Spreading Depolarization After Chronic Subdural Hematoma Evacuation: Associated Clinical Risk Factors and Influence on Clinical Outcome

被引:7
|
作者
Meadows, Christine [1 ]
Davis, Herbert [2 ]
Mohammad, Laila [3 ]
Shuttleworth, C. William [4 ]
Torbey, Michel [1 ]
Zhu, Yiliang [5 ]
Alsahara, Ali A. [1 ]
Carlson, Andrew P. [6 ]
机构
[1] Univ New Mexico, Sch Med, Dept Neurol, Albuquerque, NM 87131 USA
[2] Univ New Mexico, Sch Med, Dept Internal Med, Albuquerque, NM 87131 USA
[3] Ann & Robert H Lurie Childrens Hosp Chicago, Chicago, IL 60611 USA
[4] Univ New Mexico, Sch Med, Dept Neurosci, Albuquerque, NM 87131 USA
[5] Univ New Mexico, Sch Med, Clin Translat Sci Ctr, Albuquerque, NM 87131 USA
[6] Univ New Mexico, Sch Med, Dept Neurosurg, Albuquerque, NM 87131 USA
基金
美国国家卫生研究院;
关键词
Spreading depolarization; Cortical spreading depression; Chronic subdural hematoma; Neurophysiology; Neurologic deficits; NEUROLOGICAL DEFICITS; DEPRESSION;
D O I
10.1007/s12028-021-01339-5
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
Background Chronic subdural hematoma (cSDH) is a common neurosurgical condition responsible for excess morbidity, particularly in the geriatric population. Recovery after evacuation is complicated by fluctuating neurological deficits in a high proportion of patients. We previously demonstrated that spreading depolarizations (SDs) may be responsible for some of these events. In this study, we aim to determine candidate risk factors for probable SD and assess the influence of probable SD on outcome. Methods We used two cohorts who underwent surgery for cSDH. The first cohort (n = 40) had electrocorticographic monitoring to detect SD. In the second cohort (n = 345), we retrospectively identified subjects with suspected SD based on the presence of transient neurological symptoms not explained by structural etiology or ictal activity on electroencephalography. We extracted standard demographic and outcome variables for comparisons and modeling. Results Of 345 subjects, 80 (23%) were identified in the retrospective cohort as having probable SD. Potential risk factors included history of hypertension, worse clinical presentation on the Glasgow Coma Scale, and lower Hounsfield unit density and volume of the preoperative subdural hematoma. Probable SD was associated with multiple worse-outcome measures, including length of stay and clinical outcomes, but not increased mortality. On a multivariable analysis, probable SD was independently associated with worse outcome, determined by the Glasgow Outcome Scale score at the first clinic follow-up (odds ratio 1.793, 95% confidence interval 1.022-3.146) and longer hospital length of stay (odds ratio 7.952, 95% confidence interval 4.062-15.563). Conclusions Unexplained neurological deficits after surgery for cSDH occur in nearly a quarter of patients and may be explained by SD. We identified several potential candidate risk factors. Patients with probable SD have worse outcomes, independent of other baseline risk factors. Further data with gold standard monitoring are needed to evaluate for possible predictors of SD to target therapies to a high-risk population.
引用
收藏
页码:105 / 111
页数:7
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