Impact of the ''Back to Sleep'' campaign on sudden infant death syndrome in Minnesota

Diffuse axonal injury (DAI) was diagnoses according to axonal reaction proved as balls by Palmgren's silver impregnation and axonal lesions by immunohistochemical investigation of ubiquitin and low molecular weight neurofilaments (68 kD). Diffuse axonal injury was found in 16 cases from a group of 36 persons deceased of craniocerebral trauma (44%). Diagnosis was based on the presence of axonal retraction balls in 15 cases; the balls showed also a striking positivity with antibodies against ubiquitin and low molecular neurofilaments as well. In the last patient who died 10 hours after a head injury, too early for axonal retraction balls to be formed, diagnosis of DAI could be settled because of the presence of axonal swellings immunohistochemically positive for ubiquitin and neurofilaments. A control groups of 6 persons after sudden death showed both axonal widenings and swellings but their immunohistochemistry was negative. Immunohistochemical methods of proving ubiquitin and low molecular weight neurofilaments represent substantial contribution to diagnosis of diffuse axonal injury. Earlier phase of axonal lesions than in simple histology can be observed and histological diagnosis of axonal injury independently confirmed.     

CD46 (membrane cofactor protein of complement, measles virus receptor): structural and functional divergence among species (review)

OBJECT: In this retrospective study, the authors analyzed the frequency, anatomical distribution, and appearance of traumatic brain lesions in 42 patients in a posttraumatic persistent vegetative state. METHODS: Cerebral magnetic resonance (MR) imaging was used to detect the number of lesions, which ranged from as few as five to as many as 19, with a mean of 11 lesions. In all 42 cases there was evidence on MR imaging of diffuse axonal injury, and injury to the corpus callosum was detected in all patients. The second most common area of diffuse axonal injury involved the dorsolateral aspect of the rostral brainstem (74% of patients). In addition, 65% of these patients exhibited white matter injury in the corona radiata and the frontal and temporal lobes. Lesions to the basal ganglia or thalamus were seen in 52% and 40% of patients, respectively. Magnetic resonance imaging showed some evidence of cortical contusion in 48% of patients in this study; the frontal and temporal lobes were most frequently involved. Injury to the parahippocampal gyrus was detected in 45% of patients; in this subgroup there was an 80% incidence of contralateral peduncular lesions in the midbrain. The most common pattern of injury (74% in this series) was the combination of focal lesions of the corpus callosum and the dorsolateral brainstem. In patients with no evidence of diffuse axonal injury in the upper brainstem (26% in this series), callosal lesions were most often associated with basal ganglia lesions. Lesions of the corona radiata and lobar white matter were equally distributed in patients with or without dorsolateral brainstem injury. Moreover, cortical contusions and thalamic, parahippocampal, and cerebral peduncular lesions were also similarly distributed in both groups. CONCLUSIONS: The data indicate that diffuse axonal injury may be the major form of primary brain damage in the posttraumatic persistent vegetative state. In addition, the authors demonstrated in this study that MR imaging, in conjunction with a precise clinical correlation, may provide useful supportive information for the accurate diagnosis of a persistent vegetative state after traumatic brain injury.     

Effects of basic fibroblast growth factor on hippocampal neurons after axonal injury

OBJECTIVE: Axons of adult central nervous system neurons fail to regenerate after diffuse axonal injury in head trauma. Basic fibroblast growth factor (bFGF) has been reported to enhance neuritic extensions after neuronal injury in immature nerve cells. To investigate the effects of bFGF on adult neurons and axonal reoutgrowth, differentiated nerve cells were axonally transected and bFGF was applied. DESIGN: Cell culture study with primary rat hippocampal neurons. MATERIALS AND METHODS: After axotomy, hippocampal cultures were maintained untreated or in the presence of 0.5, 1, 10, or 20 ng/mL bFGF and evaluated over a 7-day period after injury. MEASUREMENTS AND MAIN RESULTS: Seven days after injury, axotomy decreased cell survival to 65%, increased [3H]arachidonic acid release 1.8-fold from prelabeled cells, and showed negligible effects on neuronal dendrites. bFGF reduced this neurodegeneration at all doses applied. bFGF at 10 ng/mL most efficiently increased live cells to 85% and decreased [3H]arachidonic acid release from prelabeled cells to control values (p < 0.01, vs. damaged cells). Furthermore, 10 ng/mL bFGF induced axonal branching and the longest axonal re-extensions from 60 +/- 8 to 377 +/- 10 microns 7 days after injury (p < 0.01, vs. damaged cells). CONCLUSIONS: bFGF increased cell survival and supported axonal re-elongations in adult hippocampal neurons in vitro when applied after axotomy. bFGF may play a role in new therapeutic concepts for the management of axonal injury after head trauma.     

