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PubMed2000

[Head and brain injuries. Place of imaging].

This article considers the various mechanisms of brain injury and specifies the most efficient radiologic technique for assessing patients, depending on clinical presentation. The brain injuries include either extracerebral and intracerebral lesions. The former require rapid diagnosis and therapy and the latter determine management in an intensive therapy, unit and outcome. Standard X-rays are obsolete. The CT, rapidly performed, is the most relevant imaging procedure for surgical lesions. Cortical contusions and diffuse axonal injuries are underestimated by CT and best depicted by MRI. Only late MRI has a strong correlation with neuropsychological outcome. In terms of prognosis, MRI needs to be evaluated. The indications include: a) unstable neurological status: CT; b) moderate head injury: CT may help to decide hospital admission; c) severe head injury: initial CT may be followed by MRI; d) long-term consequences: MRI. Special Indications: a) angio-MRI: suspicion of vascular lesion; b) CT with thin slices and bone window: depressed skull fracture; c) teleradiology (image transfer): to decide a patient transport from a peripheral hospital to a neurosurgical centre. In conclusion, CT remains the first-line examination to detect immediately life-threatening lesions. MRI is the examination of choice for full assessment of brain lesions.

Brain Injuries↗
PubMedDate not supplied

Proton MR spectroscopic findings correspond to neuropsychological function in traumatic brain injury.

BACKGROUND AND PURPOSE: Traumatic brain injury (TBI) causes substantial irreversible damage to neurons. Our aim was to investigate whether proton MR spectroscopic measures of diffuse cellular integrity were related to neuropsychological dysfunction after TBI. METHODS: Twelve patients with TBI (mean, 53 +/- 23 days postinjury) and 14 control subjects were included in the study using paired MR spectroscopy and neuropsychological assessment. N-acetylaspartate (NAA), creatine, and choline were measured in normal-appearing occipitoparietal white and occipital gray matter using short-echo quantitative spectroscopy. A composite measure of neuropsychological function was calculated from z-scored individual tests probing the major functional domains commonly impaired after head trauma. RESULTS: Patients with TBI displayed reduced NAA in white matter and elevated choline in gray matter, suggestive of neuronal injury and inflammation, respectively. NAA and creatine in white and gray matter were significantly associated with composite neuropsychological function and many individual neuropsychological tests. Gray matter choline, although abnormal, was not related to neuropsychological function. CONCLUSION: The concordance between neurometabolic levels and behavioral function supports the hypothesis that diffuse axonal injury is an important contributor to brain dysfunction after TBI.

Adolescent↗
PubMed1990

Morphology and neurophysiology of focal axonal injury experimentally induced in the guinea pig optic nerve.

A new model of focal axonal injury was reproduced by rapid and controlled elongation (uniaxial stretch) of the guinea pig optic nerve. Light microscopy study of optic nerve specimens after horseradish peroxidase injection into the vitreous of the animal's eye showed that axonal lesions were identical to those seen in human and primate post-traumatic diffuse axonal injury (DAI). The lesions were characterized by the formation of terminal clubs in severed axons and focal axonal enlargements in those axons that were lesioned-in-continuity. Visual-evoked potentials upon flash stimulation were recorded before and after injury. Mean amplitude and mean latency of occipital peaks were significantly elongated in the acute post-traumatic phase. Electron microscopy examination showed that the main axonal changes observed in this model were cytoskeleton disorganization, accumulation of axoplasm membrane-bound bodies at the site of terminal balls and dilatations-in-continuity and detachment of the axolemma from the myelin sheath. Such axonal alterations were similar to those found in many other biological models of central and peripheral axonal injuries in which the lesion was produced by invasive methods. This model is unique since it reproduces the same mechanism of injury and the identical lesions that have been demonstrated in humans and primates with post-traumatic (DAI).

Animals↗
PubMed2005

[Pediatric head injuries: a retrospective analysis of 280 patients.].

