Search PubMed⌕ Search

Biomedical subjects

Cristina Sarti

Publications and source records attributed to Cristina Sarti.

7 recordsLinked to original sources

Postmortem examination of vascular lesions in cognitive impairment: a survey among neuropathological services.

BACKGROUND AND PURPOSE: A full appreciation of the presence of cerebral vascular lesions in cognitively impaired patients can be ultimately reached at the neuropathological level. However, there are no detailed guidelines regarding what neuropathologists should look for at autopsy in cases of suspected vascular dementia or vascular cognitive impairment. We aimed at surveying the postmortem neuropathological procedures used in different centers in examining brain lesions of presumable or possible vascular origin in cognitively impaired patients. METHODS: Thirteen laboratories participated in the survey by filling in a semistructured questionnaire. We reviewed sampling and histology procedures in use and the neuropathological definitions of some of these lesions. Neuropathological criteria for the definition of a vascular origin of the dementing process were also surveyed. RESULTS: A large variability across centers was observed in the procedures used for the neuropathological examination and the histology techniques. Heterogeneity existed also in the definition of commonly found lesions (eg, white matter alterations, small vessel disease), interpretation of whether or not the lesions were reputed to be of vascular origin, and consequently in the interpretation of the cause of cognitive decline. CONCLUSIONS: The appreciation of the presence of neuropathologically verified vascular lesions in cognitively impaired cases may be heavily influenced by the laboratory tools used and also by the heterogeneity of the criteria applied in different centers. Harmonization of neuropathological procedures is badly needed in the field of vascular dementia and vascular cognitive impairment to better understand the association between various vascular lesions and clinical symptoms such as cognitive impairment.

Artifacts↗

Acute inflammatory events and ischemic stroke subtypes.

BACKGROUND: Recent studies have suggested that previous infection may be a risk factor for ischemic stroke mainly in young and middle-aged patients. The present study sought to further investigate the association between recent inflammatory events (IE) and ischemic stroke without age restriction and to determine the role of recent IE in different ischemic stroke subtypes. METHODS: We performed a case-control study with 93 consecutive hospitalized stroke patients and 200 (107 hospital and 93 community) controls. Acute IE, both infective and non-infective, occurring in the previous 30 days were assessed using a standard questionnaire. The TOAST criteria were used for ischemic stroke subtypes classification. RESULTS: Acute IE in the previous 30 and 7 days were significantly and independently associated with ischemic stroke (37/93 vs. 47/200; OR 2.23, 95% CI 1.26-3.96 and 17/93 vs.16/200; OR 2.45, 95% IC 1.11-5.39, respectively). Stratifying for stroke subtypes, acute IE significantly and independently increased the risk of atherothrombotic (OR 5.72, 95% CI 2.14-15.25) and cardioembolic stroke (OR 3.02, 95%CI 1.20-7.63). CONCLUSIONS: Acute IE increase the risk of acute ischemic stroke of atherothrombotic and cardioembolic type independently of other predisposing factors. Implications for daily clinical practice, in relation to prevention and treatment of IE in patients at risk, have to be explored.

Acute Disease↗

Cognitive impairment and chronic cerebral hypoperfusion: what can be learned from experimental models.

The relation between chronic cerebral hypoperfusion and cognitive functions has not been completely clarified. The resolution of cerebral hypoperfusion states, such as those induced by arteriovenous malformations or carotid stenosis/occlusion, has been reported to improve mental decline in humans. Subcortical vascular dementia is another human condition supposed to be linked with chronic cerebral hypoxia/ischemia. The extent of this cause/effect relation is, however, difficult to be assessed in humans, where different factors, such as ageing or subtle degenerative processes, can coexist and interact influencing cognitive performances. Experimental studies can help to elucidate this relation because they can use models of pure chronic/moderate cerebral hypoperfusion. An experimental model of chronic ischemia is the bilateral common carotid artery occlusion in the rat. In this paper, we present a review of experimental studies that evaluated cognitive functions in the rat with bilateral common carotid artery occlusion. We then present an experimental model of bilateral common carotid artery occlusion in the rat modified with respect to previous papers regarding both the surgical procedure and the neurocognitive evaluation that is focused on cognitive domains depending on subcortical-frontal circuits. We propose this model to investigate subcortical vascular dementia.

