Early and persistent impaired percent alpha variability on continuous electroencephalography monitoring as predictive of poor outcome after traumatic brain injury

2002 ◽  
Vol 97 (1) ◽  
pp. 84-92 ◽  
Author(s):  
Paul M. Vespa ◽  
W. John Boscardin ◽  
David A. Hovda ◽  
David L. McArthur ◽  
Marc R. Nuwer ◽  
...  

Object. Early prediction of outcomes in patients after they suffer traumatic brain injury (TBI) is often nonspecific and based on initial imaging and clinical findings alone, without direct physiological testing. Improved outcome prediction is desirable for ethical, social, and financial reasons. The goal of this study was to determine the usefulness of continuous electroencephalography (EEG) monitoring in determining prognosis early after TBI, while the patient is in the intensive care unit. Methods. The authors hypothesized that the reduced percentage of alpha variability (PAV) in continuous EEG tracings indicates a poor prognosis. Prospective continuous EEG monitoring was performed in 89 consecutive patients with moderate to severe TBI (Glasgow Coma Scale [GCS] Scores 3–12) from 0 to 10 days after injury. The PAV was calculated daily, and the time course and trends of the PAV were analyzed in comparison with the patient's Glasgow Outcome Scale (GOS) score at the time of discharge. In patients with GCS scores of 8 or lower, a PAV value of 0.1 or lower is highly predictive of a poor outcome or death (positive predictive value 86%). The determinant PAV value was obtained by Day 3 after injury. Persistent PAV values of 0.1 or lower over several days or worsening of the PAV to a value of 0.1 or lower indicated a high likelihood of poor outcome (GOS Scores 1 and 2). In comparison with the combination of traditional initial clinical indicators of outcome (GCS score, pupillary response to light, patient age, results of computerized tomography scanning, and early hypotension or hypoxemia), the early PAV value during the initial 3 days after injury independently improved prognostic ability (p < 0.01). Conclusions. Continuous EEG monitoring performed with particular attention paid to the PAV is a sensitive and specific method of prognosis that can indicate outcomes in patients with moderate to severe TBI within 3 days postinjury.

1999 ◽  
Vol 91 (5) ◽  
pp. 750-760 ◽  
Author(s):  
Paul M. Vespa ◽  
Marc R. Nuwer ◽  
Valeriy Nenov ◽  
Elisabeth Ronne-Engstrom ◽  
David A. Hovda ◽  
...  

Object. The early pathophysiological features of traumatic brain injury observed in the intensive care unit (ICU) have been described in terms of altered cerebral blood flow, altered brain metabolism, and neurochemical excitotoxicity. Seizures occur in animal models of brain injury and in human brain injury. Previous studies of posttraumatic seizures in humans have been based principally on clinical observations without a systematic approach to electroencephalographic (EEG) recording of seizures. The purpose of this study was to determine prospectively the incidence of convulsive and nonconvulsive seizures by using continuous EEG monitoring in patients in the ICU during the initial 14 days postinjury.Methods. Ninety-four patients with moderate-to-severe brain injuries underwent continuous EEG monitoring beginning at admission to the ICU (mean delay 9.6 ± 5.4 hours) and extending up to 14 days postinjury. Convulsive and nonconvulsive seizures occurred in 21 (22%) of the 94 patients, with six of them displaying status epilepticus. In more than half of the patients (52%) the seizures were nonconvulsive and were diagnosed on the basis of EEG studies alone. All six patients with status epilepticus died, compared with a mortality rate of 24% (18 of 73) in the nonseizure group (p < 0.001). The patients with status epilepticus had a shorter mean length of stay (9.14 ± 5.9 days compared with 14 ± 9 days [t-test, p < 0.03]). Seizures occurred despite initiation of prophylactic phenytoin on admission to the emergency room, with maintenance at mean levels of 16.6 ± 2.8 mg/dl. No differences in key prognostic factors (such as the Glasgow Coma Scale score, early hypoxemia, early hypotension, or 1-month Glasgow Outcome Scale score) were found between the patients with seizures and those without.Conclusions. Seizures occur in more than one in five patients during the 1st week after moderate-to-severe brain injury and may play a role in the pathobiological conditions associated with brain injury.


