Central Nervous System Findings in a Tenth Decade Autopsy Population

Peress, Nancy S.; Kane, Walter C.; Aronson, Stanley M

doi:10.1016/s0079-6123(08)60707-4

Cited by 75 publications

(47 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This interesting finding could explain our previous data [110,111] concerning a more favorable outcome in diabetic patients owing to the higher prevalence of lacunar strokes and it could provide a possible explanation for this issue, based on the minor grade of immunoinflammatory activation of both early and late acute phase of ischemic stroke in these patients, possibly related to the minor extent of ischemic brain damage. It is likely that a minor grade of chronic inflammatory response in cerebral small vessels could be involved in diabetic brain microangiopathy owing to the minor diameter of the pathogenesis of the diabetic lacunae [113]. Moreover, we observed a lower grade of ICAM 1 activation in diabetic patients with lacunar stroke.…”

Section: Inflammation In Acute Stroke Subtypesmentioning

confidence: 51%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

128

View full text Add to dashboard Cite

Determining the cause of stroke does influence choices for management. categorization of subtypes of ischemic stroke has had considerable study, but definitions are hard to formulate and their application for diagnosis in an individual patient is often problematic. Cerebral ischemia initiates a complex cascade of events at genomic, molecular, and cellular levels, and inflammation is important in this cascade. In 1993 for For the Trial of Org 10172 in Acute Stroke Treatment (TOAST), Adams et al] conducted a placebo-controlled, randomized, blinded study of the low-molecular-weight heparinoid given to patients within 24 hours after stroke and developed a system for diagnosis of subtype of ischemic stroke that uses components of existing diagnostic schemes. The type of acute ischemic stroke was classified according to the TOAST classification: 1) Large Artery AtheroSclerosis (LAAS); 2) CardioEmbolic Infarct (CEI); 3) LACunar infarct (LAC); 4) stroke of Other Determined Etiology (ODE); 5) stroke of UnDetermined Etiology (UDE) (see Fig. (1)). On the basis of pathophysiologic differences of each stroke subtype it's possible to hypothesize a different pattern of immuno-inflammatory activation in relation of ischemic stroke subtype. A nonspecific systemic inflammatory response occurs after both ischemic and hemorrhagic stroke, either as part of the process of brain damage or in response to complications such as deep venous thrombosis. Several studies have reported that higher levels of inflammatory markers such as C-reactive protein (CRP) and interleukin-6 (IL-6) are associated with worse outcome after ischemic stroke.Our group reported that patients with cardioembolic subtype showed significantly higher median plasma levels of TNF-, IL-6, IL-1 whereas the lacunar subtype showed significantly lower median plasma levels of TNF-, IL-6 and IL-1 . Our findings underlined the significant association was noted between the severity of neurological deficit at admission, the diagnostic subtype and some inflammatory variables.

show abstract

Section: Inflammation In Acute Stroke Subtypesmentioning

confidence: 51%

Inflammation in Ischemic Stroke Subtypes

Tuttolomondo

Raimondo²,

Pecoraro³

et al. 2012

CPD

128

View full text Add to dashboard Cite

show abstract

“…This interesting finding could explain our previous data (7-9) concerning a more favorable outcome in diabetic patients owing to the higher prevalence of lacunar strokes and it could provide a possible explanation for this issue, based on the minor grade of immunoinflammatory activation of both early and late acute phase of ischemic stroke in these patients, possibly related to the minor extent of ischemic brain damage. It is likely that a minor grade of chronic inflammatory response in cerebral small vessels could be involved in diabetic brain microangiopathy owing to the minor diameter of the arterioles (40-200 um vs 200-800 urn) concerned in the pathogenesis of the diabetic lacunae (18). Moreover, we observed a lower grade of ICAM I activation in diabetic patients with lacunar stroke.…”

Section: Il-lfj: Interleukin I-fj; Il-6: Interleukin-ti; Tnf-a: Tumormentioning

confidence: 51%

Immunoinflammatory Activation during the Acute Phase of Lacunar and Non-Lacunar Ischemic Stroke: Association with Time of Onset and Diabetic State

