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PubMed2005

Abnormal motor preparation in severe traumatic brain injury with good recovery.

Movement-related cortical potentials (MRCPs) were examined in seven patients with severe traumatic brain injury (TBI) and 12 matched control subjects. All patients had clinically established good recovery by the time of testing. Flexion movements of the index finger of the left or right hand were recorded in two (alternating and repetitive) self-paced conditions and in one externally triggered condition. In control subjects, the bereitschaftspotential (BP) component of MRCP was detected approximately 2000 msec prior to movement onset in the self-paced conditions and was larger and earlier in the alternating compared to the repetitive condition. The BP component was absent in the externally triggered condition. In TBI patients, the BP was greatly reduced and no difference between the alternating-repetitive conditions was detected; in contrast, only small differences were present in the controls for the negative slope (NS) and MP components and no difference for the reafferent positivity (RAP) component. A dipole analysis indicated the supplementary motor area and the premotor area as the likely generators of BP and NS' components, respectively. Gradientrecalled echo magnetic resonance imaging allowed the detection of a number of small hypointense lesions primarily located in the frontal lobes, as in diffuse axonal injury. This pattern of results indicates a selective deficit in motor preparation and a relatively spared pattern of activation during and following movement in these patients. Imaging data appear generally consistent with the pattern of MRCPs observed in the patient group. Implications of these results for the problem of slowness in TBI patients are discussed.

Adult↗
PubMedDate not supplied

Severe head injury in children--analyzing the better outcome over a decade and the role of major improvements in intensive care.

We suggest a few possible explanations, including improvement of intensive care, as the main cause, for the improved outcome after severe head injury in children and present the predictors of outcome observed in a contemporary series. From January 1984 to June 1988 we saw 117 children (ages 0-14) with postresuscitation GCS (Glasgow Come Scale) scores of 3-8. The more recent cohort of children seen in 1994-1996 was made up of 152 patients. Apart from standard statistics we used a segmentation method called CHAID (SSPS software). Previously known predictors of outcome are found still to apply in our series. Although in the recent period there was a lower proportion of patients with GCS 3-4 (11% versus 32%), a higher percentage had suffered multiple trauma (56% versus 33%). The rates of craniotomy and of ICP monitoring were similar (66% and 61%). Comparison of the two cohorts for outcome at discharge and through 1 year shows that mortality fell from 33% to 10% and the proportion achieving improvement of neurological status increased from 24% to 56%. CHAID analysis showed that the mortality rates of patients within specific groups declined significantly over the two periods: (1) a significant reduction in mortality was seen in patients with GCS 5-7, especially those with diffuse axonal injury (DAI) (17.3% to 0%); (2) no child admitted in shock survived in the earlier period, whereas 7 with GCS 4-6 survived during the recent period. The best model for mortality prediction includes GCS, and in the GCS 4-7 subgroup, the presence of subdural hematoma. It seems that the trend toward better immediate outcome is continuous, and this is the more striking when the severity of injury is taken into consideration. Our belief is that the modern medical and surgical techniques, although incurring higher costs and necessitating ongoing intensity, are well worth the effort.

Adolescent↗
PubMed2003

Correlation of regional metabolic rates of glucose with glasgow coma scale after traumatic brain injury.