Osteomyelitis pubis occurring after spontaneous vaginal delivery: a case presentation

A 30-year-old Palestinian collapsed when under interrogation by the Israeli General Security Service and was declared brain dead 3 days later. Information on the circumstances and interrogation methods was denied on security grounds. Autopsy disclosed extensive anterior chest and shoulder bruising and acute subdural haemorrhage but no other trauma. On this evidence, violent shaking was postulated as the mechanism of injury. Later, this was admitted by Israeli investigators and corroborated by histopathologically proved diffuse axonal injury and retinal haemorrhages. This is the first reported case of fatal shaken adult syndrome.     

Mild head trauma

Patients with mild traumatic brain injury constitute the overwhelming majority of head-injured patients seen in the emergency department. The indications for radiologic imaging in these patients are still undergoing study and revision. The Glasgow Coma Scale is a widely used triage score for head injury, but is less useful at identifying which patients with mild head injuries have intracranial pathology. There have been several retrospective studies and a few prospective studies examining the indications for imaging in mild to moderate head trauma. They all show that it is not easy to predict which patients will have CT abnormalities, and that some of these patients do go on to require neurosurgery. No set of clinical predictors have yet been put together that is capable of identifying all patients who are safe to be discharged without a CT scan. Pharmacologic therapy to help reduce axonal damage after head trauma and thus minimize the postconcussive sequelae of mild traumatic brain injury remains a challenge for physicians and neurobiologists into the next century.     

Characterization of diffuse axonal pathology and selective hippocampal damage following inertial brain trauma in the pig

Dynamic deformation applied to white matter tracts is a common feature of human brain trauma, and may result in diffuse axonal injury (DAI). To produce DAI in an experimental model, we have utilized nonimpact inertial loading to induce brain trauma in miniature swine. This species was chosen due to its large gyrencephalic brain with substantial white matter domains. Twenty anesthetized (2% isoflurane) miniature swine were subjected to pure impulsive centroidal rotation 110 degrees in the coronal plane in 4 to 6 ms; peak accelerations ranged from 0.6 to 1.7 x 10(5) rad/s2. Seven days following injury, the brains were fixed (4% paraformaldehyde). Histopathologic examination was performed on 40 microns sections stained with cresyl violet (Nissl), antibodies targeting neurofilament (axonal damage), GFAP (astrocytes), and pig IgG (protein extravasation). Widespread multifocal axonal injury was observed in combination with gliosis throughout the brain, most commonly in the root of gyri and at the interface of the gray and white matter. Very little vascular disruption was noted in regions of axonal injury. Neuronal damage was primarily found in the CA1 and CA3 subfields of the hippocampus. These results suggest that this model is clinically relevant and useful for evaluating mechanisms of inertial brain trauma.     

Lipoprotein profiles and serum peroxide levels of aged women consuming palmolein or oleic acid-rich sunflower oil diets

In order to determine whether axonal injury (AI) is a factor in cases of penetrating head injury, the brains of 14 patients who died shortly after sustaining a fatal gunshot wound (GSW) to the head were examined, and the presence of AI determined using immunohistochemical staining for amyloid precursor protein (APP). The distribution of AI was mapped throughout the cerebral hemispheres and brain stem. AI was present in all cases in a diffuse distribution distant to the missle track with severe involvement of the brain stem in all cases. There was no axonal APP immunoreactivity in the direct region of the missle track at the point of primary axotomy. The APP-positive AI in these cases is likely to be a mixture of primary and secondary AI as APP immunostaining is unable to distinguish primary AI due to mechanical deformation from AI secondary to hypoxic-ischemic damage.     

