Severity Of Diffuse Axonal Injury Research Articles

Diffuse Axonal Injury Pattern Predicts Timing of In-Hospital Neurologic Recovery: A Retrospective Case Series

Diffuse axonal injury (DAI) is a devastating traumatic neurological injury with variable prognosis. Although outcomes such as mortality have been described, the time course of neurological progression is poorly understood. We investigated the association between DAI neuroanatomical injury pattern and neurological recovery timing. A retrospective review of our institution's trauma registry identified patients diagnosed with DAI from 2017-2021. Neuroradiologist review of head CT was used to score DAI severity. In-hospital neurological exams were reviewed, and GCS was calculated for all patients throughout the hospital stay. Categorical variables were analyzed using Fisher's exact test and continuous variables were analyzed using Kruskal-Wallis test. Nineteen DAI patients (Grade 1=8; Grade 2=1; Grade 3=10) were included (mean age 31 years, 79% male). Mean Rotterdam CT score, Injury Severity Scale, and admission GCS were comparable across DAI grades. Mean time in days to follow commands was shorter for those with Grade 1 DAI (9.3) compared to Grade 2 (17 days) or Grade 3 (19 days) DAI (p=0.02). Throughout hospitalization, patients with Grade 1 DAI had higher motor (p=0.006), eye (p=0.001), and total GCS (p=0.011) score compared to those with Grade 2 or 3 DAI. At the time of discharge, total GCS and the frequency of command following was similar across DAI grades. Patients with Grade 1 DAI demonstrated the fastest short-term neurological recovery, although final discharge neurological examination was comparable across DAI grades. DAI classification can provide useful short-term prognostic information regarding in-hospital neurological improvement.

To assess and analyze the clinical outcome of conservative and operative management of head injury in acute subdural haematoma

Traumatic acute subdural haematoma (SDH) continue to have high mortality & morbidity despite the advent of rapid transportation, CT Scan and Intensive care management. The general surgical procedures for Acute SDH is Craniotomy with removal of haematoma & decompressive craniectomy if necessary. This is a study based in department of surgery. After taking complete history and detailed examination and investigation (CT Scan) was be done. Decision of surgery was be taken by the consultant neurosurgeon of the acute Subdural Haematoma, involvement of aloquent areas and associated other injury of brain.200 patients with head injury who reported at casualty of Gandhi Medical College, and Hamidia Hospital, Bhopal.In our study, Mode of Injury found to be Assault were 20%, Fall were 27% & RTA 53% in Conservative whereas Assault were 06%, Fall were 14% & RTA 80%.The chi-square statistic is 96.3397. The p-value is < 0.00001. The result is significant at p < 0.05. These findings indicate that the thickness/size of acute SDH significantly correlates with the type of management to be done for the patient.Acute subdural haematoma is the major cause of significant morbidity and mortality due to traumatic head injury. Acute subdual haematoma is commonly associated with countercoup injuries and diffuse axonal injury (DAI). The clinical presentation in patients with acute SDH is related to raised ICP and the severity of DAI. C.T. Scan is the investigation of choice in patients with head injury.

Functional plasticity in lateral hypothalamus and its prediction of cognitive impairment in patients with diffuse axonal injury: evidence from a resting-state functional connectivity study.

Diffuse axonal injury (DAI) is a common pathological process after traumatic brain injury, which may cause survivors severe functional disorders, including cognitive impairment and physical disability. Recent literature indicated lateral hypothalamus and medial hypothalamus damage during DAI. Thus, we aim to investigate whether there is imaging evidence of hypothalamic injury in patients with DAI and its clinical association. Twenty-four patients with diagnosed DAI and 26 age and sex-matched healthy controls underwent resting-state functional MRI. We assessed the lateral hypothalamus and medial hypothalamus functional connectivity with seed-based analysis in DAI. Furthermore, a partial correlation was used to measure its clinical association. The prediction of the severity of DAI from the altered lateral hypothalamus and medial hypothalamus connectivity was conducted using a general linear model. Compared with healthy control, the DAI group showed significantly decreased lateral hypothalamus functional connectivity with the basal ganglia and cingulate gyrus, which was positively correlated with mini-mental state examination scores (Bonferroni correction at P < 0.0125). Importantly, this disrupted functional connectivity can be used to predict the patients' cognitive state reliably (P = 0.006; P = 0.009, respectively) in DAI. Moreover, we also observed increased connectivity of medial hypothalamus with the superior temporal gyrus and the regions around the operculum. Furthermore, there was a trend of negative correlation between the medial hypothalamus functional connectivity changes to the right superior temporal gyrus and the disability rating scale scores in the DAI group. Our results suggest that there are alterations of medial hypothalamus and lateral hypothalamus connectivity in DAI and further understand its clinical symptoms, including related cognitive impairment.