UNLABELLED: After traumatic brain injury (TBI), subcortical white matter damage may induce a functional disconnection leading to a dissociation of regional cerebral metabolic rate of glucose (CMRglc) between the cerebral cortex and deeper brain regions. Therefore, thalamic and brain stem CMRglc may have a closer correlation than does the cerebral cortex with depth of coma after TBI. METHODS: Eleven adult healthy volunteers and 23 adult patients with TBI (median initial Glasgow Coma Scale score [GCSini], 8) underwent (18)F-FDG PET within 5 d after injury. The CMRglc of cortical areas (remote from hemorrhagic lesions), striatum, thalamus, brain stem, cerebellar cortex, and whole brain was compared with severity of injury and the level of consciousness evaluated using GCSini and the Glasgow Coma Scale score at the time of PET (GCSpet). RESULTS: The regional CMRglc of the brain stem is relatively unaffected by the TBI. Compared with healthy volunteers, TBI patients exhibited significantly depressed CMRglc in the striatum (3.9 +/- 1.3 vs. 5.1 +/- 0.9 mg/100 g/min, P < 0.05) and thalamus (3.1 +/- 1.0 vs. 4.3 +/- 0.9 mg/100 g/min, P < 0.05). CMRglc levels were not statistically lower in the cerebellum (2.9 +/- 0.8 vs. 3.5 +/- 0.8 mg/100 g/min, P = NS) and brain stem (2.5 +/- 0.5 vs. 2.6 +/- 0.5 mg/100 g/min, P = NS). However, compared between comatose and noncomatose patients, CMRglc values in the thalamus (2.7 +/- 0.7 vs. 3.6 +/- 1.2 mg/100 g/min, P < 0.05), brain stem (2.2 +/- 0.4 vs. 2.8 +/- 0.5 mg/100 g/min, P < 0.01), and cerebellar cortex (2.6 +/- 0.5 vs. 3.4 +/- 1.0 mg/100 g/min, P < 0.05) were significantly lower in comatose patients. When individual values of regional CMRglc were plotted against posttraumatic level of consciousness, CMRglc values for the thalamus, brain stem, and cerebellum significantly correlated with the level of consciousness at the time of PET (r = 0.58, P < 0.01; r = 0.66, P < 0.01; r = 0.64, P < 0.01, respectively). CT or MRI findings were normal for the analyzed structures except for 3 patients with diffuse axonal injury of the brain stem. The presence of shear injury was associated with poor GCSini (P < 0.05.) but was not related to GCSpet and brain stem CMRglc. CONCLUSION: A PET investigation using (18)F FDG demonstrated a significant difference in glucose metabolism in the thalamus, brain stem, and cerebellum between comatose and noncomatose patients acutely after TBI. The metabolic rate of glucose in these regions significantly correlated with the level of consciousness at the time of PET.

Adolescent↗
PubMed2002

[Brain contusion: morphology, pathogenesis and treatment].

Focal cerebral contusions can be dynamic and expansive, leading to a delayed neurological deterioration. In head--injured patients, the rise in intracranial pressure (ICP), subsequent to uncontrollable swelling, is the only and the most frequent cause of death. Studies show that brain swelling, after traumatic brain injury (TBI), is caused by brain edema rather than cerebral blood volume (CBV). CBV is reduced in proportion to cerebral blood flow (CBF) reduction, following a severe TBI. Cerebrovascular damages, leading to subsequent reductions in regional CBF, may play an important role in secondary cell damages following TBI. The histological examination revealed the formation of microthrombosis in the contused area, extending from the center to the peripheral areas within 6 hours after injury. In the pericontusional zone and surrounding parenchyma, vasoresponsivity may be nearly three times normal, which suggests hypersensitivity to hyperventilation and other phenomena. Glutamate is the most widely distributed excitatory neurotransmitter in the mammalian brain. However, when glutamate is present in excessive quantities, it may overactivate specific ion channels, especially the N-methyl-D-aspartate channel. A shift of potassium into the extracellular space will result in rapid swelling of astrocytes, which absorb quantities of potassium to preserve ionic homeostasis. This process may cause rapid cytotoxic edema, which is probably, a major factor in causation of posttraumatic raised ICP. The presence of a focal contusion and primary or secondary ischemic events were the clinical features most strongly correlated with high dialysate of glutamate. Raised ICP was significantly more common, and outcome was worse in patients with high levels of glutamate. Contusion is a key factor in the development of blood brain barrier (BBB) permeability. BBB endures at least 7 days post TBI. Biphasing opening of the BBB, following head trauma and a possible second wave of secondary brain damage, was confirmed. Brain tissue pO2 monitoring might become an important tool in the treatment regime for TBI patients. Histologically the loss of CA3 pyramidal cells in the hippocampus was observed ipsilaterally in the cortical contusion and bilaterally in diffuse axonal injury. Aggressive, early hyperventilation after TBI augments neuronal death in CA3 hippocampus. Due to high mortality associated with such cerebral contusions, a standard practice has evolved into evacuating contusions in patients who had deterioration in the level of consciousness, lesions more than 30 sec and CT suggestion of raised ICP.

Blood-Brain Barrier↗
PubMed2004

Recovery of ambulation after traumatic brain injury.