Animals↗

Persistent impairment of gait performances and working memory after bilateral common carotid artery occlusion in the adult Wistar rat.

BACKGROUND: The clinical and pathophysiological effects of a chronic reduction of cerebral blood flow in humans are not completely known. We investigated whether rats subjected to bilateral common carotid artery occlusion (bCCA-o) developed focal neurological deficits, gait dysfunction, and working memory alterations. METHODS: Eighteen male Wistar rats were subjected to bCCA-o, 13 were sham-operated. We assessed sensorimotor functions, gait on a 60 cm-long elevated bridge, and working memory (object recognition and Y maze tests) before and 30, 60, and 90 days after surgery. Histological analysis was performed in a subgroup of 10 rats. RESULTS: No rat showed sensorimotor alterations after surgery. Although gait performances of both bCCA-o and sham-operated rats declined over time, the differences reached statistical significance only for the bCCA-o group (mean+/-SE: 26.8+/-5.0; 22.4+/-4.9; 24.5+/-5.5 cm at 30, 60, and 90 days, respectively) in comparison with baseline (52.9+/-5.2 cm; P<0.05). At 60 and 90 days, bCCA-o rats in comparison with sham-operated rats showed decreased performances on object recognition (discrimination index: 0.15+/-0.03 vs. 0.29+/-0.05 at 60 days and 0.10+/-0.04 vs. 0.41+/-0.07 at 90 days; P<0.05) and on Y maze test (alternating rats: 9.9 vs. 85.7% at 60 days and 16.6 vs. 100% at 90 days; P<0.01). In none of the animals were cerebral infarcts detected. Selective neuronal necrosis was observed in the cortex and hippocampus of both bCCA-o and sham-operated rats without any obvious difference. CONCLUSIONS: bCCA-o in the Wistar rat induces persistent and progressive gait and working memory impairment without producing sensorimotor deficit or cerebral infarcts. This model may help to elucidate some physiopathological aspects of neurological impairment associated with states of cerebral chronic ischemia.

Animals↗

Failure of radiation therapy for brain involvement in Erdheim Chester disease.

A patient with suprasellar and brain stem involvement in Erdheim Chester disease (ECD) underwent magnetic resonance (MR) imaging and proton MR spectroscopy (1H MRS) of the ventral pons before and 1, 4 and 18 months after external whole-brain (24 Gy) radiotherapy. By revealing a decrease of the N-acetyl-aspartate/choline ratio in the pons, 1H MR spectroscopy anticipated lesions growth on MR imaging. In line with the results in four patients reported in the literature, our observation indicates that external radiation therapy is not effective for intracranial involvement in ECD.

Brain↗

Pathological lesions in vascular dementia.

According to current diagnostic criteria, a definite diagnosis of vascular dementia (VaD) can be reached on pathological grounds by showing the presence of vascular lesions and the absence of degenerative changes exceeding those expected for age. However, while it is commonly accepted that VaD is a group of heterogeneous entities rather than a process with a unique pathological substrate, the spectrum of vessel and parenchyma changes etiologically associated with the clinical syndrome remains basically unidentified. The review of some recent clinical-pathological series shows that different studies have assessed the presence of dissimilar vascular lesions and that, in many cases, no pathological definition was given. This has hindered the clarification of clinical-pathological correlations in the field of VaD. In this scenario, the use of animal models of cerebrovascular diseases may help to elucidate the type of lesions possibly linked with cognitive impairment in humans and might provide insight into some of the pathophysiological mechanisms of vascular cognitive impairment. A consensus is today needed in order to harmonize the pathological examination of vascular lesions in cases of dementia. An ongoing survey aimed at collecting information about the procedures used in different pathological laboratories in the assessment of lesions possibly associated with dementia is finally presented.

Dementia, Vascular↗