Diffuse axonal injury has a characteristic multidimensional MRI signature in the human brain.

Axonal injury is a major contributor to the clinical symptomatology in patients with traumatic brain injury. Conventional neuroradiological tools, such as CT and MRI, are insensitive to diffuse axonal injury (DAI) caused by trauma. Diffusion tensor MRI parameters may change in DAI lesions; however, the nature of these changes is inconsistent. Multidimensional MRI is an emerging approach that combines T1, T2, and diffusion, and replaces voxel-averaged values with distributions, which allows selective isolation of specific potential abnormal components. By performing a combined post-mortem multidimensional MRI and histopathology study, we aimed to investigate T1-T2-diffusion changes linked to DAI and to define their histopathological correlates. Corpora callosa derived from eight subjects who had sustained traumatic brain injury, and three control brain donors underwent post-mortem ex vivo MRI at 7 T. Multidimensional, diffusion tensor, and quantitative T1 and T2 MRI data were acquired and processed. Following MRI acquisition, slices from the same tissue were tested for amyloid precursor protein (APP) immunoreactivity to define DAI severity. A robust image co-registration method was applied to accurately match MRI-derived parameters and histopathology, after which 12 regions of interest per tissue block were selected based on APP density, but blind to MRI. We identified abnormal multidimensional T1-T2, diffusion-T2, and diffusion-T1 components that are strongly associated with DAI and used them to generate axonal injury images. We found that compared to control white matter, mild and severe DAI lesions contained significantly larger abnormal T1-T2 component (P = 0.005 and P < 0.001, respectively), and significantly larger abnormal diffusion-T2 component (P = 0.005 and P < 0.001, respectively). Furthermore, within patients with traumatic brain injury the multidimensional MRI biomarkers differentiated normal-appearing white matter from mild and severe DAI lesions, with significantly larger abnormal T1-T2 and diffusion-T2 components (P = 0.003 and P < 0.001, respectively, for T1-T2; P = 0.022 and P < 0.001, respectively, for diffusion-T2). Conversely, none of the conventional quantitative MRI parameters were able to differentiate lesions and normal-appearing white matter. Lastly, we found that the abnormal T1-T2, diffusion-T1, and diffusion-T2 components and their axonal damage images were strongly correlated with quantitative APP staining (r = 0.876, P < 0.001; r = 0.727, P < 0.001; and r = 0.743, P < 0.001, respectively), while producing negligible intensities in grey matter and in normal-appearing white matter. These results suggest that multidimensional MRI may provide non-invasive biomarkers for detection of DAI, which is the pathological substrate for neurological disorders ranging from concussion to severe traumatic brain injury.

Age, Sex and Cerebral Microbleed Effects On White Matter Degradation After Traumatic Brain Injury

