Prognostic implications of early multimodality evoked potentials in severely head-injured patients

1981 ◽  
Vol 55 (2) ◽  
pp. 227-236 ◽  
Author(s):  
Richard P. Greenberg ◽  
Pauline G. Newlon ◽  
Marti S. Hyatt ◽  
Raj K. Narayan ◽  
Donald P. Becker
Keyword(s):  
Patient Outcome ◽  
Head Injury ◽  
Evoked Potentials ◽  
Grade Group ◽  
Systemic Complications ◽  
Content Type ◽  
Head Injured ◽  
Multimodality Evoked Potentials ◽  
Mass Lesions ◽  
Injured Patients

✓ Results of multimodality evoked potential (MEP) studies recorded from 100 comatose patients soon after severe head injury were analyzed prospectively, using a previously established grading system, to assess the prognostic value of MEP's with respect to patient outcome, to evaluate the effect of clinically relevant sequelae of head injury on the prediction of outcome by MEP's, and to describe time to clinical recovery as a function of initial MEP grade. Graded MEP's, when recorded in the first few days after head injury, could predict patient outcome at 1 year with approximately 80% accuracy. Exclusion from the analysis of patients who died from causes unrelated to the brain and those with severe systemic complications that occurred after the evoked potentials were recorded improved the accuracy of outcome prediction to nearly 100%. The presence of a mass lesion requiring surgery reduces the probability of good to moderate outcome for a given MEP grade group by approximately 25% to 40% from that seen in patients without mass lesions. The clinical outcome predicted shortly after head injury by MEP grades may not be realized for many months. Patients with mild MEP abnormality (Grade I or II) generally reach their outcome by 3 to 6 months, whereas those with more severe deficits (Grade III) may not show improvement for at least 1 year.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

High-risk mild head injury

1997 ◽  
Vol 87 (2) ◽  
pp. 234-238 ◽  
Author(s):  
John N. K. Hsiang ◽  
Theresa Yeung ◽  
Ashley L. M. Yu ◽  
Wai S. Poon
Keyword(s):  
Head Injury ◽  
High Risk ◽  
Mild Head Injury ◽  
Radiographic Findings ◽  
Content Type ◽  
Head Injured ◽  
Definition Of ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

✓ The generally accepted definition of mild head injury includes Glasgow Coma Scale (GCS) scores of 13 to 15. However, many studies have shown that there is a heterogeneous pathophysiology among patients with GCS scores in this range. The current definition of mild head injury is misleading because patients classified in this category can have severe sequelae. Therefore, a prospective study of 1360 head-injured patients with GCS scores ranging from 13 to 15 who were admitted to the neurosurgery service during 1994 and 1995 was undertaken to modify the current definition of mild head injury. Data regarding patients' age, sex, GCS score, radiographic findings, neurosurgical intervention, and 6-month outcome were collected and analyzed. The results of this study showed that patients with lower GCS scores tended to have suffered more serious injury. There was a statistically significant trend across GCS scores for percentage of patients with positive acute radiographic findings, percentage receiving neurosurgical interventions, and percentage with poor outcome. The presence of postinjury vomiting did not correlate with findings of acute radiographic abnormalities. Based on the results of this study, the authors divided all head-injured patients with GCS scores ranging from 13 to 15 into mild head injury and high-risk mild head injury groups. Mild head injury is defined as a GCS score of 15 without acute radiographic abnormalities, whereas high-risk mild head injury is defined as GCS scores of 13 or 14, or a GCS score of 15 with acute radiographic abnormalities. This more precise definition of mild head injury is simple to use and may help avoid the confusion caused by the current classification.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors

1992 ◽  
Vol 77 (5) ◽  
pp. 694-699 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Claramae H. Miller ◽  
Franklin C. Wagner ◽  
Sally J. DeNardo ◽  
Gerald L. DeNardo ◽  
...  
Keyword(s):  
Head Injury ◽  
Cellular Immunity ◽  
Severe Head Injury ◽  
Normal Subjects ◽  
Lymphocyte Function ◽  
Serum Factors ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Effect of apolipoprotein E genotype on hematoma volume after trauma

