions involving small arterial vessels (< 200 microns in diameter). The lesions consisted of moderate-to-severe arteriolosclerosis in two cases, and mild-to-moderate arteriolosclerosis in a case of Alzheimer's disease with severe cerebral amyloid angiopathy. Parenchymal lesions consisted of small cortical and subcortical infarcts, most of them smaller than 0.1 cm in average diameter, and subcortical leukoencephalopathy severe in two cases and mild-to-moderate in the third case. Severe atherosclerosis not accompanied by large infarcts was also present in one case. Arterial changes affecting small, distal branches causing sometimes small parenchymal lesions in association with diffuse cerebral white matter disease, appear to be the anatomical substrate that accompanies progressive cognitive impairment in some patients who are frequently diagnosed with Alzheimer's disease because in their clinical records there is neither history of strokes nor stepwise progression of symptoms.

Aged↗
PubMed1996

A preliminary open trial with nimodipine in patients with cognitive impairment and leukoaraiosis.

We treated, in a preliminary open trial, 31 patients presenting with cognitive impairment, progressive bilateral motor dysfunction, and leukoaraiosis on computed tomography (CT) with a 90-mg daily dose of nimodipine for a period as long as 1 year (minimum: 96 days, maximum: 424 days), to study the safety and possible effects on functional and cognitive conditions throughout this period. Of the 29 patients who had been followed for at least 9 months, most (82%) remained stable or improved as evaluated by the Global Deterioration Scale. A significant improvement was observed in the total Sandoz Clinical Assessment Geriatric scale score (44.66 +/- 7.17 at baseline vs. 36.86 +/- 9.34 at exit, analysis-of-variance time effect, p < 0.0001). These data indicate that nimodipine, chronically administered in patients presenting with cognitive impairment, progressive bilateral motor dysfunction, and leukoaraiosis on CT, is safe and might have beneficial effect, to be confirmed by a randomized trial.

Adult↗
PubMed1996

Cerebral white matter is highly vulnerable to ischemia.

BACKGROUND AND PURPOSE: The effects of ischemia on the cerebral white matter structure seldom have been studied possibly because white matter is generally considered less vulnerable to ischemia than gray matter. The objective of this study was to evaluate the early (< or = 24 hours) structural effects of experimental focal ischemia on the cerebral white matter of the rat as a preliminary step to investigating human conditions of unknown pathogenesis that are characterized by selective damage to the white matter. METHODS: Twenty-eight rats, including four controls, had a middle cerebral artery occluded with an intravascular filament for periods ranging between 0.5 and 24 hours. Brain samples from the subcortical white matter were examined with light and electron microscopic methods, and the abnormalities were quantified with an image-analysis system. RESULTS: As early as 30 minutes after the arterial occlusion, there was conspicuous swelling of oligodendrocytes and astrocytes; after 3 hours, large numbers of oligodendrocytes were lethally injured. These changes preceded by several hours the appearance of necrotic neurons in the cortex and basal ganglia. Vacuolation and pallor of the white matter were very marked after 24 hours and reflected the segmental swelling of myelinated axons, the formation of spaces between myelin sheaths and axolemma and astrocyte swelling. CONCLUSIONS: These results suggest that the cerebral white matter is highly vulnerable to the effects of focal ischemia. Pathological changes in oligodendrocytes and myelinated axons appear early and seem to be concomitant with, but independent of neuronal perikaryal injury. Modifications of this experimental model of focal ischemia could provide the means to test the hypothesis that selected types of human leukoencephalopathies have an ischemic origin.

Animals↗
PubMed1996

[Large trials in the secondary prevention of stroke].

To date, no drug has been demonstrated as efficacious in the treatment of acute ischemic stroke. Therefore, primary and secondary prevention play a fundamental role. Besides adequate control of risk factors, trials and meta-analyses have demonstrated that both medical and surgical therapy are effective in secondary prevention of stroke. In patients with atherothrombotic transient ischemic attack (TIA) or minor stroke and carotid stenosis > 70%, surgical therapy (endarterectomy) is the treatment of choice, while antiplatelet drugs are the elective treatment in the case of stenosis < 70%. Acetylsalicylic acid is the first choice medical treatment, but the optimal dosage is still a matter of debate. Ticlopidine has an efficacy similar to that of aspirin, but shows a certain number of side effects; recently a European study has shown the efficacy of dipyridamole, and the superiority of the combination dipyridamole-aspirin vs low-dose aspirin. In the secondary prevention of cardioembolic stroke, oral anticoagulants have higher efficacy than antiplatelet drugs, at least in selected groups of patients.

Anticoagulants↗
PubMed1995

Strokes in childhood.

Brain infarcts and brain hemorrhages in patients younger than 20 years are significantly less common than among those older than 65 years; also, their clinical expressions are different from those common to older patients. Congenital defects involving the heart and the arteries supplying the brain are among the most common causes of stroke in the young. In addition to the structural changes affecting the heart and blood vessels, various genetic disorders (hematologic, mitochondrial, and others) are being identified as significant risk factors in an increasing number of young stroke victims.