Metabolic activation of 2,6-dichlorobenzonitrile, an olfactory-specific toxicant, by rat, rabbit, and human cytochromes P450

The authors posit that cellular edema is the major contributor to brain swelling in diffuse head injury and that the contribution of vasogenic edema may be overemphasized. The objective of this study was to determine the early time course of blood-brain barrier (BBB) changes in diffuse closed head injury and to what extent barrier permeability is affected by the secondary insults of hypoxia and hypotension. The BBB disruption was quantified and visualized using T1-weighted magnetic resonance (MR) imaging following intravenous administration of the MR contrast agent gadolinium-diethylenetriamine pentaacetic acid. To avoid the effect of blood volume changes, the maximum signal intensity (SI) enhancement was used to calculate the difference in BBB disruption. A new impact-acceleration model was used to induce closed head injury. Forty-five adult Sprague-Dawley rats were separated into four groups: Group I, sham operated (four animals), Group II, hypoxia and hypotension (four animals), Group III, trauma only (23 animals), and Group IV, trauma coupled with hypoxia and hypotension (14 animals). After trauma was induced, a 30-minute insult of hypoxia (PaO2 40 mm Hg) and hypotension (mean arterial blood pressure 30 mm Hg) was imposed, after which the animals were resuscitated. In the trauma-induced animals, the SI increased dramatically immediately after impact. By 15 minutes permeability decreased exponentially and by 30 minutes it was equal to that of control animals. When trauma was coupled with secondary insult, the SI enhancement was lower after the trauma, consistent with reduced blood pressure and blood flow. However, the SI increased dramatically on reperfusion and was equal to that of control by 60 minutes after the combined insult. In conclusion, the authors suggest that closed head injury is associated with a rapid and transient BBB opening that begins at the time of the trauma and lasts no more than 30 minutes. It has also been shown that addition of posttraumatic secondary insult-hypoxia and hypotension-prolongs the time of BBB breakdown after closed head injury. The authors further conclude that MR imaging is an excellent technique to follow (time resolution 1-1.5 minutes) the evolution of trauma-induced BBB damage noninvasively from as early as a few minutes up to hours or even longer after the trauma occurs.     

Significance of intracranial hypertension in severe head injury

Measurements of intracranial pressure (ICP) were begun within hours of injury in 160 patients with severe brain trauma, and continued in the intensive care unit. Some degree of increased ICP (greater than 10 mm Hg) was present on admission in most cases (82%), and in all but two of the 62 patients with intracranial mass lesions requiring surgical decompression; ICP was over 20 mm Hg on admission in 44% of cases, and over 40 mm Hg in 10%. In patients with mass lesions only very high ICP (greater than 40 mm Hg) on admission was significantly associated with a poor neurological picture and outcome from injury, while in patients with diffuse brain injury any increase in ICP above 10 mm Hg was associated with a poorer neurological status and a worse outcome. Despite intensive measures aimed at prevention of intracranial hypertension, ICP rose over 20 mm Hg during the monitoring period in 64 of the 160 patients (40%). Postoperative increases in ICP over 20 mm Hg (mean) were seen in 52% of the patients who had had intracranial masses evacuated, and could not be controlled by therapy in half of these cases. Even in patients without mass lesions, ICP rose above 20 mm Hg in a third of the cases, despite artificial ventilation and steroid therapy. Of the 48 patients who died, severe intracranial hypertension was the primary cause of death in nearly half and even moderately increased ICP (greater than 20 mm Hg) was associated with higher morbidity in patients with mass lesions and those with diffuse brain injury. Measurement of ICP should be included in management of patients with severe head injury.     

Acute administration of cocaine, but not amphetamine, increases the level of synaptotagmin IV mRNA in the dorsal striatum of rat

We reviewed the real and potential ocular problems in all head and neck injuries at a tertiary care and regional trauma center from April of 1994 to March of 1995. Through a retrospective study, 127 charts were reviewed, specifically looking at the mechanism of injury, types of injury, whether there was any ocular trauma noted in the chart, and whether there was a consultation to the ophthalmology department. Forty-one of these patients were seen by an ophthalmologist as the initial consultant for ocular and orbital injuries recognized by the emergency staff. In the 86 remaining patients, signs of potential ocular injury were recorded in the chart in 62 (72%) of these patients, yet an ophthalmology consultation was requested for only 23 of them (37%). This survey reveals the lack of awareness in a regional trauma center of certain ocular and periocular signs that may be indicative of more serious ocular injuries. It is the purpose of this article to highlight these concerns to the various health professionals involved with head and neck trauma patients in the hope that the patients will, in the end, benefit from a more thorough and complete assessment of the potential ocular and periocular injuries.     