Mild traumatic brain injury (mTBI) affects white matter (WM) integrity and accelerates neurodegeneration. This study assesses the effects of age, sex, and cerebral microbleed (CMB) load as predictors of WM integrity in 70 subjects aged 18-77 imaged acutely and ~6 months after mTBI using diffusion tensor imaging (DTI). Two-tensor unscented Kalman tractography was used to segment and cluster 73 WM structures and to map changes in their mean fractional anisotropy (FA), a surrogate measure of WM integrity. Dimensionality reduction of mean FA feature vectors was implemented using principal component (PC) analysis, and two prominent PCs were used as responses in a multivariate analysis of covariance. Acutely and chronically, older age was significantly associated with lower FA (F2,65 = 8.7, p < .001, η2 = 0.2; F2,65 = 12.3, p < .001, η2 = 0.3, respectively), notably in the corpus callosum and in dorsolateral temporal structures, confirming older adults’ WM vulnerability to mTBI. Chronically, sex was associated with mean FA (F2,65 = 5.0, p = 0.01, η2 = 0.1), indicating males’ greater susceptibility to WM degradation. Acutely, a significant association was observed between CMB load and mean FA (F2,65 = 5.1, p = 0.009, η2 = 0.1), suggesting that CMBs reflect the acute severity of diffuse axonal injury. Together, these findings indicate that older age, male sex, and CMB load are risk factors for WM degeneration. Future research should examine how sex- and age-mediated WM degradation lead to cognitive decline and connectome degeneration after mTBI.

Subcallosal haemorrhage as a sign of diffuse axonal injury in patients with traumatic brain injury

To identify the relationship between subcallosal haemorrhage and diffuse axonal injury (DAI) grading. Computed tomography (CT) and magnetic resonance imaging (MRI) images of all patients with traumatic brain injury over the past 5 years were reviewed. Subcallosal haemorrhage was defined as the presence of haemorrhage on admission CT underneath the corpus callosum. Grading of DAI was performed using MRI or CT exclusive of subcallosal haemorrhage status. The association of demographic factors, mechanism of injury, Glasgow Coma Scale (GCS) on admission, and positive subcallosal haemorrhage status with the presence of moderate-severe DAI was assessed. Receiver operating characteristic (ROC) curve analysis was used to evaluate the performance of subcallosal haemorrhage status in predicting DAI severity. Median modified Rankin Scale (mRS) scores were compared between subcallosal haemorrhage positive and negative cases. The images of 1,150 patients were reviewed with 301 patients showing DAI. Of those, 64 patients (21.2%) and 237 patients (78.7%) were positive and negative for subcallosal haemorrhage, respectively. Isolated subcallosal haemorrhage was noted in 15 patients (23.4%). A subcallosal haemorrhage positive status (OR=5.16, p<0.001) was statistically significantly associated with moderate-severe DAI. The ROC curve for predicting moderate-severe DAI with subcallosal haemorrhage status showed an area under the curve of 0.625 (95% confidence interval [CI]: 0.561-0.688, p<0.001). The median mRS score was significantly higher (p<0.001) in the subcallosal haemorrhage positive group (median 4.5, interquartile range [IQR] 2-6) versus the negative group (median 2, IQR 2-3). Isolated subcallosal haemorrhage group showed moderate-severe DAI in 80% (12/15) of cases. Subcallosal haemorrhage is a highly specific radiographic predictor of moderate-severe DAI (grade 2-3).

Serum levels of tau protein increase according to the severity of the injury in DAI rat model.

Traumatic brain injury (TBI) in the form of diffuse axonal injury (DAI) is difficult to diagnose in the early phase of the injury. Early diagnosis of DAI may provide opportunity for developing treatment and management strategies. Tau protein has been demonstrated to increase in the early phase of TBI with high diagnostic accuracy in patients with DAI. We tested the biological plausibility of tau protein using a rat DAI model by evaluating the association between serum tau levels and the severity of brain injury.DAI was induced in animals using the Marmarou model.After a survival of 60 minutes, rats were anesthetized and sacrificed after obtaining blood samples (5ml) from the heart. Eighteenratswereemployedin the present studyand were randomly subjected to sham-operated control (n=4), mild DAI (n=7), and severe DAI (n=7). Of seven severe DAI rats, two rats that had focal injury caused by skull fracture were excluded in the measurement of tau protein level. The serum levels of tau protein in the rat DAI model were found to increase significantly and consistently according to the severity of the injury.Rats with DAI showed significantly higher serum levels of tau protein compared to sham rats; the severe DAI rats had higher levels of tau than moderate DAI and sham rats (sham vs. mild, P=0.02; mild vs. severe, P=0.02). In conclusion, serum tau protein levels may be useful as a biomarker for diagnosing and estimating the severity of DAI in the early phase.