Adolescent↗
PubMed1995

The significance of cerebral white matter abnormalities 100 years after Binswanger's report. A review.

BACKGROUND: Changes in the cerebral hemispheric white matter are detected with increasing frequency by CT and MRI among persons older than 60 years. The pathogenesis, clinical significance, and morphological substrate of these changes are incompletely understood. Patients who have such neuroimaging abnormalities are sometimes diagnosed with "Binswanger's disease," an eponym that has generated much confusion because of its imprecise meaning. The objectives of this study were to determine whether the term Binswanger's disease merits acceptance as a distinct clinicopathologic entity, to deduce the clinical significance of these white matter abnormalities from the analysis of appropriate publications, and to evaluate studies that correlate in vivo changes in the cerebral white matter with pathological features. SUMMARY OF REVIEW: We evaluated Binswanger's original case description and, after conducting a Medline search, reviewed more than 160 publications, mostly in the English language, on the subject of white matter abnormalities detectable by currently used neuroimaging methods (ie, leukoaraiosis). CONCLUSIONS: Binswanger's original description appears to be insufficient for the purpose of defining a new nosological entity. After evaluating the vaguely outlined pathological correlates described in a few of these subcortical cerebral leukoencephalopathies, we conclude that the clinical significance of leukoaraiosis remains incompletely defined. However, its frequency increases with age independent of other risk factors, and in nondemented subjects leukoaraiosis is associated with deficits in selected cognitive functions. Moreover, leukoaraiosis correlates with an increased risk for the subsequent development of strokes. We make specific suggestions for future studies that may help to clarify this topic.

Aged↗
PubMed1993

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

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.

Brain Ischemia↗
PubMed1993

Cerebrospinal fluid proteins in patients with leucoaraiosis: possible abnormalities in blood-brain barrier function.

Some CSF protein abnormalities have been proposed as a possible marker for vascular dementia. We studied the CSF protein levels and albumin ratio in 21 patients (mean age 64.04 +/- 7.5) with progressive bilateral motor impairment, and a CT picture of leucoaraiosis. Seven of these patients also presented with dementia. Twenty-seven Alzheimer's disease patients (mean age 59.59 +/- 5.30) without leucoaraiosis were taken as controls. We also evaluated the correlations of the albumin ratio values with the diagnosis of dementia, the severity of cognitive impairment, the degree of cerebral atrophy and presence of infarcts on CT, and the abnormalities in CSF circulation, found on isotopic cisternography, in the leucoaraiosis group. After controlling for age and sex, the patients with leucoaraiosis showed greater CSF albumin levels (0.27 g/l +/- 0.11 vs. 0.21 g/l +/- 0.06; covariance analysis P = 0.066), CSF IgG values (4.68 mg/100 ml +/- 1.45 vs. 2.85 mg/100 ml +/- 1.03; covariance analysis P < 0.001), and a higher albumin ratio (0.0078 +/- 0.0027 vs. 0.0058 +/- 0.0019; covariance analysis P = 0.013) than those with Alzheimer's disease. The variations of these parameters were not apparently related to the presence of dementia in the leucoaraiosis group. A significantly higher albumin ratio was observed in patients with a slowed CSF circulation compared to those with normal CSF circulation (0.0086 +/- 0.0028 vs. 0.0059 +/- 0.0019; covariance analysis P = 0.05). We conclude that, independently from the presence of dementia, patients with leucoaraiosis have CSF abnormalities consistent with functional blood-brain barrier alterations.

Aged↗
PubMed1991

Cytomegalovirus encephalitis in a non-immunocompromised patient: CSF diagnosis by in situ hybridization cells.

Cytomegalovirus (CMV) encephalitis in immunologically normal patients is rarely reported in the literature. CMV infection was diagnosed by viral DNA probe techniques on CSF cells in a 32-year-old, immunologically normal male presenting with a severe clinical picture due to encephalitis. Administration of ganciclovir was followed by an immediate improvement in the patient's condition. More sensitive techniques for CMV detection could allow to discover more cases of CMV encephalitis in non-immunocompromised patients than previously recognized.

Adult↗
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

Is subcortical vascular dementia a clinical entity for clinical drug trials?

Several therapeutic trials have been performed for vascular dementia, with drugs differing in type and mechanism of action. The results have been almost invariably inconclusive. Given the current notion that there are different subtypes of vascular dementia according to pathophysiological mechanisms, it is reasonable to suspect that one of the main causes of the disappointing results was that the study samples included patients not fitting with the rationale of selective treatments. Testing this hypothesis is difficult because characterization of patients in relation to different subtypes of vascular dementia is not available for most studies. However, attempts are ongoing to reclassify patients entered in some trials for post hoc subgroup analyses with some preliminary interesting results. We propose that (1) specific subtypes of vascular dementia should be the target in any single trial using a treatment with a proper rationale; and (2) subcortical vascular dementia, caused by small vessel disease leading to lacunar infarcts and subcortical white matter changes, represents a clinically and radiologically well-defined entity to be considered for future trials designed specifically for testing adequate drugs.

Cerebral Cortex↗