OBJECTIVES: To identify variables that are predictive of independent ambulation after traumatic brain injury (TBI) and to define the time course of recovery. DESIGN: Retrospective review of consecutive admissions of patients with severe TBI over a 32-month period. SETTING: Brain injury unit in an acute, inpatient rehabilitation hospital. PARTICIPANTS: Of 264 patients screened, 116 met criteria that included the ability to participate in motor and functional evaluation on admission to acute rehabilitation, and the absence of other neurologic disorders or fractures that affect one's ability to ambulate. INTERVENTION: Inpatient rehabilitation on a specialized TBI unit by an interdisciplinary team.Main outcome measures Recovery of independent ambulation and time to recover independent ambulation. RESULTS: Of eligible patients, 73.3% achieved independent ambulation by latest follow-up (up to 5.1 mo). Patients who achieved independent ambulation were significantly younger (P<.05), had better gait scores on admission (P<.05), and tended to be less severely injured-based on duration of posttraumatic amnesia (PTA; P=.058)-than those who did not ambulate independently. There were no differences in recovery based on neuropathologic profile. Mean time to independent ambulation +/- standard deviation was 5.7+/-4.3 weeks; of those achieving independent ambulation, 82.4% did so by 2 months and 94.1% by 3 months. If not independent by 3 months postinjury, patients had a 13.9% chance of recovery. Multivariate regression analysis generated prediction models for time to independent ambulation, using admission FIM instrument scores and age (38% of variance); initial gait score, loss of consciousness, and age (40% of variance); or initial gait score and PTA (58% of variance), when restricted to just those patients with diffuse axonal injury. CONCLUSIONS: Most patients with severe TBI achieved independent ambulation; the vast majority did so within 3 months postinjury. Functional measures, injury severity measures, and age can help guide prognosis and expectations for time to recover.

Activities of Daily Living↗
PubMed2002

ERPs and behavioural indices of long-term preattentive and attentive deficits after closed head injury.

Attentional deficits are often reported even years after sustaining a closed head injury (CHI). Disturbance of cognitive attentional functions following CHI has been documented in both behavioural and event-related brain potential (ERP) studies. Recently, the possibility that the sequelae of CHI extend to preattentive processes of attention has been pointed out. We used a paradigm that makes it possible to assess simultaneously the processing of relevant information and involuntary mechanisms of attention to gain further insight in this matter. Eleven patients with CHI greater than 1 year post-trauma and 14 age-matched control subjects were engaged in the performance of a continuous visual reaction time (RT) discrimination task while ignoring streams of auditory task-irrelevant stimuli. The main characteristic in the paradigm was that all visual stimuli were shortly preceded by an auditory stimulus, which could be a repeated (90%) or a different (deviant) tone. We measured performance on the discrimination task, and ERP indices of preattentive (mismatch negativity MMN) and attentive information processing (P1, N165, P3b). In relation to control subjects, CHI patients showed an attenuation of the MMN evoked by the deviant-tone. In response to the visual stimuli, CHI patients showed a delay of P1, and a reduction of the N165 and P3b components. Moreover, they had slower RT and missed more responses in a visual discrimination task. These results indicate both preattentive and attentive deficits, which is consistent with the typical diffuse axonal injury (DAI) resulting after CHI.

Adult↗
PubMed1991

Traumatic brain injuries: structural changes.

A host of complications and consequences may follow a contusion or other brain injury of any sort. An appreciation of the temporal evolution of the contusion from a microscopic standpoint is useful to a full understanding of the process by which physical force damages the brain and how the brain reacts to this damage. Some disruptions of the blood brain barrier quite early will result in extracellular edema. The microscopic appearance of an edematous area is usually spongy with numerous vacuoles. The neuropil may appear bubbly, and glial cells may be swollen. If edema has been long standing, the vacuoles may be larger and in fact a small cyst may appear in the white matter. If focal cerebral edema is not present for long periods of time and the underlying cause has been corrected, residual fluid and electrolytes are eventually removed, restoring the neuropil to a normal state, leaving no sign of its presence. However, in longer standing lesions, myelin pallor and some reactive gliosis may remain indefinitely. Neurons may show swelling very early and for a short period of time, which gives way to shrinkage, eosinophilia, and nuclear pyknosis. These changes may be observed at the periphery of lesions for as long as 5 or 6 months after the initial event. Before dissolution, nuclear pyknosis may remain in the tissue for many days and possibly longer, and may even become mineralized in situ (ferruginated neurons) to remain for years. In a traumatic lesion, swollen and ballooned axons may be found in and around the contusion but also at great distances from it (diffuse axonal injury). Axonal ballooning may be observed between 24 and 48 h postinjury and may persist wherever found for many years. Selective axonal calcification has been observed in humans as well as in experimental trauma. At about 7-10 days postinjury increased numbers of astroglia probably are present. Over the ensuing weeks and months, and probably years, astrocytes increase in number and in fibrillary appearance, eventually resulting in a glial scar in and about the injured area. It is thought that this reactive gliosis results in restoration of the blood-brain barrier in the damaged area.