Severe head trauma. Review of the factors influencing the prognosis

A series of 72 severely head injured patients are reported, 24 (33%) with surgical intracranial hematomas. All patients were intensively cared for under the same therapeutic regime; intracranial pressure (ICP) was monitored and treated if increased. The series mortality was 39%. Uncontrollable increase of ICP (UI-ICP), always fatal, was observed in 18% of patients and in 13 of 28 deaths (46%); the incidence of UI-ICP among deaths was higher in patients less than in those more than 40 years old (55% vs 25%). Patients with UI-ICP were frequently deeply comatose and with arterial hypotension on admission; almost all died in the first days. Patients directly admitted from the scene with well staffed Life Flight Helicopter Emergency Care compared with those directly admitted from the scene with different type of ambulance service (paramedics, police, firemen and private) had a mortality rate significantly less (20% vs 54%) and an incidence of UI-ICP strongly lower both among patients (5% vs 29%) and among deaths (25% vs 54%). Thus in this small series intensive care after admission was not effective to obtain good results if patients had received poor preadmission emergency care. Review of the literature on main clinical predictors of outcome in severe head injury, have made possible some observations. Ischemic and intracranial hypertension brain lesions were generally present in patients killed by head trauma; while diffuse axonal injury, frequently responsible for vegetative, severe disability survival and late deaths, was observed only in 20-30% of postmortem examinations. Old age, poor neurological status and cardiocirculatory and respiratory disturbances prior to and upon admission positively worsened the outcome, while intracranial hematomas had a more variable predictive value. Intracranial hypertension was a definitively ominous predictor only if very high when the risk to be or become uncontrollable seems to be much elevated. UI-ICP, often fatal despite any aggressive therapy, was the single most frequent killer after severe head injury, responsible for about half of all deaths after admission. The different outcome among severe head injury series could be conceivably related to a different frequency of UI-ICP. Besides the severity of head injury and delay and mode of admission, we suggest that preadmission respiratory and cardiocirculatory and the quality of emergency medical system could strongly affect the incidence of uncontrollable increase of ICP in admitted patients and thus the mortality rate and favorable recovery of the series. The advanced preadmission emergency care service with intensive care after admission could significantly explain the better results often observed in severe head injury series.     

Shearing injuries of parasagittal white matter, corpus callosum and basal ganglia: possible radiological evidences of hemiplegia in diffuse axonal injury

The relationship between spastic hemiplegia in diffuse axonal injury (DAI) and neuroradiological findings was studied in 100 cases. These cases were prospectively collected from the files of Automobile Insurance Rating Organization in Japan between 1993 from to 1996. Requirements for entry to this study were as follows: presence of initial unconsciousness after head injury without any lucid interval. Existence of CT scan or MRI film obtained within 12 hours of injury showing no significant mass effects, as well as follow-up CT scan or MRI film obtained more than 3 months after the injury. Psychosocial outcome was described both by the medical professional and the caregiver. The hemiplegia was rated severe, mild, or none. The outcome and diffuse ventriculomegaly were classified as reported by the authors previously. Spastic hemiplegia or quadriplegia was documented in the chronic stage in 63 cases, including 53 severe cases with difficulty in walking and 10 mild cases with only pyramidal signs detected. Chi-square analysis showed significant correlation between hemiplegia and the DAI outcome level or ventriculomegaly rating. Focal brain contusion was noticed in 33 cases, but did not correlate with the hemiplegia at all. Radiological findings included 25 cases of parasagittal white matter injury (gliding contusion), 20 cases of callosal injury, 19 cases of basal ganglionic region injury, 5 cases of brain-stem injury, and 3 cases of cerebellar injury. Chi-square analyses of hemiplegia and contralateral presence of these injuries were significant in the former three types of injury. Presence of at least one of these 3 lesions was defined as GCB injury. There were altogether 46 GCB injury cases which were significantly correlated with contralateral hemiplegia by chi-square analysis and by Spearman rank analysis. Partial correlation analysis with hemiplegia as the target variable indicated highly significant correlation only with GCB injury and outcome level. In conclusion, spastic hemiplegia in DAI is a manifestation of primary shear injury. Neuroradiological findings of GCB injury were statistically able to be significantly correlated with the presence of hemiplegia, and suggested pyramidal tract injury either at the corona radiata or the internal capsule level.     

Langerhans histiocytosis and acute monoblastic leukemia type LMA4

A 9-year-old girl with rigidospastic quadriplegia as post-traumatic sequela was reported. The distribution of lesions observed on a MRI implied diffuse axonal injury; involvement of the substantia nigra was also detected. L-Dopa administration was remarkably effective for relief of the rigidity. As a result, she became able to walk on her knees and communicate by writing letters. L-Dopa administration should be considered for patients who show rigidity as sequela of diffuse axonal injury with involvement of the substantia nigra.     