2015 ◽  
Vol 16 (2) ◽  
pp. 167-176 ◽  
Author(s):  
Brent R. O’Neill ◽  
Michael H. Handler ◽  
Suhong Tong ◽  
Kevin E. Chapman

OBJECT Seizures may cause diagnostic confusion and be a source of metabolic stress after traumatic brain injury (TBI) in children. The incidence of electroencephalography (EEG)-confirmed seizures and of subclinical seizures in the pediatric population with TBI is not well known. METHODS A routine protocol for continuous EEG (cEEG) monitoring was initiated for all patients with moderate or severe TBI at a Level 1 pediatric trauma center. Over a 3.5-year period, all patients with TBI who underwent cEEG monitoring, both according to protocol and those with mild head injuries who underwent cEEG monitoring at the discretion of the treating team, were identified prospectively. Clinical data were collected and analyzed. RESULTS Over the study period, 594 children were admitted with TBI, and 144 of these children underwent cEEG monitoring. One hundred two (71%) of these 144 children had moderate or severe TBI. Abusive head trauma (AHT) was the most common mechanism of injury (65 patients, 45%) in children with cEEG monitoring. Seizures were identified on cEEG in 43 patients (30%). Forty (93%) of these 43 patients had subclinical seizures, including 17 (40%) with only subclinical seizures and 23 (53%) with both clinical and subclinical seizures. Fifty-three percent of patients with seizures experienced status epilepticus. Age less than 2.4 years and AHT mechanism were strongly correlated with presence of seizures (odds ratios 8.7 and 6.0, respectively). Those patients with only subclinical seizures had the same risk factors as the other groups. The presence of seizures did not correlate with discharge disposition but was correlated with longer hospital stay and intensive care unit stay. CONCLUSIONS Continuous EEG monitoring identifies a significant number of subclinical seizures acutely after TBI. Children younger than 2.4 years of age and victims of AHT are particularly vulnerable to subclinical seizures, and seizures in general. Continuous EEG monitoring allows for accurate diagnosis and timely treatment of posttraumatic seizures, and may mitigate secondary injury to the traumatized brain.


Neurosurgery ◽  
2017 ◽  
Vol 64 (CN_suppl_1) ◽  
pp. 249-250
Author(s):  
Yirui Sun ◽  
Jian Yu ◽  
Qiang Yuan ◽  
Jin Hu

Abstract INTRODUCTION Seizure is a common complication for severe traumatic brain injury (TBI). Valproic acid (VPA) is a first-line antiepileptic drug, though its metabolism is affected by genetic polymorphisms and varies between individuals. The aim of this study was to investigate such association and to explore its influence on the occurrence of early post-traumatic seizure. METHODS A case control study was conducted from 2012 to 2016 recruiting adult patients with severe TBI. Continuous electroencephalograph (EEG) monitoring was performed for 7 days. Genetic polymorphisms in UGT1A6, UGT2B7, CYP2C9, and CYP2C19 were analyzed in association with daily VPA plasma concentrations, adjusted dosages, and occurrence seizures. RESULTS >Among the 395 recruited patients, eight-three (21%) had early post-traumatic seizure, of which 30 (36.14%) were non-convulsive. Most seizures were first detected on day 1 (34.94%) and day 2 (46.99%) after injury. Patients with seizure had longer ICU length of stay and relatively lower VPA plasma concentrations. Patients with UGT1A6_19T>G/541A>G/552A>C double heterozygosities or CYP2C9 extensive metabolizers (EMs) initially had lower adjusted VPA plasma concentrations (power >0.99) and accordingly require higher VPA dosages during later time of treatment (power >0.99). The odds ratio indicated a higher risk of early post-traumatic seizure occurrence in male patients (OR 1.96, 95% CI 1.01-3.81, P = 0.043), age over 65 (OR 2.13, 95% CI 1.01-4.48), and with UGT1A6_19T>G/541A>G/552A>C double heterozygosities (OR 2.38, 95% CI 1.11-5.10, P = 0.02). CONCLUSION Continuous EEG monitoring are necessary to detect both convulsive and non-convulsive early post-traumatic seizures in severe TBI patients. UGT1A6/CYP2C9 polymorphisms have influence on VPA metabolism. UGT1A6_19T>G/541A>G/552A>C double heterozygositie is associated with occurrence of early post-traumatic seizures in addition to patients' age and gender. Further investigations with larger sample size are required to confirm the difference.


