Lacunes.

Mohr, J. P.

doi:10.1161/01.str.13.1.3

Cited by 181 publications

(77 citation statements)

References 55 publications

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“…Mohr, in a 1982 review of lacunar infarcts, commented that "this surprisingly leisure mode of onset" characterizes many lacunar strokes. 8 Progression occurs in different patterns and time courses depending on stroke subtype. Patients with intracerebral hemorrhage develop gradual worsening of focal signs usually over minutes, occasionally a few hours, followed by headache, vomiting, and decreased consciousness.…”

Section: How Common Is Worsening and In Whichmentioning

confidence: 99%

“…10 Lacunar infarcts are caused in the great majority of patients by occlusive disease, either lipohyalinosis or atheromatous branch disease, involving the penetrating artery (and sometimes also adjacent penetrating arteries) supplying the territory involved in the small, deep infarcts. 8 These penetrating arteries are widely considered to be end arteries with little potential for collateralization. Recent studies using newer magnetic resonance technology show that patients whose perfusion-weighted images (PWI) show a larger area of involvement than the diffusion-weighted images (DWI) who have occlusive lesions on magnetic resonance angiography and do not reperfuse develop larger infarcts and more severe clinical deficits than those patients with open arteries and no PWIϾDWI mismatch.…”

Section: What Factors Are Present In Patients With Noncardioembolic Smentioning

confidence: 99%

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Worsening in Ischemic Stroke Patients: Is it Time for a New Strategy?

Caplan

2002

Stroke

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Section: How Common Is Worsening and In Whichmentioning

confidence: 99%

Section: What Factors Are Present In Patients With Noncardioembolic Smentioning

confidence: 99%

Worsening in Ischemic Stroke Patients: Is it Time for a New Strategy?

Caplan

2002

Stroke

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“…They are typically characterised by a regular shape that is frequently rounded or tube-like with a diameter of 0.2 -2 cm [11][12][13]. SSI account for up to 25% of all strokes [14] and occur predominantly in patients with small vessel disease, such as diabetes and hypertension [10].…”

Section: Introductionmentioning

confidence: 99%

Inverse mismatch and lesion growth in small subcortical ischaemic stroke

et al. 2010

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OBJECTIVE: Infarction typically develops within the borders of an initial hypoperfused tissue. We prospectively investigated whether in small subcortical stroke patients infarct growth can occur beyond the margins of the affected vascular territories. METHODS: In 19 consecutive patients, stroke MRI was performed within 14 h after ictus, and at days 2 and 6 (± 1). Size of diffusion and perfusion disturbances were determined. Infarct volume measured on T2-weighted images on day 6 was considered as imaging endpoint. RESULTS: At the initial examination, the mean diffusion lesion [apparent diffusion coefficient (ADC) lesion size, 1.82 ± 1.2 ml] was larger (p = 0.0002) than the perfusion lesion [mean transit time (MTT) lesion size, 0.72 ± 0.69 ml]. Such an "inverse mismatch" (ADC lesion > MTT lesion) was present in 14/19 patients at baseline and in all patients on day 2. Final lesion volume at day 6 was 3.2 ± 1.6 ml which was larger than the initial perfusion deficit (p = 0.02). CONCLUSION: In small subcortical ischaemic stroke "inverse mismatch" is frequent and infarction develops beyond the initial perfusion disturbance. This indicates that cytotoxic processes probably triggered by the infarct core are a dominant mechanism for lesion growth. Areas with normal perfusion but which are threatened by cytotoxic damage developing over several days seem prime targets for neuroprotective therapy. We prospectively investigated whether in small subcortical stroke patients infarct growth can occur beyond the margins of the affected vascular territories.Methods: In 19 consecutive patients, stroke MRI was performed within 14 hours after ictus, and at days 2 and 6 (±1). Size of diffusion and perfusion disturbances were determined.Infarct volume measured on T2-weighted images on day 6 was considered as imaging endpoint.Results: At the initial examination, the mean diffusion lesion (ADC lesion size: 1.82±1.2 ml) was larger (p=0.0002) than the perfusion lesion (MTT lesion size: 0.72±0.69ml). Such an "Inverse Mismatch" (ADC lesion > MTT lesion) was present in 14/19 patients at baseline and in all patients on day 2. Final lesion volume at day 6 was 3.2±1.6ml which was larger than the initial perfusion deficit (p=0.02).Conclusion: In small subcortical ischaemic stroke "Inverse Mismatch" is frequent and infarction develops beyond the initial perfusion disturbance, This indicates that cytotoxic processes probably triggered by the infarct core are a dominant mechanism for lesion growth.Areas with normal perfusion but which are threatened by cytotoxic damage developing over several days seem prime targets for neuroprotective therapy.2

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“…There is evidence that hypertension accelerates the atherosclerotic process in the larger cerebral vessels and is the most important factor in the development and progression of cerebral atherosclerosis. In hypertensive subjects, atherosclerosis and atherosclerosis-related hyalinosis have been found in small vessels ( < 2 mm in diameter), such as the arterioles supplying basal ganglia [44].…”

Section: A Therosclerosis and Thromboembolismmentioning

confidence: 99%

Pathogenetic mechanisms in vascular dementia

et al. 1994

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Summary. Vascular dementia accounts for approximately20% of all cases of dementia and for about 50% in subjects over 80 years. Thromboembolism with multiple cerebral infarcts was considered to be almost the only pathogenetic pathway of vascular dementia, with multiinfarct dementia as its clinical manifestation. However, there is a great heterogeneity of vascular dementia syndromes and pathological subtypes, as documented by the number of pathogenetic mechanisms now known to underlie the clinical picture. They include thromboembolism and extracerebral and cerebral factors. Among the extracerebral factors are ischemic hypoxic dementia (i.e., dementia due to hypoperfusion), vasculitis, hyperviscosity and abnormalities of hemostasis. Among the cerebral factors are lipohyalinosis, cerebral amyloid angiopathy, disruption of the blood-brain barrier and altered regulation of cerebral blood flow. Therefore, the approach to vascular dementia should take the heterogeneity into account. In this context, the importance of non-infarct type should be considered; subcortical white matter disorder seems to be a noteworthy common pathway of vascular dementia produced by various vascular mechanisms. Finally, the heterogeneity of the vascular mechanisms involved in vascular d~mentia -namely hypoperfusion -might be a factor that can be positively influenced by targeted therapeutic intervention.

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Lacunes.

Cited by 181 publications

References 55 publications

Worsening in Ischemic Stroke Patients: Is it Time for a New Strategy?

Worsening in Ischemic Stroke Patients: Is it Time for a New Strategy?

Inverse mismatch and lesion growth in small subcortical ischaemic stroke

Pathogenetic mechanisms in vascular dementia

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