2002 ◽  
Vol 96 (1) ◽  
pp. 90-96 ◽  
Author(s):  
Imran Liaquat ◽  
Laurence T. Dunn ◽  
James A. R. Nicoll ◽  
Graham M. Teasdale ◽  
John D. Norrie
Keyword(s):  
Head Injury ◽  
Ct Scan ◽  
Injury Severity ◽  
Univariate Analysis ◽  
Hematoma Volume ◽  
Patient Age ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The apolipoprotein E-ϵ4 (APOE-ϵ4) allele is associated with poor outcome after head injury and spontaneous intracerebral hemorrhage (SICH). The aims of this study were to determine if patients in whom one or more APOE-ϵ4 alleles are present are more likely to sustain intracranial mass lesions after head injury and to determine whether there is an isoform-specific effect on the size of the intracranial hematoma. Methods. The authors performed a computerized volumetric analysis of 142 hematomas visible on computerized tomography (CT) scans obtained in 129 patients. The APOE genotype was determined by subjecting buccal smear samples to polymerase chain reaction and restriction enzyme digestion. Allele frequencies were similar in head-injured patients with and without intracranial hematomas (p = 0.36). Univariate analysis revealed that in those patients with one or more APOE-ϵ4 alleles hematoma volume was greater (cube root—transformed values) than that found in patients without the APOE-ϵ4 allele (3.1 cm compared with 2.5 cm, p = 0.0039). The results of univariate analysis also suggested significant effects of patient age, injury severity (mild, moderate, or severe according to admission Glasgow Coma Scale scores) and hematoma location (extraaxial, intraaxial, or both) on hematoma volume. The mechanism of injury (assault, fall, or other) was marginally associated with hematoma volume (p = 0.052). Time from injury to CT scan, hypoxia, and hypotension had no significant effect on hematoma volume. The results of multiple linear regression analysis showed that the presence of an APOE-ϵ4 allele and an extraaxial hematoma location were independent predictors of hematoma volume, after adjusting for patient age, hours between injury and CT scan, injury severity, and injury mechanism. Conclusions. Larger hematomas were found in head-injured patients with one or more APOE-ϵ4 alleles than in patients without the allele. This may contribute to the poorer outcomes observed in these patients.

Failure of prophylactic barbiturate coma in the treatment of severe head injury

1985 ◽  
Vol 62 (3) ◽  
pp. 383-388 ◽  
Author(s):  
John D. Ward ◽  
Donald P. Becker ◽  
J. Douglas Miller ◽  
Sung C. Choi ◽  
Anthony Marmarou ◽  
...  
Keyword(s):  
Head Injury ◽  
Severe Head Injury ◽  
Controlled Trial ◽  
Neurological Status ◽  
Treated Group ◽  
Control Group ◽  
Barbiturate Coma ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients

✓ In certain subgroups of severely head-injured patients, the mortality rate remains unacceptably high. The authors describe a randomized, controlled trial of prophylactic pentobarbital therapy in a group of these patients. Pentobarbital was started as soon as possible after the head injury, regardless of the intracranial pressure (ICP), and was continued for a prescribed period of time. The study included 53 consecutive head-injured patients over the age of 12 years, who had either an acute intradural hematoma (subdural and/or intracerebral, large enough to warrant surgical decompression), or no mass lesion but whose best motor response was abnormal flexion or extension. All patients in the study were randomly assigned to a control group (26 cases) or a pentobarbital-treated group (27 cases) once the diagnosis had been made and informed consent obtained. All patients were treated with the same protocol of aggressive resuscitation, prompt diagnosis and treatment of mass lesions, and intensive care, with close follow-up monitoring. The randomization was effective in producing a close match between the control and treated groups with respect to age, sex distribution, cause of injury, neurological status, intracranial lesions, prevalence of early systemic insults, midline shift, and initial ICP. Outcome was essentially the same in each group. There was no difference between groups in the incidence of elevated ICP, the duration of ICP elevation, or the response of ICP elevations to treatment. Arterial hypotension occurred in 14 patients (54%) in the treated group and only two patients (7percnt;) in the untreated group. Based on these data the authors cannot recommend the prophylactic use of pentobarbital coma in the treatment of patients with severe head injury. They also believe that its use is accompanied by significant side effects which can potentially worsen the condition of a patient with severe head injury.