2002 ◽  
Vol 96 (1) ◽  
pp. 103-108 ◽  
Author(s):  
Michael N. Diringer ◽  
Tom O. Videen ◽  
Kent Yundt ◽  
Allyson R. Zazulia ◽  
Venkatesh Aiyagari ◽  
...  

Object. Recently, concern has been raised that hyperventilation following severe traumatic brain injury (TBI) could lead to cerebral ischemia. In acute ischemic stroke, in which the baseline metabolic rate is normal, reduction in cerebral blood flow (CBF) below a threshold of 18 to 20 ml/100 g/min is associated with energy failure. In severe TBI, however, the metabolic rate of cerebral oxygen (CMRO2) is low. The authors previously reported that moderate hyperventilation lowered global hemispheric CBF to 25 ml/100 g/min but did not alter CMRO2. In the present study they sought to determine if hyperventilation lowers CBF below the ischemic threshold of 18 to 20 ml/100 g/min in any brain region and if those reductions cause energy failure (defined as a fall in CMRO2). Methods. Two groups of patients were studied. The moderate hyperventilation group (nine patients) underwent hyperventilation to PaCO2 of 30 ± 2 mm Hg early after TBI, regardless of intracranial pressure (ICP). The severe hyperventilation group (four patients) underwent hyperventilation to PaCO2 of 25 ± 2 mm Hg 1 to 5 days postinjury while ICP was elevated (20–30 mm Hg). The ICP, mean arterial blood pressure, and jugular venous O2 content were monitored, and cerebral perfusion pressure was maintained at 70 mm Hg or higher by using vasopressors when needed. All data are given as the mean ± standard deviation unless specified otherwise. The moderate hyperventilation group was studied 11.2 ± 1.6 hours (range 8–14 hours) postinjury, the admission Glasgow Coma Scale (GCS) score was 5.6 ± 1.8, the mean age was 27 ± 9 years, and eight of the nine patients were men. In the severe hyperventilation group, the admission GCS score was 4.3 ± 1.5, the mean age was 31 ± 6 years, and all patients were men. Positron emission tomography measurements of regional CBF, cerebral blood volume, CMRO2, and oxygen extraction fraction (OEF) were obtained before and during hyperventilation. In all 13 patients an automated search routine was used to identify 2.1-cm spherical nonoverlapping regions with CBF values below thresholds of 20, 15, and 10 ml/100 g/min during hyperventilation, and the change in CMRO2 in those regions was determined. In the regions in which CBF was less than 20 ml/100 g/min during hyperventilation, it fell from 26 ± 6.2 to 13.7 ± 1 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.59 (p < 0.0001), and CMRO2 was unchanged (1.12 ± 0.29 compared with 1.14 ± 0.03 ml/100 g/min; p = 0.8). In the regions in which CBF was less than 15 ml/100 g/min during hyperventilation, it fell from 23.3 ± 6.6 to 11.1 ± 1.2 ml/100 g/min (p < 0.0001), OEF rose from 0.31 to 0.63 (p < 0.0001), and CMRO2 was unchanged (0.98 ± 0.19 compared with 0.97 ± 0.23 ml/100 g/min; p = 0.92). In the regions in which CBF was less than 10 ml/100 g/min during hyperventilation, it fell from 18.2 ± 4.5 to 8.1 ± 0 ml/100 g/min (p < 0.0001), OEF rose from 0.3 to 0.71 (p < 0.0001), and CMRO2 was unchanged (0.78 ± 0.26 compared with 0.84 ± 0.32 ml/100 g/min; p = 0.64). Conclusions. After severe TBI, brief hyperventilation produced large reductions in CBF but not energy failure, even in regions in which CBF fell below the threshold for energy failure defined in acute ischemia. Oxygen metabolism was preserved due to the low baseline metabolic rate and compensatory increases in OEF; thus, these reductions in CBF are unlikely to cause further brain injury.


