Original ArticleA Proposal for the Classification of Etiologies of Neurologic Deterioration after Acute Ischemic Stroke
Introduction
Neurologic deterioration (ND) is common after ischemic stroke, occurring in up to one third of all patients. Nearly half of the patients who experience ND will do so within the first 48 hours of the index stroke,1, 2, 3 and this significantly contributes to morbidity and mortality.2, 4, 5
The distinction between and definitions for etiologies of ND have not yet been described. Certain structural changes may contribute to potentially nonreversible worsening neurologic status after stroke (eg, focal cerebral edema and hemorrhagic transformation); however, other systemic issues may introduce secondary structural damage or may transiently disrupt neurologic function (eg, infection and metabolic abnormalities). Primary (cerebral) causes of ND may only be amenable to reperfusion and recanalization, but the permanence of secondary (systemic) damage–producing ND is not clearly elucidated. Secondary neurologic damage may be mitigated by early recognition and intervention, as is potentially the case for infection with fever and leukocytosis during episodes of ND.6
In the present study, we propose standard definitions for ND etiology and analyze the clinical outcomes associated with specific ND etiologies. We expect that this information will aid neurologists in identifying the cause of ND in acute stroke and provide the patient and their families with more accurate prognostic information and provide uniform definitions for classifying ND in subsequent investigations.
Section snippets
Patient Population
We conducted a single-center retrospective analysis of all consecutive patients who presented with acute ischemic stroke between July 2008 and December 2010 using a prospective registry.7 Patients were excluded if they experienced an in-hospital stroke, presented more than 48 hours after last seen normal, or had an unknown time of last seen normal because ND is more likely to occur earlier after the cerebrovascular event and is the target for neuroprotection.8 ND was defined as the first
Results
Of 596 patients screened, 366 met inclusion criteria (median age 65 years, 41.4% women, 68.3% black). One hundred twenty-eight (34.9%) experienced at least 1 episode of ND (median age 69 years, 42.2% women, 68.7% black). Demographic information comparing patients with and without ND are displayed in Table 2.
Discussion
In the present study, we have identified likely causes of first-time ND following acute ischemic stroke in more than 90% of all cases. The most common etiology of ND was progressive stroke, occurring 38.3% of the time and among 13.4% of the total population of ischemic stroke patients studied. ND because of edema was the most frequently observed in cardioembolic strokes (40.9% of all cases of edema). However, there were no other clinically significant relationships between stroke etiology and
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Epileptic activity in neurological deterioration after ischemic stroke, a continuous EEG study
2019, Clinical NeurophysiologyCitation Excerpt :Despite improvement in prevention and monitoring of complications, early neurological deterioration (ND) after IS occurs in up to 38% of cases (Seners et al., 2014, 2018) and is associated with a four-fold increase in death or dependency at 3 months compared to patients without ND (Seners et al., 2014). In about half of cases, ND is caused by haemorrhagic conversion, oedema, recurrent ischemia or systemic medical complications that either impair blood oxygenation or increase neuronal metabolism (Karepov et al., 2006; Siegler et al., 2013). In the remaining 50% of cases, the underlying mechanism of ND remains unclear, preventing the development of adequate management strategies (Jauch et al., 2013).
Sources of funding: The project described was supported by award numbers 5 T32 HS013852-10 from the Agency for Healthcare Research and Quality, 3 P60 MD000502-08S1 from the National Institute on Minority Health and Health Disparities, National Institutes of Health, and 13PRE13830003 from the American Heart Association. The content is solely the responsibility of the authors and does not necessarily represent the official views of the Agency for Healthcare Research and Quality, American Heart Association, or the National Institutes of Health.