Determination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver operating—characteristic curves: an observational study in 291 patients

2001 ◽  
Vol 94 (3) ◽  
pp. 412-416 ◽  
Author(s):  
Iain Robert Chambers ◽  
Lynne Treadwell ◽  
A. David Mendelow
Keyword(s):  
Cerebral Perfusion ◽  
Operating Characteristic ◽  
Perfusion Pressure ◽  
Roc Curves ◽  
Content Type ◽  
Head Injured ◽  
Mass Lesions ◽  
Injured Patients ◽  
Fine Print

Object. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are frequently monitored in severely head injured patients. To establish which one (ICP or CPP) is more predictive of outcome and to examine whether there are significant threshold levels in the determination of outcome, receiver—operating characteristic (ROC) curves were used to analyze data in a large series of head-injured patients. Methods. Data were obtained from a total of 291 severely head injured patients (207 adults and 84 children). Outcome was categorized as either independent (good recovery or moderate disability) or poor (severely disabled, vegetative, or dead) by using the Glasgow Outcome Scale; patients were also grouped according to the Marshall computerized tomography scan classification. Conclusions. The maximum value of a 2-minute rolling average of ICP readings (defined as ICPmax) and the minimum value of the CPP readings (CPPmin) were then used to calculate the sensitivity and specificity of the ROC curves over a range of values. Using ROC curves, a threshold value for CPPmin of 55 mm Hg and for ICPmax of 35 mm Hg appear to be the best predictors in adults. For children the levels appear to be 43 to 45 mm Hg for CPPmin and 35 mm Hg for ICPmax. Higher levels of CPPmin seem important in adults with mass lesions. These CPP thresholds (45 mm Hg for children and 55 mm Hg for adults) are lower than previously predicted and may be clinically important, especially in children, in whom a lower blood pressure level is normal. Also, CPP management at higher levels may be more important in adults with mass lesions. A larger observational series would improve the accuracy of these predictions.

Flaccidity after Head Injury

Neurosurgery ◽  
1981 ◽  
Vol 9 (3) ◽  
pp. 242-248 ◽  
Author(s):  
John F. Butterworth ◽  
John B. Selhorst ◽  
Richard P. Greenberg ◽  
Douglas Miller ◽  
Steven K. Gudeman
Keyword(s):  
Head Injury ◽  
High Serum ◽  
Respiratory Complications ◽  
Intracranial Mass ◽  
Cord Injury ◽  
Head Injured ◽  
Spinal Subdural Hematoma ◽  
Mass Lesions ◽  
Injured Patients ◽  
Prompt Diagnosis

Abstract Upon admission, 17 of 223 (8%) consecutive patients with severe head injury exhibited a flaccid, wholly unresponsive motor examination. In this study alcoholic intoxication neither caused depressed motor responsiveness in head-injured patients with high serum ethanol levels nor accounted for the motor examination in those exhibiting the flaccid state. Flaccidity was attributed principally to impaired ventilation in 4 patients, a major intracranial mass in 12. and a spinal cord injury in 1. Compared to the larger group of head-injured patients, the flaccid patients had a significantly greater incidence of hypercapnia (P &lt; 0.001), acidosis (P &lt; 0.01), and both elevated and uncontrollable intracranial pressure (ICP) (P&lt; 0.001). These findings and the high mortality rate (76%) in this study suggest that the magnitude of respiratory complications and the severity of mechanical brain injury are greater in flaccid patients. The flaccid patients undergoing surgical decompression for major intracranial mass lesions (11 cases) have all died and. although still small in number, this group may represent an important subset with a poor prognosis. Nonetheless, a protocol that encourages rapid radiological and electrophysiological assessment and vigorous surgical and ICP management until the probable cause of flaccidity is identified and treated has benefit. The flaccid state was reversed and a good recovery was attained after the restoration of blood pressure and/or ventilation in 2 patients who appeared to have sustained a very grave head injury. In another patient, absent somatosensory evoked potentials greatly facilitated the diagnosis of a spinal subdural hematoma. This program of prompt diagnosis and intense therapy did not result in a protracted course or undue numbers of severely braindamaged survivors.