Factors Affecting Diffuse Axonal Injury under Blunt Impact and Proposal for a Head Injury Criteria: A Finite Element Analysis.

Diffuse axonal injury (DAI) is the most common pathological feature of brain injury which accounts for half of the traumatic lesions in the United States. Although direct shear strain measures indicate DAI, it is localized and varies greatly in the brain. It has limitations when correlated with the possibility and severity of DAI in different brain regions along different planes for variable factors. Rather, a statistical strain measure such as peak shear strain possibility (PSSP) is proposed as a head injury criteria. In this study, computer tomography (CT) was used to derive a finite element model of the skull-brain complex including viscoelastic behavior for brain material. It was simulated under blunt impact for variable factors such as five impact directions, four impact velocities, and four head sizes. Nodal shear strain measures were obtained for seven brain regions along three planes. Proposed PSSPs for different shear strain level (10%90%) were calculated. Considering 30% shear strain as the critical level, PSSPs were 0.49 for corpus callosum and 0.71 for the brain stem along the sagittal plane, and 0.63 for frontal impact. Among eighty simulation cases (240 strain measures), the corpus callosum and brain stem have the highest possibility (30%) of DAI. Frontal impact is the most dangerous direction, followed by side-back and back impact. For all impact directions, the highest PSSP along the sagittal plane indicates the predominance of rotational motion of the brain for causing DAI. Head size variation has the least effect on DAI possibility. At higher impact velocities, DAI possibility increases nonlinearly. Hence, these proposed criteria are expected to predict DAI under variable factors.

Diffuse Axonal Injury: Epidemiology, Outcome and Associated Risk Factors.

Diffuse axonal injury (DAI), a type of traumatic injury, is known for its severe consequences. However, there are few studies describing the outcomes of DAI and the risk factors associated with it. This study aimed to describe the outcome for patients with a primary diagnosis of DAI 6 months after trauma and to identify sociodemographic and clinical factors associated with mortality and dependence at this time point. Seventy-eight patients with DAI were recruited from July 2013 to February 2014 in a prospective cohort study. Patient outcome was analyzed using the Extended Glasgow Outcome Scale (GOS-E) within 6 months of the traumatic injury. The mean Injury Severity Score was 35.0 (SD = 11.9), and the mean New Injury Severity Score (NISS) was 46.2 (SD = 15.9). Mild DAI was observed in 44.9% of the patients and severe DAI in 35.9%. Six months after trauma, 30.8% of the patients had died, and 45.1% had shown full recovery according to the GOS-E. In the logistic regression model, the severity variables – DAI with hypoxia, as measured by peripheral oxygen saturation, and hypotension with NISS value – had a statistically significant association with patient mortality; on the other hand, severity of DAI and length of hospital stay were the only significant predictors for dependence. Therefore, severity of DAI emerged as a risk factor for both mortality and dependence.

Serum Neurofilament Light Protein as a Marker for Diffuse Axonal Injury: Results from a Case Series Study.

Diffuse axonal injury (DAI) is an important cause of morbidity in patients with traumatic brain injury (TBI). There is currently no simple and reliable technique for early identification of patients with DAI, or to prognosticate long-term outcome in this patient group. In the present study, we examined acute serum concentrations of neurofilament light (NFL) in nine patients with severe TBI and DAI using a novel ultrasensitive single molecule array (Simoa) assay. The relationships between the NFL concentrations and MRI in the acute stage as well as clinical outcome and magnetic resonance diffusion tensor imaging (MR-DTI) parameters at 12 months were analyzed. We found that the mean NFL concentrations among the patients displayed a 30-fold increase compared with controls, and that NFL completely discriminated between the patients and controls. We also found a relationship between serum NFL and MR-DTI parameters, with higher NFL concentrations in patients with higher trace (R2 = 0.79) and lower fractional anisotropy (FA) (R 2 = 0.83). These results suggest that serum NFL may be a valuable blood biomarker for TBI, reflecting the severity of DAI.