Licata

Tuttolomondo

Corrao

et al. 2006

Int J Immunopathol Pharmacol

View full text Add to dashboard Cite

Several studies have stressed the involvement of inflammation in the pathophysiology of acute brain ischemia, but the role of immunoinflammatory activation in diabetic stroke patients has not yet been fully evaluated. The aim of our study was to evaluate immunoinflammatory activation of acute phase of stroke in relation to time of symptoms onset, diabetic state and diagnostic subtype. We enrolled 60 patients (32 diabetics; 28 non-diabetics) with acute ischemic stroke and 123 subjects without acute ischemic stroke, and measured levels of IL-lP, TNF-a, IL-6, IL-I0, E-selectin, P-selectin, sICAM-l, sVCAM-l, VWF, 24-72 hand 7-10 days after stroke onset; TPA, PAI-l plasma levels at 24-72h. Our stroke patients exhibited significantly higher plasma levels of cytokines, selectins, adhesion molecules and PAl-I, and diabetic stroke patients exhibited higher plasma levels of PAI-l in comparison with non-diabetic ones. Lacunar strokes in comparison with those non-lacunar exhibited significantly lower levels of TNF-a and ILI-P, P-selectin and ICAM-l. Moreover, diabetic patients with lacunar strokes exhibited a minor grade ofimmunoinflammatory activation ofthe acute phase at 24-72h and 7-10 days after stroke onset. The minor grade of immunoinflammatory activation of patients with lacunar strokes, particularly diabetic ones, could be related to the minor extension of the infarct size, owing to the typical microvascular disease of diabetic subjects which could also explain the reported better outcome of this subtype of ischemic stroke.The epidemiologic relationship between diabetes and stroke is well confirmed (I), but the clinical and prognostic profile of ischemic stroke in diabetic patients in comparison with non-diabetic ones and in relation to diagnostic subtype, appears unclear (2-3). An immunoinflammatory cascade (4) involving endothelial and coagulation functions represents the pathogenetic background of neuronal damage in ischemic stroke. Indeed, there is evidence that brain injury, secondary to arterial occlusion, is characterized by acute local inflammation (5). Moreover, during reperfusion after acute ischemia, polymorphonuclear neutrophils (PMN) are believed to exacerbate tissue damage by both the physical obstruction of vessels and the release of oxygen radicals, proinflammatory cytokines and cytolytic enzymes (4-5). Thus, if clinical and prognostic differences exist between diabetic and non-diabetic

show abstract

“…Whatever the explanation, our data seem to be in line with previous results showing that infarcts occurring in the brain stem supplied by paramedian-penetrating branches are 3-to 4-times more common in diabetic patients than in nondiabetic patients. 23 There are several limitations of this study. First, because the results are based on a registry from a large tertiary hospital located in urban areas, selection bias may be present.…”

Section: Discussionmentioning

confidence: 91%

Risk Factors and Stroke Mechanisms in Atherosclerotic Stroke

Kim

Nah

Park

et al. 2012

Stroke

267

139

View full text Add to dashboard Cite

Previous studies have addressed the differences in risk factors and stroke mechanisms between ICAS and ECAS, 2,3 but the results are inconsistent. Whereas some reported that hypertension, diabetes mellitus, and metabolic syndrome (MetS) are more closely associated with ICAS, 4-8 this was not confirmed by others. 9-11 It also remains unclear whether the risk factors and stroke mechanisms differ between anterior and posterior circulation atherosclerosis. 12Previous studies examined a small number of patients at single hospitals. 6,7,11 Most importantly, prospective studies that used detailed examinations, including advanced brain and vascular imaging, are scarce. The purpose of this study was to elucidate the differences in the risk factors and mechanisms of stroke between ICAS and ECAS, and between anterior and posterior circulation atherosclerosis. We developed a Background and Purpose-The aim of this study was to investigate differences in risk factors and stroke mechanisms between intracranial atherosclerosis (ICAS) and extracranial atherosclerosis (ECAS) and between anterior and posterior circulation atherosclerosis. Methods-A multicenter, prospective, Web-based registry was performed on atherosclerotic strokes using diffusionweighted magnetic resonance imaging and magnetic resonance angiography. Stroke mechanisms were categorized as artery-to-artery embolism, in situ thrombo-occlusion, local branch occlusion, or hemodynamic impairment. Results-One-thousand patients were enrolled from 9 university hospitals. Age (odds ratio [OR]

show abstract

Central Nervous System Findings in a Tenth Decade Autopsy Population

Cited by 75 publications

References 6 publications

Inflammation in Ischemic Stroke Subtypes

Inflammation in Ischemic Stroke Subtypes

Immunoinflammatory Activation during the Acute Phase of Lacunar and Non-Lacunar Ischemic Stroke: Association with Time of Onset and Diabetic State

Risk Factors and Stroke Mechanisms in Atherosclerotic Stroke

Contact Info

Product

Resources

About