Astrocytes↗
PubMed2005

Brain damage and axonal injury in a Scottish cohort of neonatal deaths.

Despite the clinical and medicolegal significance attached to perinatal asphyxia, the neuropathological basis of this condition remains obscure. There are very few studies in the literature which correlate the pathological findings in neonatal brains with detailed epidemiological data, and none which are population based. In a Scotland-wide study of neonatal deaths, 70 brains have been examined. On the basis of glial and macrophage reactions, we previously identified infants with putative antepartum brain damage in this cohort and have related these reactions to signs of birth asphyxia. The present study explores the extent of neuronal/axonal injury in these infants since this is likely to be the basis for neurological deficits in surviving infants. We have also investigated these brains for beta-amyloid precursor protein (betaAPP) positivity to determine whether this is a useful marker of neuronal injury in neonates. Neuronal eosinophilia and karyorrhexes were detected in 43% and 27% of the cohort, respectively; maximally in the subiculum and ventral pons, but often present elsewhere. White matter damage was detected in 24% of cases but without classic cystic lesions of periventricular leucomalacia. betaAPP positivity was present in neuronal soma in 52% of cases and, in axons, in 27% of cases, and was seen from as early as 25-weeks gestation. Axonal bulbs were clearly delineated by betaAPP positivity and were usually located in the cerebral white matter and internal capsule, and infrequently in the brain stem. Although white matter damage and betaAPP axonal positivity were often detected in the same cases (P = 0.034), these features also occurred independently of each other. Both neuronal karyorrhexes and white matter betaAPP positivity were significantly correlated with the features of birth asphyxia, particularly a history of seizures. Immunocytochemistry for both betaAPP and glial fibrillary acidic protein proved useful in detecting neuropathological features which escaped detection on routine examination, particularly in preterm infants. The presence together of recent and older damage in individual brains suggests that there is an ongoing neuronal response to cerebral insults. We find that betaAPP is a useful marker of white matter damage in the neonatal brain. Immunopositivity for betaAPP in these circumstances is not attributable to inflicted or accidental trauma. While birth-related trauma cannot be ruled out, hypoxia/ischaemia is a likely cause in these infants. However, the exact pathogenesis of neuronal/axonal injury in the neonatal brain remains unclear.

Amyloid beta-Protein Precursor↗
PubMed2002

Resuscitation from severe hemorrhagic shock after traumatic brain injury using saline, shed blood, or a blood substitute.