びまん性軸索損傷の急性期重症度評価におけるSusceptibility Weighted Imagingの有用性

びまん性軸索損傷の急性期重症度評価におけるSusceptibility Weighted Imagingの有用性

Intraventricular hemorrhage on initial computed tomography as marker of diffuse axonal injury after traumatic brain injury.

Intraventricular hemorrhage (IVH) on initial computed tomography (CT) was reported to predict lesions of diffuse axonal injury (DAI) in the corpus callosum (CC) on subsequent magnetic resonance imaging (MRI). We aimed to examine the relationship between initial CT findings and DAI lesions detected on MRI as well as the relationship between the severity of IVH (IVH score) and severity of DAI (DAI staging). A consecutive 140 patients with traumatic brain injury (TBI) who underwent MRI within 30 days after onset were revisited. We reviewed their initial CT for the following six findings: Status of basal cistern, status of mid-line shift, epidural hematoma, IVH, subarachnoid hemorrhage, and volume of hemorrhagic mass and IVH score were assigned in each patient. Based on MRI findings, patients were divided into DAI and non-DAI groups and were assigned a DAI staging. Then, to confirm that the IVH on initial CT predicts DAI lesions on MRI, we used multi-variate analysis of the six CT findings, including IVH, and examined the relationship between IVH score and DAI staging. The IVH detected on CT was the only predictor of DAI (p=0.0139). The IVH score and DAI staging showed significant positive correlation (p<0.0003). IVH score in DAI stage 3 (with DAI involving the brain stem; p=0.0025) or stage 2 (with DAI involving CC; p=0.0042) was significantly higher than that of DAI stage 0 (no DAI lesions). In conclusion, IVH on initial CT is the only marker of DAI on subsequent MRI, specifically severe DAI (stage 2 or 3).

The therapeutic influence of epsilon3 isoform of apolipoprotein E on pathophysiological mechanisms of secondary brain injury evolution after experimental traumatic brain injury

Purpose. To test the therapeutic potential of apolipoprotein E isoform epsilon3, whose synthesis in nerve tissue was induced by means of gene therapy, in an experimental traumatic brain injury (TBI) model, and to substantiate its mechanism of therapeutic action based on current literature data.Methods. To determine structural and functional changes associated with severe diffuse TBI, adult male Wistar rats were subjected to weight drop impact acceleration injury and evaluated at day 10 after trauma. A mixture of DOTAP liposomes and 25 µg of recombinant plasmid pCMV-APOE3 cDNA was infused intraventicularly immediately after TBI using ALZET osmotic pumps. The hippocampal CA1 regions were analyzed by means of light and electron microscopy, morphometry, immunocytochemical and confocal analysis using markers selective for neurons (NeuN) and astrocytes (GFAP). The neurofunctional outcome was assessed in an open field test.Results. The research data have shown that cationic liposome-mediated APOE3 gene transfer has a beneficial effect on hippocampal structure and ultrastructure, diminishes neuronal loss and severity of diffuse axonal injury, gliosis and microglial reaction, as well as aids regression of posttraumatic stress and anxiety.Conclusion. According to literature data, possible mechanisms of apoE therapeutic action are (1) normalization of neural cellular lipid component, (2) its role in regulating reactive gliosis and inflammatory response of CNS to injury, (3) antioxidant effects of apolipoprotein E, (4) regulation of cell death mechanisms, (5) influence of apolipoprotein E on differential gene expression and regulation of genomic response of CNS cells to injury

Serial Changes in Diffusion Tensor Imaging Metrics of Corpus Callosum in Moderate Traumatic Brain Injury Patients and Their Correlation With Neuropsychometric Tests