1994 ◽  
Vol 81 (5) ◽  
pp. 726-733 ◽  
Author(s):  
Ricardo E. Jorge ◽  
Robert G. Robinson ◽  
Sergio E. Starkstein ◽  
Stephan V. Arndt

✓ The authors examine those factors that contributed to deterioration in social functioning, activities of daily living, or intellectual functioning during a 1-year period after traumatic brain injury (TBI). Fifty-two patients suffering an acute TBI were evaluated for existence and severity of mood disorders and impairment during their hospital stays and at 3-, 6-, and 12-month follow-up examinations. Patients whose scores on intellectual function, social function, or daily activities deteriorated during the 1-year period after trauma were considered to have a poor outcome. Eleven of 52 patients had a poor outcome in social function, which was associated with race, right-hemisphere lesions, intellectual impairment, and prolonged major depression. Seven of 52 patients had a poor outcome in daily activities, which was associated with a major depression of more than 6 months' duration and severity of Hamilton Depression Rating Scale scores. Eleven of these patients had a poor outcome in cognitive function, which was associated with cognitive impairment immediately after TBI. A major depression lasting more than 6 months was associated with deterioration of social functioning and activities of daily living during the 1-year period after TBI.


2009 ◽  
Vol 110 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Magnus Olivecrona ◽  
Bo Zetterlund ◽  
Marie Rodling-Wahlström ◽  
Silvana Naredi ◽  
Lars-Owe D. Koskinen

Object The authors prospectively studied the occurrence of clinical and nonclinical electroencephalographically verified seizures during treatment with an intracranial pressure (ICP)–targeted protocol in patients with traumatic brain injury (TBI). Methods All patients treated for TBI at the Department of Neurosurgery, University Hospital Umeå, Sweden, were eligible for the study. The inclusion was consecutive and based on the availability of the electroencephalographic (EEG) monitoring equipment. Patients were included irrespective of pupil size, pupil reaction, or level of consciousness as long as their first measured cerebral perfusion pressure was > 10 mm Hg. The patients were treated in a protocol-guided manner with an ICP-targeted treatment based on the Lund concept. The patients were continuously sedated with midazolam, fentanyl, propofol, or thiopental, or combinations thereof. Five-lead continuous EEG monitoring was performed with the electrodes at F3, F4, P3, P4, and a midline reference. Sensitivity was set at 100 μV per cm and filter settings 0.5–70 Hz. Amplitude-integrated EEG recording and relative band power trends were displayed. The trends were analyzed offline by trained clinical neurophysiologists. Results Forty-seven patients (mean age 40 years) were studied. Their median Glasgow Coma Scale score at the time of sedation and intubation was 6 (range 3–15). In 8.5% of the patients clinical seizures were observed before sedation and intubation. Continuous EEG monitoring was performed for a total of 7334 hours. During this time neither EEG nor clinical seizures were observed. Conclusions Our protocol-guided ICP targeted treatment seems to protect patients with severe TBI from clinical and subclinical seizures and thus reduces the risk of secondary brain injury.


1999 ◽  
Vol 7 (3) ◽  
pp. E1 ◽  
Author(s):  
Paul M. Vespa ◽  
Marc R. Nuwer ◽  
Valeriy Nenov ◽  
Elisabeth Ronne-Engstrom ◽  
David A. Hovda ◽  
...  