The original purpose of this study was to compare initial resuscitation of hemorrhagic hypotension after traumatic brain injury (TBI) with saline and shed blood. Based on those results, the protocol was modified and saline was compared to a blood substitute, diaspirin cross-linked hemoglobin (DCLHb). Two series of experiments were performed in anesthetized and mechanically ventilated (FiO2 = 0.4) pigs (35-45 kg). In Series 1, fluid percussion TBI (6-8 ATM) was followed by a 30% hemorrhage. At 120 min post-TBI, initial resuscitation consisted of either shed blood (n = 7) or a bolus of 3x shed blood volume as saline (n = 13). Saline supplements were then administered to all pigs to maintain a systolic arterial blood pressure (SAP) of >100 mmHg and a heart rate (HR) of <110 beats/min. In Series 2, TBI (4-5 ATM) was followed by a 35% hemorrhage. At 60 min post-TBI, initial resuscitation consisted of either 500 mL of DCLHb (n = 6) or 500 mL of saline (n = 5). This was followed by saline supplements to all pigs to maintain a SAP of >100 mmHg and a HR of <110 beats/min. In Series 1, most systemic markers of resuscitation (e.g., SAP, HR, cardiac output, filling pressures, lactate, etc.) were normalized, but there were 0/7 vs. 5/13 deaths within 5 h (P = 0.058) with blood vs. saline. At constant arterial O2 saturation (SaO2), mixed venous O2 saturation (SvO2), cerebral perfusion pressure (CPP), and cerebral venous O2 saturation (ScvO2) were all higher, intracranial pressure (ICP) was lower, and CO2 reactivity was preserved with blood vs. saline (all P < 0.05). In Series 2, SAP, ICP, CPP, and lactate were higher with DCLHb vs. saline (all P< 0.05). Cardiac output was lower even though filling pressure was markedly elevated with DCLHb vs. saline (both P< 0.05). Neither SvO2 nor cerebrovascular CO2 reactivity were improved, and ScvO2 was lower with DCLHb vs. saline (P < 0.05). All survived at least 72 h with neuropathologic changes that included sub-arachnoid hemorrhage, midline cerebellar necrosis, and diffuse axonal injury. These changes were similar with DCLHb vs. saline. Thus, whole blood was more effective than saline for resuscitation of TBI, whereas DCLHb was no more, and according to many variables, less effective than saline resuscitation. These experimental results are comparable to those in a recent multicenter trial using DCLHb for the treatment of severe traumatic shock. Further investigations in similar experimental models might provide some plausible explanations why DCLHb unexpectedly increased mortality in patients.

Animals↗
PubMed2006

Noninvasive detection of cuprizone induced axonal damage and demyelination in the mouse corpus callosum.

Previously, we tested the prediction that axonal damage results in decreased axial diffusivity (lambda(parallel)) while demyelination leads to increased radial diffusivity (lambda(perpendicular)). Cuprizone treatment of C57BL/6 mice was a highly reproducible model of CNS white matter demyelination and remyelination affecting the corpus callosum (CC). In the present study, six C57BL/6 male mice were fed 0.2% cuprizone for 12 weeks followed by 12 weeks of recovery on normal chow. The control mice were fed normal chow and imaged in parallel. Biweekly in vivo DTI examinations showed transient decrease of lambda(parallel) in CC at 2-6 weeks of cuprizone treatment. Immunostaining for nonphosphorylated neurofilaments demonstrated corresponding axonal damage at 4 weeks of treatment. Significant demyelination was evident from loss of Luxol fast blue staining at 6-12 weeks of cuprizone ingestion and was paralleled by increased lambda(perpendicular) values, followed by partial normalization during the remyelination phase. The sensitivity of lambda(perpendicular) to detect demyelination may be modulated in the presence of axonal damage during the early stage of demyelination at 4 weeks of cuprizone treatment. Our results suggest that lambda(parallel) and lambda(perpendicular) may be useful in vivo surrogate markers of axonal and myelin damage in mouse CNS white matter.

Animals↗
PubMed2005

Acquired lesions of the corpus callosum: MR imaging.

In this pictorial review, we illustrate acquired diseases or conditions of the corpus callosum that may be found by magnetic resonance (MR) imaging of the brain, including infarction, bleeding, diffuse axonal injury, multiple sclerosis, acute disseminated encephalomyelitis, Marchiafava-Bignami disease, glioblastoma, gliomatosis cerebri, lymphoma, metastasis, germinoma, infections, metabolic diseases, transient splenial lesion, dilated Virchow-Robin spaces, wallerian degeneration after hemispheric damage and focal splenial gliosis. MR imaging is useful for the detection and differential diagnosis of corpus callosal lesions. Due to the anatomical shape and location of the corpus callosum, both coronal and sagittal fluid-attenuated inversion recovery images are most useful for visualizing lesions of this structure.

Brain Diseases↗
PubMed2001

Differential diagnosis of posterior fossa multiple sclerosis lesions--neuroradiological aspects.

