Histopathological Correlates of Leuko-Araiosis in Patients with Ischemic Stroke

Inzitari, Domenico; Mascalchi, Mario; Giordano, G.P.; Marini, Paolo; Sità, D.; Abbamondi, Anna Laura

doi:10.1159/000116461

Cited by 21 publications

(11 citation statements)

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“…The results of this study however, do not prove that the leuko-araiosis observed in pure SDAT has the same origin as in MID [36]. Although the presence of severe white matter palor has been shown to coexist with cere bral amyloid angiopathy in postmortem cases of Alz heimer's disease [37], an electron-microscopic study showed quantitative differences in loss of nerve fibers between cases of progressive subcortical vascular en cephalopathy of Binswanger type and SDAT [38].…”

Section: Discussioncontrasting

confidence: 88%

Cerebral Blood Flow and Oxygen Metabolism in Leuko-Araiosis

Reuck¹,

Aken²,

Decoo³

et al. 1990

Cerebrovasc Dis

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Regional blood flow and oxygen metabolism were determined by positron emission tomography using the steady-state technique with ¹⁵0, in 2 patients with posthypoxic ischemic leukoencephalopathy, in 6 patients with leuko-araiosis and dementia, and in 6 patients with leuko-araiosis without dementia. Comparison between the three groups allowed us to conclude that leuko-araiosis is associated with a lowered cerebral blood flow, which is more pronounced and widespread in demented patients and more restricted to the white matter in nondemented ones.

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Section: Discussioncontrasting

confidence: 88%

Cerebral Blood Flow and Oxygen Metabolism in Leuko-Araiosis

Reuck¹,

Aken²,

Decoo³

et al. 1990

Cerebrovasc Dis

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“…In cases of hypoxic/ischemic injury, histological changes of the WM can range from coagulative necrosis and cavitation to non-specific tissue changes such as sponginess, patchy demyelination, and astrocytic proliferation [88]. Such changes are consistent with the lesions seen in patients with leukoaraiosis [89], suggesting that ischemia is closely associated with the condition [88]. In particular, leukoaraiosis is characterized by non-inflammatory collagenosis of the periventricular veins [13,22], resulting in thickening of the vessel walls and narrowing, or even occlusion, of the lumen [13].…”

Section: Introductionmentioning

confidence: 90%

Venous hemodynamics in neurological disorders: an analytical review with hydrodynamic analysis

Beggs

2013

BMC Med

109

102

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Venous abnormalities contribute to the pathophysiology of several neurological conditions. This paper reviews the literature regarding venous abnormalities in multiple sclerosis (MS), leukoaraiosis, and normal-pressure hydrocephalus (NPH). The review is supplemented with hydrodynamic analysis to assess the effects on cerebrospinal fluid (CSF) dynamics and cerebral blood flow (CBF) of venous hypertension in general, and chronic cerebrospinal venous insufficiency (CCSVI) in particular.CCSVI-like venous anomalies seem unlikely to account for reduced CBF in patients with MS, thus other mechanisms must be at work, which increase the hydraulic resistance of the cerebral vascular bed in MS. Similarly, hydrodynamic changes appear to be responsible for reduced CBF in leukoaraiosis. The hydrodynamic properties of the periventricular veins make these vessels particularly vulnerable to ischemia and plaque formation.Venous hypertension in the dural sinuses can alter intracranial compliance. Consequently, venous hypertension may change the CSF dynamics, affecting the intracranial windkessel mechanism. MS and NPH appear to share some similar characteristics, with both conditions exhibiting increased CSF pulsatility in the aqueduct of Sylvius.CCSVI appears to be a real phenomenon associated with MS, which causes venous hypertension in the dural sinuses. However, the role of CCSVI in the pathophysiology of MS remains unclear.

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“…Various histopathologic correlates have been described, including loss of ependyma with gliosis, glial swelling, demyelination, dilated perivascular spaces, lacunar infarcts, spongiosis, arteriolar hyalinosis, amyloid angiopathy, and cyst formation. [2][3][4] A vascular etiology is strongly suggested, given the frequent association with increasing age, hypertension, stroke, and markers of cellular ischemia, including hypoxia inducible factor, neuroglobulin, and matrix metalloproteinase protein MMP7. [5][6][7] Other associations include arteriosclerosis, 8 impaired cerebral autoregulation, hypoperfusion, CSF flow disturbances, and blood-brain barrier (BBB) disruption.…”

mentioning

confidence: 99%