Topography of axonal injury as defined by amyloid precursor protein and the sector scoring method in mild and severe closed head injury

Axonal injury (AI), as defined by amyloid precursor protein (APP) positive axonal swellings, was recorded on a series of line diagrams of standard brain sections divided into 116 sectors to provide an Axonal Injury Sector Score (AISS) ranging from 0 to 116. This sector scoring method of recording axonal damage and providing a topographic overview of AI was applied to a series of 6 mild head injury cases [Glasgow Coma Scale (GCS) 13-15] and six severe head injury cases (GCS 3-8). The AISS ranged from 4 to 107 overall and varied from 4 to 88 in the mildly injured group and 76 to 107 in the severe head injury group, supporting the concept that there is a spectrum of AI in traumatic head injury and that the AISS is a measure of the extent of AI. APP immunostaining demonstrated positive axonal swellings 1.75 h after head injury and analysis of the pattern of AI in the mild and severe head injury groups showed that axons were more vulnerable than blood vessels and that the axons in the corpus callosum and fornices were the most vulnerable of all.     

Axonal cytoskeletal changes after non-disruptive axonal injury

In animal models of human diffuse axonal injury, axonal swellings leading to secondary axotomy occur between 2 and 6 h after injury. But, analysis of cytoskeletal changes associated with secondary axotomy has not been undertaken. We have carried out a quantitative analysis of cytoskeletal changes in a model of diffuse axonal injury 4 h after stretch-injury to adult guinea-pig optic nerves. The major site of axonal damage was the middle portion of the nerve. There was a statistically significant increase in the proportion of small axons with a diameter of 0.5 micron and smaller in which there was compaction of neurofilaments. Axons with a diameter greater than 2.0 microns demonstrated an increased spacing between cytoskeletal elements throughout the length of the nerve. However, in the middle segment of the nerve these larger axons demonstrated two different types of response. Either, where periaxonal spaces occurred, there was a reduction in axonal calibre, compaction of neurofilaments but no change in their number, and a loss of microtubules. Or, where intramyelinic spaces occurred there was an increased spacing between neurofilaments and microtubules with a significant loss in the number of both. Longitudinal sections showed foci of compaction of neurofilaments interspersed between regions where axonal structure was apparently normal. Neurofilament compaction was correlated with disruption of the axolemma at these foci present some hours after injury. We suggest that the time course of these axonal cytoskeletal changes after stretch-injury to central axons is shorter than those changes documented to occur during Wallerian degeneration.     

Postconcussion syndrome occurs in children.

The consensus of evidence published since 1924 suggests that parents report attention deficits, hyperactivity, or conduct disorder after pediatric head injury rather than postconcussion syndrome. In this study, the symptoms reported by children after mild (n?=?38) and moderate-severe (n?=?27) head trauma were compared to those reported after orthopedic injury (n?=?47) and to adults matched for injury severity and chronicity by using a structured interview based on diagnostic criteria for postconcussion syndrome. Pediatric head trauma caused significantly more subjective symptoms after 6 weeks than orthopedic injury. These symptoms were related to head injury severity and the child's anxiety level. When assessed in a similar manner, children report postconcussion syndrome similar to that seen in adults. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Results of treatment of multiple trauma in 130 children

Trauma remains the leading cause of death in the pediatric age group, despite recent advances in prevention and treatment. We retrospectively analyzed 130 cases of multiple trauma among 725 pediatric patients with injuries treated here during 1988-1989. Road accidents and falls from heights were the most common causes of injury. Mean age was 7 years (range 0.5-15) and the male to female ratio 2.7:1.0. Overall mortality was 9.2%. 57 patients (44%) did not get any prehospital medical care and 5 of them with injury severity scores (ISS) greater than 25 died. In contrast 11/18 (61%) of patients with ISS greater than 25 who were treated by medical teams survived. On arrival at the emergency room, 15% were hypothermic ( < 34 degrees C), and 6 were in hypovolemic shock--5 of whom died. Most common injuries were head trauma (91), limb injuries (69), abdominal trauma (34) and thoracic trauma (34). In 39 injury was severe, with pediatric trauma score (PTS) 6 or less, 12 of whom died. All deaths except 1 were associated with severe head injury and with ISS more than 25. There was no mortality in those with PTS more than 7 or ISS less than 25. Thus, the prehospital care of pediatric patients with head injury is associated with high mortality. Absence of mortality in patients with PTS of more than 7 emphasizes the importance of designated trauma centers for these patients.     