Various infratentorial pathological conditions can mimic multiple sclerosis (MS) both clinically and radiologically. We review the inflammatory, vascular, neoplastic and metabolic conditions which show features similar to those of MS on magnetic resonance imaging (MRI). Behcet's disease, Lyme disease, progressive multifocal leukoencephalopathy, neurosarcoidosis, Whipple's disease, listeria rhombencephalitis, Bickerstaff's brainstem encephalitis, vasculitis due to systemic lupus erythematosus, and acute disseminated encephalomyelitis produce inflammatory lesions similar to those of MS in the brainstem and cerebellum. Neoplastic diseases, in particular pontine gliomas and lymphomas, can mimic MS. Vascular ischaemic lesions, either due to infarction produced by occlusion of a major posterior circulation artery or due to small vessel vasculopathy, can lead to posterior fossa lesions. The MRI changes of central pontine myelinolysis can also mimic MS. Diffuse axonal injury, radiation and chemotherapy induce lesions that resemble MS, however the clinical history will exclude these possibilities. Finally, we discuss a few conditions which are similar to MS in clinical presentation but have different MRI appearances, such as brainstem cavernomas, posterior fossa tumoural lesions, aneurysms and vascular loops producing neurovascular conflicts. Analysis of the MRI findings with clinical history and laboratory data helps to narrow down the diagnosis of the infratentorial pathology.

Brain↗
PubMed1998

Quantitative electroencephalographic evaluation of non-fatal and fatal traumatic coma.

Diffuse axonal injury (DAI) is an important cause of morbidity and mortality after traumatic brain injury (TBI), and its severity is therefore a major determinant of outcome. There have been suggestions that the extent of DAI may be reflected in quantitative measures of cerebral function, including the electroencephalogram (EEG) and brain-stem auditory evoked potentials (BAEPs). It has therefore been proposed that these quantitative methods of analysis may provide objective predictors of outcome following TBI. We prospectively investigated the relationship between quantitative EEG and BAEP measures and outcome, in 60 comatose patients (47 male and 13 female; age range 1-80 years, mean 36.4) after severe, closed head injury (post-resuscitation Glasgow Coma Scale (GCS) of 8). The Spearman correlation coefficients (rs) have been calculated for quantitative EEG measures (mean regional power and interhemispheric coherence) and BAEPs with patient outcome on the Glasgow Outcome and Disability Rating Scales at 6 months and 1 year. The measures most significantly correlated with outcome (P < 0.001) are over the left hemisphere, beta activity power (amplitude squared) in the fronto-central and centro-temporal regions, and alpha activity power in the centro-temporal region. We found no correlation between interhemispheric coherence (a statistical measure of cross-correlation in the frequency domain) and outcome at either 6 months or 1 year post-injury. In 10 fatalities, we examined the relationship between interhemispheric EEG coherence prior to deaths and the histopathological severity of DAI, in concordant regions. The only significant correlation between DAI and interhemispheric coherence is seen in the alpha band at the temporo-occipital site (rs = -0.79, P = 0.007). Our data indicate that there is regional information in EEG power spectra over the left hemisphere, which could be used in prognostic predictions for patients in coma after severe TBI. We were unable to demonstrate a correlation between interhemispheric coherence and outcome, or any clear and consistent evidence of a relationship between interhemispheric coherence and the severity of DAI.

Adolescent↗
PubMed2000

The contribution of MRI in the differential diagnosis of posterior fossa damage.

In multiple sclerosis patients, magnetic resonance imaging (MRI) frequently detects lesions in the brain stem and cerebellum. However various pathologies that have a predelection to occur in posterior fossa parenchyma may share similar features with inflammatory-demyelinating lesions. In this paper, we review the contribution of MRI to the differential diagnosis of posterior fossa pathology. Vascular lesions due to chronic hypoperfusion and arteriolosclerosis or occlusion of the main supplying arteries of the posterior circulation leading to acute infarction frequently produce characteristic pontine or cerebellar lesions. Neoplastic disease, in particular pontine gliomas in younger patients may have similar MRI features and may be difficult to distinguish from inflammatory-demyelinating lesions. Central pontine myelinolysis usually occurs in severely ill patients but the pontine MRI changes have an overlapping profile with inflammatory demyelination. Diffuse axonal injury of the midbrain and brainstem after head trauma and atrophy of posterior fossa structures in degenerative diseases may appear similar on MRI to tissue changes also seen frequently in MS. Analysis of the MRI appearance and clinical information is most often useful to narrow the fairly long list of differential diagnoses of posterior fossa pathology.