To assess longitudinally the severity of diffuse axonal injury in the corpus callosum in patients with moderate traumatic brain injury (TBI) through quantitative diffusion tensor imaging and to correlate these changes with neuropsychometric tests (NPT) at 6 and 24 months after injury. Prospective longitudinal study. Sixteen patients with TBI and 17 age/sex-matched healthy controls. Patients underwent magnetic resonance imaging at 3 time points: within 2 weeks (range = 5-14 days), 6 months, and 24 months after injury. NPT could be performed only at 6 and 24 months. In patients with TBI, a significant increase in fractional anisotropy (FA) values in genu as well as an insignificant decrease in radial diffusivity (RD) and mean diffusivity values in genu and splenium were observed over time, respectively. FA, RD, and mean diffusivity values continued to be abnormal in patients compared with controls at the end of 2 years. Although some NPT scores improved over time in these patients, these were still significantly impaired compared with controls. FA and RD indices appear to be surrogate markers of microstructural alterations in patients over time and correlate significantly with some of the NPT scores. The recovery in these indices associated with recovery in neurocognitive deficits suggests that these indices may be used as an objective marker for residual injury in these patients.

Abnormal Corticospinal Excitability in Traumatic Diffuse Axonal Brain Injury

This study aimed to investigate the cortical motor excitability characteristics in diffuse axonal injury (DAI) due to severe traumatic brain injury (TBI). A variety of excitatory and inhibitory transcranial magnetic stimulation (TMS) paradigms were applied to primary motor cortices of 17 patients and 11 healthy controls. The parameters of testing included resting motor threshold (MT), motor evoked potential (MEP) area under the curve, input-output curves, MEP variability, and silent period (SP) duration. The patient group overall revealed a higher MT, smaller MEP areas, and narrower recruitment curves compared to normal controls (p < 0.05). The alterations in excitability were more pronounced with an increase in DAI severity (p < 0.005) and the presence of motor impairment (p < 0.05), while co-existence of focal lesions did not affect the degree of MEP changes. MEP variability was significantly lower in the group with motor impairment only (p < 0.05). The intracortical inhibition, as revealed by SP duration, did not exhibit any significant differences in any of the patient groups. In conclusion, our findings expand the concept that impairment of the excitatory and inhibitory phenomena in the motor cortex does not proceed in parallel and demonstrate distinct patterns of aberrations in TBI. Furthermore, these data suggest that alterations in the corticospinal excitatory mechanisms are determined predominantly by the severity of DAI, and show a significant relationship with clinical motor dysfunction following severe trauma diffusely affecting the motor cortical connections. In severe TBI, motor and functional recovery might be linked to restitution of normal corticospinal mechanisms, indexed by normalization of the cortical excitability parameters.

Cognitive Sequelae of Diffuse Axonal Injury

The results of recent studies on cognitive disability after traumatic brain injury-associated diffuse axonal injury (DAI) are inconsistent. In these studies, the diagnosis of DAI relied on cranial computed tomography. To further clarify the extent and severity of a possibly DAI-associated cognitive impairment by the use of magnetic resonance imaging (MRI) and detailed neuropsychological testing. From a databank of 299 patients with traumatic brain injury, 18 patients (age range, 17-50 years; median initial Glasgow Coma Scale score, 5) who showed an MRI lesion pattern compatible with pure DAI were identified. All of the patients had undergone MRI on a 3-T system. Pure DAI was defined by the findings of traumatic microbleeds on T2*-weighted gradient-echo images in the absence of otherwise traumatic or nontraumatic MRI abnormalities. Neuropsychological performance in the categories of attention and psychomotor speed, executive functions, spans, learning and memory, and intelligence 4 to 55 months (median, 9 months) after traumatic brain injury. All of the patients showed impairments of 1 or more cognitive subfunctions, and no cognitive domain was fundamentally spared. Memory and executive dysfunctions were most frequent, the former reaching a moderate to severe degree in half of the patients. In comparison, deficits of attention, executive functions, and short-term memory were mostly mild. Correlations between the amount of traumatic microbleeds and specific or global cognitive performance were absent. An MRI lesion pattern compatible with isolated DAI is associated with persistent cognitive impairment. The traumatic microbleed load is no sufficient parameter for the assessment of DAI severity or functional outcome.