Cerebral autoregulation following head injury

2001 ◽  
Vol 95 (5) ◽  
pp. 756-763 ◽  
Author(s):  
Marek Czosnyka ◽  
Piotr Smielewski ◽  
Stefan Piechnik ◽  
Luzius A. Steiner ◽  
John D. Pickard
Keyword(s):  
Head Injury ◽  
Cerebral Autoregulation ◽  
Perfusion Pressure ◽  
Content Type ◽  
Arterial Blood ◽  
Head Injured ◽  
The Mean ◽  
Injured Patients ◽  
The Relationship ◽  
Fine Print

Object. The goal of this study was to examine the relationship between cerebral autoregulation, intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP) after head injury by using transcranial Doppler (TCD) ultrasonography. Methods. Using ICP monitoring and TCD ultrasonography, the authors previously investigated whether the response of flow velocity (FV) in the middle cerebral artery to spontaneous variations in ABP or CPP provides reliable information about cerebral autoregulatory reserve. In the present study, this method was validated in 187 head-injured patients who were sedated and receiving mechanical ventilation. Waveforms of ICP, ABP, and FV were recorded over intervals lasting 20 to 120 minutes. Time-averaged mean FV and CPP were determined. The correlation coefficient index between FV and CPP (the mean index of autoregulation [Mx]) was calculated over 4-minute epochs and averaged for each investigation. The distribution of averaged mean FV values converged with the shape of the autoregulatory curve, indicating lower (CPP < 55 mm Hg) and upper (CPP > 105 mm Hg) thresholds of autoregulation. The relationship between the Mx and either the CPP or ABP was depicted as a U-shaped curve. Autoregulation was disturbed in the presence of intracranial hypertension (ICP ≥ 25 mm Hg) and when mean ABP was too low (ABP < 75 mm Hg) or too high (ABP > 125 mm Hg). Disturbed autoregulation (p < 0.005) and higher ICP (p < 0.005) occurred more often in patients with unfavorable outcomes than in those with favorable outcomes. Conclusions. Autoregulation not only is impaired when associated with a high ICP or low ABP, but it can also be disturbed by too high a CPP. The Mx can be used to guide intensive care therapy when CPP-oriented protocols are used.

Cerebral autoregulation following minor head injury

1997 ◽  
Vol 86 (3) ◽  
pp. 425-432 ◽  
Author(s):  
Elisabeth C. Jünger ◽  
David W. Newell ◽  
Gerald A. Grant ◽  
Anthony M. Avellino ◽  
Saadi Ghatan ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Head Injury ◽  
Cerebral Autoregulation ◽  
Minor Head Injury ◽  
Lower Blood Pressure ◽  
Content Type ◽  
Lower Blood ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI). Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

Effects of Therapeutic Pentobarbital Coma on Multimodality Evoked Potentials Recorded from Severely Head-injured Patients

Neurosurgery ◽  
1983 ◽  
Vol 12 (6) ◽  
pp. 613-619 ◽  
Author(s):  
Pauline G. Newlon ◽  
Richard P. Greenberg ◽  
Gregory G. Enas ◽  
Donald P. Becker
Keyword(s):  
Evoked Potentials ◽  
Brain Function ◽  
Brain Dysfunction ◽  
Control Group ◽  
Wave Form ◽  
Long Latency ◽  
Head Injured ◽  
The Mean ◽  
Multimodality Evoked Potentials ◽  
Injured Patients

Abstract We sought to determine whether pentobarbital (PB) coma compromises the use of evoked potentials (EPs) in the assessment of brain dysfunction and of the prognosis of severely head-injured patients. Therefore, the effects of therapeutic PB on somatosensory (SEPs, BSEPs), visual (VEPs), and auditory (BAEPs) evoked potentials recorded from 20 patients early after injury were analyzed. Seventeen head-injured patients served as controls. EP studies were obtained shortly after admission (Mean Day 2, PB present) and approximately 2 weeks after injury (Mean Day 15, PB absent). The mean serum level of PB in the treatment group was 1.9 mg/100 ml. The drug effect was assessed by comparisons between the PB and the control groups. Statistical analyses were based on differences observed between two studies in the same patient. Analyses of covariance (F tests) were performed on data from all modalities. Wave form complexity was minimally affected by the drug. Middle and long latency components of the SEP were depressed by PB, and latencies of BSEP peaks and the early components of the SEP were delayed. The amplitude of some VEP peaks was reduced by PB. The BAEP was not significantly altered. All of the observed effects of PB were determined to be due to the hypothermia exhibited by PB-treated patients (mean temperature, 36.1ºC), which was not seen in the control group (mean, 37.8ºC). It is concluded that, with appropriate interpretation, EPs can be used to monitor brain function in head-injured patients when PB therapy is used.

Sign in / Sign up

Export Citation Format

Share Document