BACKGROUND: To assess etiological factors, clinical features, radiological findings and recovery rates in pediatric head injuries. METHODS: Patients (n =280) with head injuries (age range: 0 - 16 years) hospitalized in Trakya University Department of Neurosurgery between January 1995 and 2004 were analyzed statistically. RESULTS: According to Glasgow Coma Scale (GCS) the patients had minor (GCS: 13- 15 ; 70.1% ), moderate (GCS: 9- 12; 17,1% ), or severe (GCS: 3 to 8; 6,8% ). head injuries The most common etiological factor was fall from a height (34,3%); and the most frequently associated injury was extra-spinal skeletal injury (12,9%). Fifty-one patients (18,2%) underwent neurosurgical operation. 87.5% of them recovered completely, while 12,5% showed partial recovery or died, as graded by Glasgow Outcome Scale (GOS). There was a moderately strong correlation between initial GCS and GOS (r=0,53, p=0,01). CONCLUSIONS: Nearly half of the pediatric head injuries were caused by falls with good prognoses. In the school age, motor vehicle accident (MVA) was the most frequent trauma type. MVA was the most serious type of trauma as demonstrated by its low GCS and GOS scores. Polytraumas, subdural hematomas, cerebral contusions, subarachnoid or intracerebral hemorrhages, cerebral edemas, diffuse axonal injuries, and any cranial lesion which required surgery were found to be related with poor prognosis.

Adolescent↗
PubMed2005

Early Glasgow Outcome Scale scores predict long-term functional outcome in patients with severe traumatic brain injury.

Patients sustaining severe traumatic brain injury (TBI) have variable long-term outcomes. We examined the association between Glasgow Outcome Scale (GOS) assessed at 3 months and long-term outcomes at 12 months after TBI. We studied 159 patients with severe, closed traumatic brain injuries (Glasgow Coma Scale [GCS] <or= 8) who were treated at an academic medical center and survived for a minimum of 3 months after TBI. Demographics and admission clinical data and GOS at 3 and 12 months were analyzed. Multivariate logistic regression was used to asses the relationship between 3-month GOS, demographics, and clinical data and a poor outcome, defined as GOS 1-3 assessed at 12 months after injury. The patient population was predominantly male (77%), with a median age of 30 years and a median admission GCS of 6. The logistic regression model showed that the GOS at 3 months was the best predictor of 12-month outcomes (odds ratio = 15.22, p < 0.001). The presence of prolonged hypotension, diffuse axonal injury (DAI), and fixed and dilated pupils on admission were also significant independent predictors of poor 12-month outcome (for all, p <or= 0.047). The adjusted logistic model showed a steep gradient of long-term recovery potential depending upon GOS at 3 months, ranging from an 89.4% chance of poor outcome for patients with a GOS of 2, to a 0.11% chance of poor outcome for those with a GOS of 5. The 3-month GOS is a powerful independent predictor of long-term outcome for patients with severe TBI. Prolonged hypotension, DAI, and the presence of fixed and dilated pupils were also independent predictors of poor outcome.

Adolescent↗
PubMed2000

Temporal profile of release of neurobiochemical markers of brain damage after traumatic brain injury is associated with intracranial pathology as demonstrated in cranial computerized tomography.

This study aimed at the investigation of release patterns of neuron specific enolase (NSE) and protein S-100B after traumatic brain injury (TBI) and their association with intracranial pathologic changes as demonstrated in computerized tomography (CT). We analyzed NSE and S-100B concentrations in serial venous blood samples taken one to three days after TBI in 66 patients by the use of immunoluminometric assays. These markers are considered to be specific neurobiochemical indicators of damage to glial (S-100B) or neuronal (NSE) brain tissue. Standardized neurological examination and plani- and volumetric evaluation of computerized tomography scans were performed in all patients. Patients with medium severe to severe TBI [Glasgow Coma Scale (GCS) score at the site of accident < or =12] exhibited significantly higher NSE and S-100B concentrations and a significantly longer release compared to patients with minor head injury (GCS: 13-15). Both, patients with and without visible intracerebral pathology in CT scans exhibited elevated concentrations of NSE and S-100B after TBI and a significant decrease in the follow-up blood samples. Release patterns of S-100B and NSE differed in patients with primary cortical contusions, diffuse axonal injury (DAI), and signs of cerebral edema (ICP) without focal mass lesions. All serum concentrations of NSE and S-100B were significantly correlated with the volume of contusions. The data of the present study indicate that the early release patterns of NSE and S-100 may mirror different pathophysiological consequences of traumatic brain injury.

