1998
DOI: 10.1001/archneur.55.4.481
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Different Predictors of Neurological Worsening in Different Causes of Stroke

Abstract: Determinants of neurological worsening may include causative aspects rather than just the evolution of the ischemic or hemorrhagic process itself. For a better comprehension and treatment of neurological worsening, the causative and pathophysiological conditions underlying stroke should be differentiated as early as possible.

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Cited by 110 publications
(112 citation statements)
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References 27 publications
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“…3 In the Lausanne Stroke Registry, among Ͼ3000 patients, worsening after admission occurred in 29% of all stroke patients and in 662 (34%) of noncardioembolic ischemic stroke patients. 4 Among the noncardioembolic stroke patients who worsened, 58% progressed during the first 24 hours. 4 Among 350 Japanese patients in one study, 25% progressed after admission; worsening in the hospital occurred in 26% of lacunar stroke patients.…”
Section: How Common Is Worsening and In Whichmentioning
confidence: 99%
See 1 more Smart Citation
“…3 In the Lausanne Stroke Registry, among Ͼ3000 patients, worsening after admission occurred in 29% of all stroke patients and in 662 (34%) of noncardioembolic ischemic stroke patients. 4 Among the noncardioembolic stroke patients who worsened, 58% progressed during the first 24 hours. 4 Among 350 Japanese patients in one study, 25% progressed after admission; worsening in the hospital occurred in 26% of lacunar stroke patients.…”
Section: How Common Is Worsening and In Whichmentioning
confidence: 99%
“…4 Among the noncardioembolic stroke patients who worsened, 58% progressed during the first 24 hours. 4 Among 350 Japanese patients in one study, 25% progressed after admission; worsening in the hospital occurred in 26% of lacunar stroke patients. 5 A number of studies focused on progression and worsening in series of patients with lacunar strokes.…”
Section: How Common Is Worsening and In Whichmentioning
confidence: 99%
“…Clinical worsening after lacunar infarction has been extensively reported and may result from thrombi propagation, flow limiting arterial lesion supplying the ischemic zone, and perilesional edema. 9,10 We suspect that secondary neuronal degeneration, apoptosis, or abnormal plasticity involving local synaptic interconnections may explain the delay in the development of Ondine's curse after lateral medullary infarction, ranging several days to several months postinfarct. Likewise, hypoxemia secondary to altered automatic breathing in brainstem infarctions with hypercapnia-induced cerebral vasoconstriction can increase ischemia.…”
mentioning
confidence: 99%
“…The sudden apnea during sleep may be caused by clinical worsening by thrombi propagation, reduced blood flow in the ischemic zone, and perilesional edema [6,7]. Stroke patients with Sleep-Disordered Breathing (SDB) may have potential risk for Ondine's curse as well, because most Ondine's curse occurred in the night-time.…”
Section: Discussionmentioning
confidence: 99%