Evaluation of head injury in a pediatric emergency department: pretrauma and posttrauma system

OBJECTIVE: To determine if trauma center protocols affect the number of tests and consultations performed and the length of time spent in the emergency department or hospital. DESIGN: A retrospective review and comparison of treatment for children with isolated head injury admitted to the emergency department before trauma center designation (group 1, 1985), and 5 years after implementation of trauma center protocols (group 2, 1991). SETTING: Urban children's hospital, level I trauma center. RESULTS: One hundred sixty-five children met the enrollment criteria in 1985 and 162 met the criteria in 1991. Falls were the predominant mechanism of injury (55%) for both years. For patients with moderate injury (Glasgow Coma Scale score, 9-12) or severe injury (Glasgow Coma Scale score, <9), there was no difference in radiographic or laboratory evaluation. For patients with minimal head injury (Glasgow Coma Scale score, 15, no loss of consciousness, amnesia, seizure, focal neurologic findings, or persistent symptoms) and minor head injury (Glasgow Coma Scale score, >12, and loss of consciousness or amnesia), more radiologic and laboratory studies were done in 1991 that showed no clinically significant abnormalities. Patients with minimal head injury in group 2 were 14 times more likely to have cranial computed tomographic scans performed (95% confidence interval [CI], 3.4-67); 11 times more likely to have cervical spine radiographs (95% CI, 2.2-76.6); and 23 times more likely to have hepatic enzymes obtained (95% CI, 3-491). These differences persisted when analyzed by both the age of the patient and mechanism of injury. CONCLUSIONS: Application of trauma system protocols to isolated head injury patient evaluation results in increased use of laboratory and radiologic services. These practices have the potential to increase the cost of medical care without significantly improving outcome.     

Axonal injury caused by focal cerebral ischemia in the rat

The susceptibility of axons to blunt head injury is well established. However, axonal injury following cerebral ischemia has attracted less attention than damage in gray matter. We have employed immunocytochemical methods to assess the vulnerability of axons to cerebral ischemia in vivo. Immunocytochemistry was performed using antibodies to a synaptosomal-associated protein of 25 kDa (SNAP25), which is transported by fast anterograde transport; the 68-kDa neurofilament subunit (NF68kD); and microtubule-associated protein 5 (MAP5) on sections from rats subjected to 30 min and 1, 2, and 4 h of ischemia induced by permanent middle cerebral artery (MCA) occlusion. After 4 h of occlusion, there was increased SNAP25 immunoreactivity, which was bulbous in appearance, reminiscent of the axonal swellings that occur following blunt head injury. Increased SNAP25 immunoreactivity was present in circumscribed zones in the subcortical white matter and in the axonal tracts at the border of infarction, a pattern similar to that previously described for amyloid precursor protein. Although less marked, similar changes in immunoreactivity in axons were evident following 2 h of ischemia. MAP5 and NF68kD had striking changes in immunoreactivity in axonal tracts permeating the caudate nucleus within the MCA territory at 4 h. The appearance was roughened and disorganized compared with the smooth regular staining in axons within the nonischemic areas. Profiles reminiscent of axonal bulbs were evident in MAP5-stained sections. The changes seen with NF68kD and MAP5 were also evident at 2 h but were more subtle at 1 h. There were no changes in axonal immunoreactivity with SNAP25 or NF68kD at 30 min after MCA occlusion. Altered immunoreactivity following ischemia using SNAP25, MAP5, and NF68kD provides further evidence for the progressive breakdown of the axonal cytoskeleton following an ischemic insult. NF68kD and MAP5 appear to be sensitive markers of the structural disruption of the cytoskeleton, which precedes the subsequent accumulation of SNAP25 within the damaged axons. Axonal cytoskeletal breakdown and disruption of fast axonal transport, which are well-recognized features of traumatic brain injury, are also sequalae of an ischemic insult.     

Effects of Diffuse Axonal Injury on Speed of Information Processing Following Severe Traumatic Brain Injury.

To test the hypothesis that slowed information processing in traumatic brain injury is related to diffuse axonal injury (DAI), the authors compared 10 patients with predominant DAI (diffuse group) and minimal DAI (mixed injury group) on the Symbol Digit Modalities Test, simple and choice reaction time, Trail Making Tests A and B, and the Stroop Neuropsychological Screening Test. The diffuse group was slower than the mixed injury and control groups on basic speed of processing tasks. This difference was not apparent on complex speeded tasks once basic speed of processing was controlled for. The diffuse group's slower speed of processing was not accounted for by differences in injury severity, age, or time postinjury. The diffuse group showed greater recovery over time. (PsycINFO Database Record (c) 2010 APA, all rights reserved)