Xenon-enhanced cerebral blood flow at 28% xenon provides uniquely safe access to quantitative, clinically useful cerebral blood flow information: a multicenter study.

BACKGROUND AND PURPOSE: Xe-CT measures CBF and can be used to make clinical treatment decisions. Availability has been limited, in part due to safety concerns. Due to improvements in CT technology, the concentration of inhaled xenon gas has been decreased from 32% to 28%. To our knowledge, no data exist regarding the safety profile of this concentration. We sought to better determine the safety profile of this lower concentration through a multicenter evaluation of adverse events reported by all centers currently performing xenon/CT studies in the US. MATERIALS AND METHODS: Patients were prospectively recruited at 7 centers to obtain safety and efficacy information. All studies were performed to answer a clinical question. All centers used the same xenon delivery system. CT imaging was used during a 4.3-minute inhalation of 28% xenon gas. Vital signs were monitored on all patients throughout each procedure. Occurrence and severity of adverse events were recorded by the principal investigator at each site. RESULTS: At 7 centers, 2003 studies were performed, 1486 (74.2%) in nonventilated patients. The most common indications were occlusive vascular disease and ischemic stroke; 93% of studies were considered clinically useful. Thirty-nine studies (1.9%) caused respiratory suppression of >20 seconds, all of which resolved spontaneously. Shorter respiratory pauses occurred in 119 (5.9%), and hyperventilation, in 34 (1.7%). There were 53 additional adverse events (2.9%), 7 of which were classified as severe. No adverse event resulted in any persistent neurologic change or other sequelae. CONCLUSIONS: Xe-CT CBF can be performed safely, with a very low risk of adverse events and, to date, no risk of permanent morbidity or sequelae. On the basis of the importance of the clinical information gained, Xe-CT should be made widely available.

Development of a posterior cerebral artery aneurysm subsequent to occlusion of the contralateral internal carotid artery for giant cavernous aneurysm.

We report a case of a patient who developed a left posterior cerebral artery aneurysm 5 years after balloon occlusion of the right internal carotid artery for a giant cavernous aneurysm. The location of the new aneurysm was outside of the primary collateral pathways to the contralateral, proximally occluded, anterior circulation, illustrating the complexity of hemodynamic factors contributing to the development of intracranial saccular aneurysms. The appearance of an aneurysm in this setting supports the hypothesis that degenerative factors and hemodynamic stresses are important in the etiology of intracranial aneurysms.

Traumatic brain injury: diffusion-weighted MR imaging findings.

BACKGROUND AND PURPOSE: Diffuse axonal injury (DAI) accounts for a significant portion of primary intra-axial lesions in cases of traumatic brain injury. The goal of this study was to use diffusion-weighted MR imaging to characterize DAI in the setting of acute and subacute traumatic brain injury. METHODS: Nine patients ranging in age from 26 to 78 years were examined with conventional MR imaging (including fast spin-echo T2-weighted, fluid-attenuated inversion-recovery, and gradient-echo sequences) as well as echo-planar diffusion-weighted MR imaging 1 to 18 days after traumatic injury. Lesions were characterized as DAI on the basis of their location and their appearance on conventional MR images. Trace apparent diffusion coefficient (ADC) maps were computed off-line with the diffusion-weighted and base-line images. Areas of increased signal were identified on the diffusion-weighted images, and regions of interests were used to obtain trace ADC values. RESULTS: In the nine patients studied, isotropic diffusion-weighted images showed areas of increased signal with correspondingly decreased ADC. In one case, decreased ADC was seen 18 days after the initial event. CONCLUSION: Decreased ADC can be demonstrated in patients with DAI in the acute setting and may persist into the subacute period, beyond that described for cytotoxic edema in ischemia.

Characterization of white matter lesions in multiple sclerosis and traumatic brain injury as revealed by magnetization transfer contour plots.

