Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury. (1/230)

Apolipoprotein E deficient mice have distinct memory deficits and neurochemical derangements and their recovery from closed head injury is impaired. In the present study, we examined the possibility that the neuronal derangements of apolipoprotein E deficient mice are associated with oxidative stress, which in turn affects their ability to recover from close head injury. It was found that brain phospholipid levels in apolipoprotein E deficient mice are lower than those of the controls (55+/-15% of control, P<0. 01), that the cholesterol levels of the two mice groups are similar and that the levels of conjugated dienes of the apolipoprotein E deficient mice are higher than those of control mice (132+/-15% of P<0.01). Brains of apolipoprotein E deficient mice had higher Mn-superoxide dismutase (134+/-7%), catalase (122+/-8%) and glutathione reductase (167+/-7%) activities than control (P<0.01), whereas glutathione peroxidase activity and the levels of reduced glutathione and ascorbic acid were similar in the two mouse groups. Closed head injury increased catalase and glutathione peroxidase activities in both mouse groups, whereas glutathione reductase increased only in control mice. The superoxide dismutase activity was unaffected in both groups. These findings suggest that the antioxidative metabolism of apolipoprotein E deficient mice is altered both prior to and following head injury and that antioxidative mechanisms may play a role in mediating the neuronal maintenance and repair derangements of the apolipoprotein E deficient mice.  (+info)

Clinical studies on diffuse axonal injury in patients with severe closed head injury. (2/230)

OBJECTIVE: To discuss the clinical criteria for diagnosing diffuse axonal injury (DAI). METHODS: Clinical and computed tomographic features of 117 patients with severe closed head injury were analyzed. The authors preliminarily put forward CT diagnostic criteria of DAI, that is, 1) single or multiple small intraparenchymal hemorrhages in the cerebral hemispheres (< 2 cm in diameter); 2) intraventricular hemorrhage; 3) hemorrhage in the corpus callosum; 4) small focal areas of hemorrhage adjacent to the third ventricle (< 2 cm in diameter); and 5) brain stem hemorrhage. All patients were divided into two groups, DAI and non-DAI group, according to the criteria. There were 42 patients in the DAI group and 75 patients in the non-DAI group. The injury causes, Glasgow coma scale (GCS) scores on admission, coexisting injuries and outcomes were compared between the two groups. The relationship between DAI and the outcomes in the patients with severe head injury was analyzed. RESULTS: Traffic accident was the main injury cause in the cases of DAI. GCS scores on admission in patients with DAI were significantly lower than those in patients without DAI. The incidence of diffuse brain swelling (DBS) in the DAI group was significantly higher than that in the non-DAI group, whereas the incidences of both skull fracture and epidural hematoma (EDH) in the DAI group were significantly lower than those in non-DAI group. There was no significant difference between the incidence of subarachnoid hemorrhage (SAH) and subdural hematoma (SDH) in the two groups. The incidence of poor outcome in the DAI group was significantly higher than that in the non-DAI group, although there was no significant difference between the mortalities in the two groups. CONCLUSIONS: Because DAI is a very important factor worsening the outcome of patients with head injury, it is essential to make a diagnosis as soon as possible. The clinical manifestations of DAI, however, are not specific and DAI does not show directly on CT scans, so it is difficult to make a definite diagnosis. The CT diagnostic criteria of DAI put forward in this article are practicable, though they are by no means perfect.  (+info)

Multifocal cerebellar granular layer necrosis in traumatically head-injured lambs. (3/230)

In a blunt, nonmissile, head impact model of traumatic brain injury in 4-5-week-old Merino lambs, multiple foci of internal granular layer necrosis were found in all 10 impacted animals. This lesion has not previously been reported after human or animal head injury. Temporal lobe impact contusions, predominantly microscopic (8/10) and contralateral contusions (2/10), parenchymal (10/10) and subarachnoid (10/10) hemorrhage, and widely distributed axonal injury were also observed. Although the precise pathogenesis of this focal granule cell necrosis and often attendant red cell change in Purkinje cells was unclear, an ischemic etiology due to trauma-related vascular damage is postulated.  (+info)