Adolescent↗
PubMed1999

Dysautonomia after traumatic brain injury: a forgotten syndrome?

OBJECTIVES: To better establish the clinical features, natural history, clinical management, and rehabilitation implications of dysautonomia after traumatic brain injury, and to highlight difficulties with previous nomenclature. METHODS: Retrospective file review on 35 patients with dysautonomia and 35 sex and Glasgow coma scale score matched controls. Groups were compared on injury details, CT findings, physiological indices, and evidence of infections over the first 28 days after injury, clinical progress, and rehabilitation outcome. RESULTS: the dysautonomia group were significantly worse than the control group on all variables studied except duration of stay in intensive care, the rate of clinically significant infections found, and changes in functional independence measure (FIM) scores. CONCLUSIONS: Dysautonomia is a distinct clinical syndrome, associated with severe diffuse axonal injury and preadmission hypoxia. It is associated with a poorer functional outcome; however, both the controls and patients with dysautonomia show a similar magnitude of improvement as measured by changes in FIM scores. It is argued that delayed recognition and treatment of dysautonomia results in a preventable increase in morbidity.

Adolescent↗
PubMed2000

Discrepancy of clinical symptoms and prognosis of a patient--forensic significance of "talk and die" head injury.

Deaths of patients who had talked after sustaining a head injury and were then assumed clinically to be recovering from the head trauma raise medicolegal questions about the precise causes of deaths. A forensic autopsy on a 77-year-old man who had been talking after a road traffic accident and died on the sixth day showed slight subdural hematoma, bifrontal cerebral contusions and diffuse axonal injury. No natural diseases or delayed complications of injury were found. The cause of death was certified as head injury due to a traffic accident. This is a case of "talk and die" head injury. Forensic autopsy is important in patients with "talk and die" to clarify the causal relation to the head trauma in relation to any further forensic dispute.

Journal Article↗
PubMed2001

Imaging of acute head injury in the adult.

Head injury is a leading cause of trauma deaths. Prompt recognition of treatable injuries is critical to reduce mortality. Computed tomography (CT) of the head is readily obtainable in most medical centers, and is the cornerstone of rapid diagnosis. This article explains the important prognostic features of various forms of head trauma and their manifestations on noncontrast head CT. Intra-axial lesions are considered first, with explanation of diffuse axonal injury, contusions, and parenchymal hematomas. Extra-axial hemorrhages are also detailed, including subdural hematomas, epidural hematomas, and subarachnoid hemorrhage. Finally, extracranial manifestations of head trauma are explained, with descriptions of craniofacial fractures and orbital injuries. This article should help to place the imaging features of head trauma in clinical perspective for those involved in caring for trauma victims from a diagnostic or therapeutic standpoint.

Acute Disease↗
PubMed2004

[A case of head injury accompanied by minute hemorrhage-like artifacts created by multislice CT scans].

We demonstrated a head injury case accompanied by multiple small high-density artifacts in the middle of the brain created by multislice CT scanning, due to the malfunction of a detector involved in reconstruction of the mid images. We named these objects high-density spot artifacts. The high-density spot artifacts resemble minute hemorrhages which appear as diffuse axonal injuries. Radiologists and neurosurgeons should be familiar with this the existence of artifact.

Adolescent↗
PubMed1991

Significance of magnetic resonance imaging in acute head injury.

One hundred seventy-seven patients who had incurred head trauma were studied with magnetic resonance imaging (MRI). Patients varied from those with mild injury without any focal neurological deficit to those with severe injury with post-traumatic coma. Altogether, 177 lesions were demonstrated by MRI in 123 of 177 patients within 3 days of injury using T2-weighted (SE2000/40,2000/111) and T1-weighted (IR1500/500/40) multislice sequences. In contrast, computerized tomography (CT) demonstrated 103 lesions in 90 patients. MRI was superior to CT in the diagnosis of nonhemorrhagic contusions demonstrated as a high-intensity area on T2-weighted imaging. MRI provided some information to evaluate the severity of diffuse axonal injury or to predict delayed traumatic intracerebral hematoma (DTICH).

Acute Disease↗
PubMed2006

Osteogenic effects of traumatic brain injury on experimental fracture-healing.