BACKGROUND AND PURPOSE: Magnetization transfer imaging provides information about the structural integrity of macromolecular substances, such as myelin. Our objective was to use this imaging technique and contour plotting to characterize and to define the extent of white matter lesions in multiple sclerosis and traumatic brain injury. METHODS: Magnetization transfer imaging was performed of 30 multiple sclerosis plaques and 10 traumatic white matter lesions. Magnetization transfer ratios (MTRs) were calculated for the lesions, for the normal- or abnormal-appearing surrounding white matter, and for remote normal-appearing white matter. MTR contour plots were constructed about these lesions. RESULTS: The contour plot appearance of MS plaques differed from that of traumatic white matter lesions. There was a gradual increase in MTR values at points at increasing distances from the center of the MS plaques; this was true for those lesions with and without surrounding T2 signal abnormality (halos). In contrast, there was an abrupt transition in MTR values between traumatic lesions and normal-appearing surrounding white matter. Additionally, the size of the MTR abnormality exceeded the size of the T2 signal abnormality for the MS plaques. CONCLUSION: MTR contour plots permit characterization and border definition of white matter lesions. Analysis of the contour plots suggests that MS is a centrifugal process with the lowest MTR within the center of the lesion. In contrast, traumatic white matter injuries are discrete lesions with abrupt transitions between the abnormal lesion and normal brain.

Endovascular thrombolysis for symptomatic cerebral venous thrombosis.

OBJECT: The authors sought to treat potentially catastrophic intracranial dural and deep cerebral venous thrombosis by using a multimodality endovascular approach. METHODS: Six patients aged 14 to 75 years presented with progressive symptoms of thrombotic intracranial venous occlusion. Five presented with neurological deficits, and one patient had a progressive and intractable headache. All six had known risk factors for venous thrombosis: inflammatory bowel disease (two patients), nephrotic syndrome (one), cancer (one), use of oral contraceptive pills (one), and puerperium (one). Four had combined dural and deep venous thrombosis, whereas clot formation was limited to the dural venous sinuses in two patients. All patients underwent diagnostic cerebral arteriograms followed by transvenous catheterization and selective sinus and deep venous microcatheterization. Urokinase was delivered at the proximal aspect of the thrombus in dosages of 200,000 to 1,000,000 IU. In two patients with thrombus refractory to pharmacological thrombolytic treatment, mechanical wire microsnare maceration of the thrombus resulted in sinus patency. Radiological studies obtained 24 hours after thrombolysis reconfirmed sinus/vein patency in all patients. All patients' symptoms and neurological deficits improved, and no procedural complications ensued. Follow-up periods ranged from 12 to 35 months, and all six patients remain free of any symptomatic venous reocclusion. Factors including patients' age, preexisting medical conditions, and duration of symptoms had no statistical bearing on the outcome. CONCLUSIONS: Patients with both dural and deep cerebral venous thrombosis often have a variable clinical course and an unpredictable neurological outcome. With recent improvements in interventional techniques, endovascular therapy is warranted in symptomatic patients early in the disease course, prior to morbid and potentially fatal neurological deterioration.

Proton magnetic resonance spectroscopy for detection of axonal injury in the splenium of the corpus callosum of brain-injured patients.

OBJECT: This study was conducted to determine whether proton magnetic resonance spectroscopy (MRS) is a sensitive method for detecting diffuse axonal injury, which is a primary sequela of traumatic brain injury (TBI). Diffuse axonal injury is characterized by selective damage to white matter tracts that is caused in part by the severe inertial strain created by rotational acceleration and deceleration, which is often associated with motor vehicle accidents. This axonal injury is typically difficult to detect by using conventional imaging techniques because it is microscopic in nature. The splenium was selected because it is a site vulnerable to shearing forces that produce diffuse axonal injury. METHODS: The authors used proton MRS to evaluate the splenium, the posterior commissure of the corpus callosum, in normal control volunteers and in patients with TBI. Proton MRS provided an index of neuronal and axonal viability by measuring levels of N-acetyl aspartate (NAA). CONCLUSIONS: A majority of mildly brain injured patients, as well as those more severely injured, showed diminished NAA/creatine (Cr) levels in the splenium compared with normal control volunteers. The patients displaying lowered NAA/Cr in the splenium were also likely to exhibit lowered NAA/Cr in lobar white matter. Also, the levels of NAA/Cr in the splenium of normal volunteers were higher compared with those found in lobar white matter. Decreases in NAA/Cr levels in the splenium may be a marker for diffuse injury. A proton MRS examination may be particularly useful in evaluating mildly injured patients with unexplained neurological and cognitive deficits. It is concluded that MRS is a sensitive tool in detecting axonal injury.