Cerebral blood flow and metabolism in patients with cognitive impairments after minor traumatic brain injury: PET study in a chronic state

In order to clarify the pathophysiology of cognitive impairments after mild traumatic brain injury (TBI), we studied cerebral blood flow and metabolism using positron emission computed tomography (PET). Fifty-two patients with mild TBI were divided into three groups based on magnetic resonance images (MRI) findings: normal (group N), diffuse axonal injury (DAI) (group D), and DAI with brain atrophy (group V). PET data were obtained by the steady state method using 15O labeled gases. Regional cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of oxygen (CMRO 2) were measured for each brain area. Higher cortical dysfunction was evaluated using Wechsler Adult Intelligence Scale-Revised (WAIS-R). WAIS-R scores for group V were significantly lower than for group N. In almost all patients, CBF and OEF were within normal ranges, however, CMRO 2 was decreased slightly. CMRO 2 in all regions of group V except for the bilateral parietal lobes was significantly lower than in group N. We conclude that the severity of higher cortical dysfunction in these cases correlated with a decrease of CMRO 2 and the severity of DAI.

Semiquantitative analysis of corpus callosum injury using magnetic resonance imaging indicates clinical severity in patients with diffuse axonal injury

Objective: To evaluate the hypothesis that the extent of corpus callosum injury indicates the depth of shearing lesions in the central brain structure and therefore relates to the clinical severity...

Early recovery after closed traumatic head injury: somatosensory evoked potentials and clinical findings.

To determine the ability of somatosensory evoked potentials (SEP) compared with clinical findings to monitor and predict recovery in patients suffering from closed head injury with predominantly diffuse axonal injury (DAI). Prospective cohort study. Neurologic intensive care unit (ICU) of a university hospital. Serial SEP recordings were obtained from 31 consecutive patients with closed head injury. The first SEP was recorded within 48 hrs after trauma, followed by recordings after another 2 days, after which the time interval for each consecutive recording was doubled. Clinical examinations were performed every 6 hrs during the ICU stay and daily after transfer to a general neurologic ward. None. Twenty-three of 31 patients demonstrated pathologic SEP findings at initial examination. Of these patients, 11 recovered clinically, two remained vegetative, and ten died. In all 11 patients with clinical recovery, SEP also recovered. In 8 of 31 patients, initial SEPs were normal and remained normal until discharge, all eight had a good outcome. Initial SEP findings were related with outcome at 6 months (p = .02), and follow-up studies increased the predictive value of SEP studies (p = .009). Other factors related to outcome included age, severity of DAI, and length of ICU/hospital stay. In the 11 patients with SEP and clinical recovery, early (day 2) and late (>or=2 months) recovery was documented. Early and reliable SEP indicators of improvement included N20-P25-Amplitudes (mean recovery, 8.5 days) and central conduction time (9.6 days). Pupillary light reaction (6.4 days), Babinski reflex (12.4 days), and Glasgow Coma Score (9.6 days) were the most valuable clinical findings. Recovery of the Glasgow Coma Score frequently coincided with reduction of sedatives. In most patients, recovery was detected with SEP before clinical recovery (7/11 patients, time difference 1 wk). Initial SEP findings correlate with long-term outcome in patients with closed head injury with DAI. Initial bilaterally absent cortical responses in the SEP reliably predicted death, whereas completely normal SEP findings predicted good long-term outcome. Early recovery after DAI can be detected with serial SEP recordings despite sedative medications. Electrophysiologic recovery frequently precedes clinical recovery.

Neuroimaging correlates of cognitive and functional outcome after traumatic brain injury.

Magnetic resonance imaging (MRI) may provide an estimate of the severity of diffuse axonal injury by quantitative measurements of atrophy of white matter tracts (such as corpus callosum) and of ventricular enlargement (particularly the third ventricle). However, most MRI studies failed to reveal consistent relationships between the pattern of neuropsychological impairments and the site and extent of focal structural lesions after traumatic brain injury. Functional neuroimaging techniques, such as positron emission tomography or functional MRI, may reveal areas of cerebral dysfunction in regions that look structurally intact on MRI. Studies using these techniques have suggested that the cognitive and behavioural disturbances of traumatic brain injury could be related to a defective activation of a prefrontal-cingulate network.