BACKGROUND: Heterotopic bone formation has been observed in patients with traumatic brain injury; however, an association between such an injury and enhanced fracture-healing remains unclear. To test the hypothesis that traumatic brain injury causes a systemic response that enhances fracture-healing, we established a reproducible model of traumatic brain injury in association with a standard closed fracture and measured the osteogenic response with an in vitro cell assay and assessed bone-healing with biomechanical testing. METHODS: A standard closed femoral fracture was produced in forty-three Sprague-Dawley rats. Twenty-three of the rats were subjected to additional closed head trauma that produced diffuse axonal injury similar to that observed in patients with a traumatic brain injury. Twenty-one days after the procedure, all animals were killed and fracture-healing was assessed by measuring callus size and by mechanical testing. Sera from the animals were used in subsequent in vitro experiments to measure mitogenic effects on established cell lines of committed osteoblasts, fibroblasts, and mesenchymal stem cells. RESULTS: Biomechanical assessment demonstrated that the brain-injury group had increased stiffness (p = 0.02) compared with the fracture-only group. There was no significant difference in torsional strength between the two groups. Cell culture studies showed a significant increase in the proliferative response of mesenchymal stem cells after exposure to sera from the brain-injury group compared with the response after exposure to sera from the fracture-only group (p = 0.0002). This effect was not observed in fibroblasts or committed osteoblasts. CONCLUSIONS: These results support data from previous studies that have suggested an increased osteogenic potential and an enhancement of fracture-healing secondary to traumatic brain injury. Our results further suggest that the mechanism for this enhancement is related to the presence of factors in the serum that have a mitogenic effect on undifferentiated mesenchymal stem cells.

Animals↗
PubMed1997

Airbag-induced lethal cervical trauma.

In a frontal collision of a car (taxicab) perpendicular into a streetcar with an impact speed of approximately 30 kph (20 mph), the driver survived with minor injuries. The front-seat passenger was extremely "out-of-position," with her seat positioned nearly fully forward. This in combination with her short stature led to fatal injuries resulting from the inflating airbag (U.S.-type) striking against her face and chin. At the scene, she was found essentially clinically dead, but was resuscitated and died finally 13 days later. Postmortem examination showed a complete disruption of all ventral ligaments between the base of the skull and the first and second vertebrae, a nearly complete ventral rupture of the medulla, and diffuse axonal injury of the brain.

Accidents, Traffic↗
PubMed1998

Experimental brain injury induces expression of amyloid precursor protein, which may be related to neuronal loss in the hippocampus.

Previous reports have demonstrated that some focal brain injuries increase amyloid precursor protein (APP) immunoreactivity in the region surrounding the injury where it was localized, in damaged axons and in pre-alpha 2 cells of the entorhinal cortex. However, to date, APP expression in the hippocampus remote from the impact site has not been comprehensively studied. Therefore, we have evaluated APP expression not only in the locally injured cerebral cortex but also in the hippocampus remote from the impact site. In the present paper, diffuse axonal injury was induced in rats in midline fluid percussion injury. APP expression was examined post injury using Western blot analysis and immunohistochemistry. Western blot analysis demonstrated that the expression of 100-kd APP was increased in both the cerebral cortex and hippocampus 24 h after injury. It then decreased in the hippocampus, but did not change in the cerebral cortex, 7 days after injury. Immunohistochemical studies showed increased immunoreactivity of APP in the neuronal perikarya and reactive astrocytes near the region of injury in the cerebral cortex 24 h to 7 days after injury. In the hippocampus, APP accumulated in the CA3 neurons 24 h and 3 days after injury, although no hemorrhagic lesions were seen at that site. The APP positive neurons in CA3 showed shrunken cell bodies and pyknotic nuclei 3 days after injury, and some of the neurons in CA3 had disappeared by 7 days postinjury. The results of present study suggest that traumatic brain injury induces overexpression and accumulation of APP in neuronal perikarya and that these events are followed by degeneration of CA3 neurons. Further, the decline in APP expression in the hippocampus is thought to be due to neuronal loss in CA3 subsector.

Amyloid beta-Peptides↗
PubMed1999

[A case of primary brain-stem injury recovered from persistent vegetative state after L-dopa administration].