Brain Diseases↗
PubMed2002

Neuronal and glial mGluR5 modulation prevents stretch-induced enhancement of NMDA receptor current.

Neuronal stretching in culture has been used to model diffuse axonal injury caused by head trauma, and activation of N-methyl-D-aspartate receptors (NMDARs) has been implicated in the pathophysiology of such injury. Here we report the effects of modulating injury severity and the metabotropic glutamate receptor subtype 5 (mGluR5) on NMDAR activity after stretch injury. Following mild stretch, cortical neurons plated upon a confluent layer of astrocytes (NG) exhibited both increased maximal current (I(NMDA)) and reduction in the voltage-dependent Mg2+ block. In contrast, neurons grown without an astrocyte monolayer (PN) only exhibited increased I(NMDA). In NG, surprisingly, pretreatment with either the mGluR5 agonist CHPG or the mGluR5 antagonist MPEP decreased the enhancement of I(NMDA). In contrast, in PN, MPEP similarly limited I(NMDA) changes, but CHPG was without effect. In both culture conditions, MPEP, but not CHPG, limited the stretch-reduced Mg2+ block. Severe stretch had no effect on I(NMDA) or the Mg2+ block in either culture condition, despite a correlation between injury severity and the release of lactose dehydrogenase measured postinjury. Neither CHPG nor MPEP had any direct effects upon the NMDA receptor. We conclude that mGluR5 regulates NMDAR activity during mild stretch injury, but not severe injury, by modulating both the Mg2+ block and I(NMDA).

Animals↗
PubMedDate not supplied

Spontaneously T1-hyperintense lesions of the brain on MRI: a pictorial review.

In this work, the brain lesions that cause spontaneously hyperintense T1 signal on MRI were studied under seven categories. The first category includes lesions with hemorrhagic components, such as infarct, encephalitis, intraparenchymal hematoma, cortical contusion, diffuse axonal injury, subarachnoid hemorrhage, subdural and epidural hematoma, intraventricular hemorrhage, vascular malformation and aneurysm, and hemorrhagic neoplasm. The second category includes protein-containing lesions, such as colloid cyst, craniopharyngioma, Rathke's cleft cyst, and atypical epidermoid. The third category includes lesions with fatty components, such as lipoma, dermoid, and lipomatous meningioma. Lesions with calcification or ossification, such as endocrine-metabolic disorder, calcified neoplasm, infection, and dural osteoma, constitute the fourth category, whereas the fifth category includes lesions with other mineral accumulation, such as acquired hepatocerebral degeneration and Wilson disease. The sixth category includes melanin-containing lesions, such as metastasis from melanoma and leptomeningeal melanosis. The last category is the miscellaneous group, which includes ectopic neurohypophysis, chronic stages of multiple sclerosis, and neurofibromatosis type I. The above-mentioned lesions are presented with their typical T1-hyperintense images, and the underlying reasons for those appearances in magnetic resonance imaging are discussed.

Brain Diseases↗
PubMed2002

Imaging of traumatic intracranial hemorrhage.

Traumatic intracranial hemorrhage is a leading cause of morbidity and mortality in the United States. CT remains the primary imaging modality for initial evaluation of patients who have sustained head trauma. MR imaging, which has always been important for the evaluation of subacute and chronic head trauma, has been gaining popularity and recognition as an alternative primary imaging modality.

Brain↗
PubMed2001

Prophylaxis against thromboembolism in patients with traumatic brain injury: a survey of UK practice.

Venous thromboembolism is a major complication associated with traumatic brain injury and is responsible for significant morbidity and mortality. There has been a general reluctance over the years to use anticoagulant prophylaxis for patients with head injury who have suffered intracranial bleeding or for whom intracranial surgery is needed. We conducted a postal questionnaire survey of all neurosurgical centres in the United Kingdom, enquiring about the use of thromboprophylactic methods in the management of patients with traumatic brain injury. A diversity of practice and opinion in the use of such methods was evident from the replies received. The survey highlighted concern about the failure to implement even the most simple means of prophylaxis. The evidence for the use of the various methods of prophylaxis is reviewed.

Anticoagulants↗