Prophylactic inferior vena cava filters in trauma patients at high risk: follow-up examination and risk/benefit assessment. (4/230)

PURPOSE: The efficacy of prophylactic inferior vena cava filters in selected trauma patients at high risk has come into question in relation to risk/benefit assessment. To evaluate the usefulness of prophylactic inferior vena cava filters, we reviewed our experience and overall complication rate. METHODS: From February 1991 to April 1998, the trauma registry identified 7333 admissions. One hundred eighty-seven prophylactic inferior vena cava filters were inserted. After the exclusion of 27 trauma-related deaths (none caused by thromboembolism), 160 patients were eligible for the study. The eligible patients were contacted and asked to complete a survey and return for a follow-up examination to include physical examination, Doppler scan study, vena cava duplex scanning, and fluoroscopic examination. The patients' hospital charts were reviewed in detail. The indications for prophylactic inferior vena cava filter insertion included prolonged immobilization with multiple injuries, closed head injury, pelvic fracture, spine fracture, multiple long bone fracture, and attending discretion. RESULTS: Of the 160 eligible patients, 127 were men, the mean age was 40.3 years, and the mean injury severity score was 26.1. The mean day of insertion was hospital day 6. Seventy-five patients (47%) returned for evaluation, with a mean follow-up period of 19.4 months after implantation (range, 7 to 60 months). On survey, patients had leg swelling (n = 27), lower extremity numbness (n = 14), shortness of breath (n = 9), chest pain (n = 7), and skin changes (n = 4). All the survey symptoms appeared to be attributable to patient injuries and not related to prophylactic inferior vena cava filter. Physical examination results revealed edema (n = 12) and skin changes (n = 2). Ten Doppler scan studies had results that were suggestive of venous insufficiency, nine of which had histories of deep vein thrombosis. With duplex scanning, 93% (70 of 75) of the vena cavas were visualized, and all were patent. Only 52% (39 of 75) of the prophylactic inferior vena cava filters were visualized with duplex scanning. All the prophylactic inferior vena cava filters were visualized with fluoroscopy, with no evidence of filter migration. Of the total 187 patients, 24 (12.8%) had deep vein thrombosis develop after prophylactic inferior vena cava filter insertion, including 10 of 75 (13.3%) in the follow-up group, and one patient had a nonfatal pulmonary embolism despite filter placement. Filter insertion complications occurred in 1.6% (three of 187) of patients and included one groin hematoma, one arteriovenous fistula, and one misplacement in the common iliac vein. CONCLUSION: This study's results show that prophylactic inferior vena cava filters can be placed safely with low morbidity and no attributable long-term disabilities. In this patient population with a high risk of pulmonary embolism, prophylactic inferior vena cava filters offered a 99.5% protection rate, with only one of 187 patients having a nonfatal pulmonary embolism.  (+info)

Correlation between cerebral oxygen saturation measured by near-infrared spectroscopy and jugular oxygen saturation in patients with severe closed head injury. (5/230)

Near-infrared spectroscopy has been used to monitor cerebral oxygen saturation during cerebral circulatory arrest and carotid clamping. However, its utility has not been demonstrated in more complex situations, such as in patients with head injuries. The authors tested this method during conditions that may alter the arteriovenous partition of cerebral blood in different ways. METHODS: The authors compared changes in measured cerebral oxygen saturation and other hemodynamic parameters, including jugular venous oxygen saturation, in nine patients with severe closed head injury during manipulation of arterial carbon dioxide partial pressure and after mean arterial pressure was altered by vasopressors. RESULTS: The Bland and Altman representation of cerebral oxygen saturation versus jugular oxygen saturation showed a uniform scatter. Values for changing arterial carbon dioxide partial pressure were: bias = 1.1%, 2 SD = +/-21%, absolute value; and those for alterations in mean arterial pressure: bias = 3.7%, 2 SD = +/-24%, absolute value. However, a Bland and Altman plot of changes in cerebral oxygen saturation versus changes in jugular oxygen saturation had a negative slope (alteration in arterial carbon dioxide partial pressure: bias = 2.4%, 2 SD = +/-17%, absolute value; alteration in mean arterial pressure: bias = -4.9%, 2 SD = +/-31%, absolute value). Regression analysis showed that changes in cerebral oxygen saturation were positively correlated with changes in jugular venous oxygen saturation during the carbon dioxide challenge, whereas correlation was negative during the arterial pressure challenge. CONCLUSIONS: Cerebral oxygen saturation assessed by near-infrared spectroscopy does not adequately reflect changes in jugular venous oxygen saturation in patients with severe head injury. Changes in arteriovenous partitioning, infrared-spectroscopy contamination by extracerebral signal, algorithm errors, and dissimilar tissue sampling may explain these findings.  (+info)