Cerebral extraction of oxygen, lactate production, and perfusion pressure in gunshot wound to the head: case report.

A case of gunshot wound to the head is presented, in which the patient made a satisfactory recovery after a prolonged period of elevated intracranial pressure and increased cerebral extraction of oxygen. Even though cerebral extraction of oxygen was increased in the most acute phase, the arteriojugular lactate difference was never abnormally decreased (ischemic). This finding indicated that, in this patient, increased cerebral extraction of oxygen was not sufficient to result in global cerebral ischemia (increased cerebral lactate production). To our knowledge, this is the first report on frequent serial assessment of cerebral extraction of oxygen and lactate production in severe penetrating head injury.

Fetal hippocampal transplants attenuate CA3 pyramidal cell death resulting from fluid percussion brain injury in the rat.

Transplantation of fetal neural tissue has been demonstrated to prevent neuronal loss in a number of CNS injury models including spinal cord contusion. However, no studies have examined the neuroprotective role of fetal transplants in models of traumatic brain injury. The present study examined the ability of fetal neural grafts to attenuate neuronal loss resulting from lateral fluid percussion (FP) brain injury in the rat. Lateral FP in the rat elicits a focal contusion within the parietal/temporal cortex and induces cell death in a subset of hippocampal CA3 pyramidal neurons. To examine potential neuroprotective effects of fetal neural grafts, either E16 fetal hippocampus, E16 fetal cortex, or sterile lactated Ringers was stereotaxically transplanted directly into contused cortex 2 days after FP brain injury. The effects of fetal transplants upon adjacent injured hippocampal CA3 regions were then assessed at 4 weeks after grafting utilizing quantitative image analysis. Both fetal cortex and hippocampal grafts survived within contused cortex. Fetal hippocampal grafts significantly attenuated CA3 cell death resulting from lateral fluid percussion, while fetal cortical transplants induced a small, but nonsignificant, amelioration of CA3 pyramidal loss. Thus, neuroprotection by fetal grafts appeared to be tissue specific with hippocampal, but not cortical, fetal transplants significantly reducing posttraumatic CA3 loss. In summary, fetal neural transplantation can ameliorate hippocampal cell death following experimental brain injury.

Pediatric spinal injury: the very young.

Maturity of the spine and spine-supporting structures is an important variable distinguishing spinal cord injuries in children from those in adults. Clinical data are presented from 71 children aged 12 years or younger who constituted 2.7% of 2598 spinal cord-injured patients admitted to the authors' institutions from June, 1972, to June, 1986. The 47 children with traumatic spinal cord injury averaged 6.9 years of age and included 20 girls (43%). The etiology of the pediatric injuries differed from that of adult injuries in that falls were the most common causative factor (38%) followed by automobile-related injuries (20%). Ten children (21.3%) had spinal cord injury without radiographic abnormality (SCIWORA), whereas 27 (57%) had evidence of neurological injury. Complete neurological injury was seen in 19% of all traumatic pediatric spinal cord injuries and in 40% of those with SCIWORA. The most frequent level of spinal injury was C-2 (27%, 15 cases) followed by T-10 (13%, seven cases). Upon statistical examination of the data, a subpopulation of children aged 3 years or younger emerged. These very young children had a significant difference in level of injury, requirement for surgical stability, and sex distribution compared to 4- to 12-year-old children.