Object The early pathophysiological features of traumatic brain injury observed in the intensive care unit (ICU) have been described in terms of altered cerebral blood flow, altered brain metabolism, and neurochemical excitotoxicity. Seizures occur in animal models of brain injury and in human brain injury. Previous studies of posttraumatic seizures in humans have been based principally on clinical observations without a systematic approach to electroencephalographic (EEG) recording of seizures. The purpose of this study was to determine prospectively the incidence of convulsive and nonconvulsive seizures by using continuous EEG monitoring in patients in the ICU during the initial 14 days postinjury. Methods Ninety-four patients with moderate-to-severe brain injuries underwent continuous EEG monitoring beginning at admission to the ICU (mean delay 9.6 ± 5.4 hours) and extending up to 14 days postinjury. Convulsive and nonconvulsive seizures occurred in 21 (22%) of the 94 patients, with six of them displaying status epilepticus. In more than half of the patients (52%) the seizures were nonconvulsive and were diagnosed on the basis of EEG studies alone. All six patients with status epilepticus died, compared with a mortality rate of 18 (24%) of 73 in the nonseizure group (p < 0.001). The patients with status epilepticus had a shorter mean length of stay (9.14 ± 5.9 days compared with 14 ± 9 days (t-test, p < 0.03). Seizures occurred despite initiation of prophylactic phenytoin on admission to the emergency room, with maintenance at mean levels of 16.6 ± 2.8 mg/dl. No differences in key prognostic factors (such as the Glasgow Coma Scale score, early hypoxemia, early hypotension, or 1-month Glasgow Outcome Scale score) were found between the patients with seizures and those without. Conclusions Seizures occur in more than one in five patients during the 1st week after moderate-to-severe brain injury and may play a role in the pathobiological conditions associated with brain injury.


2000 ◽  
Vol 92 (1) ◽  
pp. 7-13 ◽  
Author(s):  
Michael N. Diringer ◽  
Kent Yundt ◽  
Tom O. Videen ◽  
Robert E. Adams ◽  
Allyson R. Zazulia ◽  
...  

Object. Hyperventilation has been used for many years in the management of patients with traumatic brain injury (TBI). Concern has been raised that hyperventilation could lead to cerebral ischemia; these concerns have been magnified by reports of reduced cerebral blood flow (CBF) early after severe TBI. The authors tested the hypothesis that moderate hyperventilation induced early after TBI would not produce a reduction in CBF severe enough to cause cerebral energy failure (CBF that is insufficient to meet metabolic needs).Methods. Nine patients were studied a mean of 11.2 ± 1.6 hours (range 8–14 hours) after TBI occurred. The patients' mean Glasgow Coma Scale score was 5.6 ± 1.8 and their mean age 27 ± 9 years; eight of the patients were male. Intracranial pressure (ICP), mean arterial blood pressure, and jugular venous oxygen content were monitored and cerebral perfusion pressure was maintained at a level higher than 70 mm Hg by using vasopressors when needed. Measurements of CBF, cerebral blood volume (CBV), cerebral metabolic rate for oxygen (CMRO2), oxygen extraction fraction (OEF), and cerebral venous oxygen content (CvO2) were made before and after 30 minutes of hyperventilation to a PaCO2 of 30 ± 2 mm Hg. Ten age-matched healthy volunteers were used as normocapnic controls.Global CBF, CBV, and CvO2 did not differ between the two groups, but in the TBI patients CMRO2 and OEF were reduced (1.59 ± 0.44 ml/100 g/minute [p < 0.01] and 0.31 ± 0.06 [p < 0.0001], respectively). During hyperventilation, global CBF decreased to 25.5 ± 8.7 ml/100 g/minute (p < 0.0009), CBV fell to 2.8 ± 0.56 ml/100 g (p < 0.001), OEF rose to 0.45 ± 0.13 (p < 0.02), and CvO2 fell to 8.3 ± 3 vol% (p < 0.02); CMRO2 remained unchanged.Conclusions. The authors conclude that early, brief, moderate hyperventilation does not impair global cerebral metabolism in patients with severe TBI and, thus, is unlikely to cause further neurological injury. Additional studies are needed to assess focal changes, the effects of more severe hyperventilation, and the effects of hyperventilation in the setting of increased ICP.


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