Spontaneous ventriculostomy: report of three cases revealed by flow-sensitive phase-contrast cine MR imaging. (6/230)

Spontaneous ventriculostomy is a rare condition that occurs with the spontaneous rupture of a ventricle, resulting in a communication between the ventricular system and the subarachnoid space. Three cases of spontaneous ventriculostomy through the floor of the third ventricle that occurred in cases of chronic obstructive hydrocephalus are presented. The communication was identified via flow-sensitive phase-contrast cine MR imaging. Spontaneous ventriculostomy is probably a result of a rupture of the normally thin membrane that forms the floor of the third ventricle and, with long-standing obstructive hydrocephalus, creates an internal drainage pathway that spontaneously compensates for the hydrocephalus.  (+info)

Refractory symptomatic schizophrenia resulting from frontal lobe lesion: response to clozapine. (7/230)

A 34-year-old man with a 10-year history of persistent auditory hallucinations and passivity delusions had failed to respond to a variety of conventional antipsychotic medications. He had a history of head trauma 8 years before the onset of psychiatric symptoms. Recent investigations revealed a post-traumatic infarct, situated in the left frontal lobe, on a magnetic resonance imaging scan. Treatment with clozapine for more than 2 years resulted in a marked improvement in his psychotic symptoms. The localization of the brain lesion may be related to the etiology of his symptoms and to the clinical response to clozapine.  (+info)

Experimental closed head injury: analysis of neurological outcome, blood-brain barrier dysfunction, intracranial neutrophil infiltration, and neuronal cell death in mice deficient in genes for pro-inflammatory cytokines. (8/230)

Cytokines are important mediators of intracranial inflammation following traumatic brain injury (TBI). In the present study, the neurological impairment and mortality, blood-brain barrier (BBB) function, intracranial polymorphonuclear leukocyte (PMN) accumulation, and posttraumatic neuronal cell death were monitored in mice lacking the genes for tumor necrosis factor (TNF)/lymphotoxin-alpha (LT-alpha) (TNF/LT-alpha-/-) and interleukin-6 (IL-6) and in wild-type (WT) littermates subjected to experimental closed head injury (total n = 107). The posttraumatic mortality was significantly increased in TNF/LT-alpha-/- mice (40%; P < 0.02) compared with WT animals (10%). The IL-6-/- mice also showed a higher mortality (17%) than their WT littermates (5.6%), but the difference was not statistically significant (P > 0.05). The neurological severity score was similar among all groups from 1 to 72 hours after trauma, whereas at 7 days, the TNF/LT-alpha-/- mice showed a tendency toward better neurological recovery than their WT littermates. Interestingly, neither the degree of BBB dysfunction nor the number of infiltrating PMNs in the injured hemisphere was different between WT and cytokine-deficient mice. Furthermore, the analysis of brain sections by in situ DNA nick end labeling (TUNEL histochemistry) at 24 hours and 7 days after head injury revealed a similar extent of posttraumatic intracranial cell death in all animals. These results show that the pathophysiological sequelae of TBI are not significantly altered in mice lacking the genes for the proinflammatory cytokines TNF, LT-alpha, and IL-6. Nevertheless, the increased posttraumatic mortality in TNF/LT-alpha-deficient mice suggests a protective effect of these cytokines by mechanisms that have not been elucidated yet.  (+info)