A 51-year-old male was transferred to our hospital just after traffic accident. On admission, the patient was comatose (Glasgow Coma Scale of 6) and showed a left hemiparesis with a left oculomotor nerve palsy. Computed tomography demonstrated a traumatic subarachnoid hemorrhage without mass lesion. Magnetic resonance imaging showed high intensity lesions on the left dorsolateral midbrain and the right cerebral peduncle. The distribution of lesions implied diffuse axonal injury involving dopaminergic systems such as the substantia nigra and the ventral tegmental area. After several months of conservative management, the patient showed no recovery and was diagnosed as persistent vegetable state. The administration of L-dopa was then started and the patient showed remarkable neurological improvement. Therefore the patient's neurological status was thought to be modified with primary brain stem injury and accompanying traumatic Parkinson's syndrome. It is important to understand "pseudo" persistent vegetative state in the management of patients showing prolonged consciousness disturbance. L-dopa should be considered as the drugs of pharmacological intervention for the patients of masked parkinsonism behind "pseudo" persistent vegetative state whose dopaminergic systems might have been damaged.

Accidents, Traffic↗
PubMed1990

Relation between intracranial pressure, computed tomographic lesion, and neuropsychological outcome.

Long-term neuropsychological recovery of 24 severe head-injured patients was examined and correlated with acute measurements of intracranial pressure (ICP) and diffuse computed tomographic (CT) lesions. Intracranial hypertension (ICP greater than or equal to 20 mm Hg) was present acutely in 12 patients and absent in 12 patients. CT diagnoses of diffuse swelling (DS) was present in 12 patients, and diffuse axonal injury (DAI) in 12 patients. During chronic recovery, neuropsychological dysfunctioning was found in all cases. Patients with acute ICP elevations showed more intellectual and memory losses than those without acute ICP elevations. No neuropsychological differences were found between patients with DS and DAI injuries. The findings suggest secondary brain insults caused by intracranial hypertension may be more disruptive to long-term neuropsychological functioning than diffuse lesion type.

Accidents, Traffic↗
PubMed1983

Comprehensive monitoring and computerized tomographic follow up in patients with acute severe head injury: coma-outcome correlations.

In 88 patients with acute severe head injury the Glasgow coma scale (GCS), computerized tomography and autonomic monitoring during the first 24 hours were used to characterize different types of post-traumatic brain dysfunction. A subgroup is defined--GCS 8.1--with signs of diffuse brain swelling and autonomic instability which included two cases with dorsal midbrain lesions. These preliminary results suggest that autonomic instability is a valid criterion for identifying patients suffering from diffuse axonal injury.

Atrophy↗
PubMed2004

Deficits in facial emotion perception in adults with recent traumatic brain injury.

UNLABELLED: We examined whether facial emotion perception was compromised in adults with recent traumatic brain injury (TBI). Few studies have examined emotion perception in TBI; those that have, examined chronic patients only. Recent and chronic TBI populations differ according to degree of functional reorganization of the brain, use of compensatory strategies, and severity of cognitive impairments--any of which might differentially affect presentation of emotion perception deficits. A secondary aim of the study was to utilize the TBI population--in whom diffuse axonal injury (DAI) is a cardinal neurological feature--to examine the suggestion of Adolphs et al. [Journal of Neuroscience 20(7) (2000) 2683] that damage to white matter tracts should give rise to emotion perception deficits. METHODS: Thirty TBI participants and 30 age-matched controls were tested. A 2 x 3 mixed design was employed. The dependent variable was accuracy on neutral and emotional face perception tests. RESULTS: (1) The TBI group performed significantly less accurately than the matched controls on the facial emotion perception tasks, whereas the groups performed equivalently on a non-emotional face perception control task. (2) A sub-group of TBI participants without evidence of focal injury to areas of the brain most commonly implicated in facial emotion perception was as impaired on the emotion perception tasks as a second sub-group who had sustained focal lesions to these areas. This suggests an alternative neurological mechanism for deficits in the first sub-group, such as DAI. CONCLUSIONS: Patients with recently acquired TBI are impaired in their ability to perceive emotions in faces. DAI alone may cause facial emotion perception deficits.

Adult↗