Tumour associated epilepsy (TAE) is a poorly understood manifestation of many gliomas, meningiomas and metastatic brain tumours that has important clinical and social implications. Etiological mechanisms underlying tumour associated epilepsy include theories invoking peritumoural amino acid disturbances, local metabolic imbalances, cerebral oedema, pH abnormalities, morphological changes in the neuropil, changes in neuronal and glial enzyme and protein expression and altered immunological activity. It has also been suggested that the pathology involves perturbations in distribution and function of the NMDA subclass of glutamate receptors. The often capricious response of the seizure disorder following removal of the causative neoplasms suggests multiple factors are involved. Further understanding about the pathogenesis of TAE will await the development and characterisation of suitable animal models that demonstrate the clinical manifestations and physiological changes comparable to those seen in human cerebral tumours. With such a model it is hoped that progress may one day be made in understanding and subsequently treating this debilitating clinical problem.

N-Acetylaspartate (NAA) is considered a neuron-specific metabolite and its reduction a marker of neuronal loss. The objective of this study was to evaluate the time course of NAA changes in varying grades of traumatic brain injury (TBI), in concert with the disturbance of energy metabolites (ATP). Since NAA is synthesized by the mitochondria, it was hypothesized that changes in NAA would follow ATP. The impact acceleration model was used to produce three grades of TBI. Sprague-Dawley rats were divided into the following four groups: sham control (n = 12); moderate TBI (n = 36); severe TBI (n = 36); and severe TBI coupled with hypoxia-hypotension (n = 16). Animals were sacrificed at different time points ranging from 1 min to 120 h postinjury, and the brain was processed for high-performance liquid chromatography (HPLC) analysis of NAA and ATP. After moderate TBI, NAA reduced gradually by 35% at 6 h and 46% at 15 h, accompanied by a 57% and 45% reduction in ATP. A spontaneous recovery of NAA to 86% of baseline at 120 h was paralleled by a restoration in ATP. In severe TBI, NAA fell suddenly and did not recover, showing critical reduction (60%) at 48 h. ATP was reduced by 70% and also did not recover. Maximum NAA and ATP decrease occurred with secondary insult (80% and 90%, respectively, at 48 h). These data show that, at 48 h post diffuse TBI, reduction of NAA is graded according to the severity of insult. NAA recovers if the degree of injury is moderate and not accompanied by secondary insult. The highly similar time course and correlation between NAA and ATP supports the notion that NAA reduction is related to energetic impairment.

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The radial approach in CTO PCI is as fast and successful as the femoral approach with comparable in hospital MACE. However, there are far less access site complications with radial approach.

It is well established in mechanical head trauma that posttraumatic secondary insults, such as hypoxia and hypotension exacerbate neuronal injury and lead to worse outcome. In this study, the neuroprotective effect of hypothermia on the reduction of supraventricular subcortical neuronal damage was evaluated using an impact-acceleration model of diffuse traumatic brain injury coupled with both moderate and severe periods of hypoxia and hypotension. A total of 135 adult male Sprague-Dawley rats (340-375 g) were divided into three experimental studies: (I) physiological evaluation (n = 36); (II) quantitative analysis of the effect of trauma coupled with moderate and severe hypotension on neuronal damage assessed at 4 (n = 39) and 24 h (n = 24); and (III) the neuroprotective effect of hypothermia following moderate secondary insult (n = 36). Induction of hypothermia occurred at 15 min postinjury, to a level of 30 degrees C for 60 min. At the designated time points (4 and 24 h), the animals were sacrificed via standard transcardial perfusion techniques for histological processing. Quantitative assessment of neuronal damage using routine H&E staining at 4 hours showed neuronal damage which correlated with the severity of secondary insult. Animals exposed to trauma alone had a mean number of damaged neurons of 7.61 +/- 3.08/high powered field (hpf) compared with a mean of 1.21 +/- 0.30/hpf in the sham operated group (p = 0.015). Animals exposed to trauma with 10 min of hypoxia and hypotension (THH-10) showed a statistically significant number of damaged neurons compared to the sham-operated animals (7.50 +/- 2.15 damaged neurons/hpf, p = 0.013), whereas, neuronal damage in animals undergoing trauma with a 30-min secondary insult of hypoxia and hypotension (THH-30) was markedly increased (100 +/- 30.20/hpf, p = 0.002). Statistical analysis showed no significant difference in neuronal damage in animals subjected to secondary insult alone. At 24 h, the evolution of neuronal damage in the trauma alone group (5.08 +/- 1.63/hpf) was relatively static; however, there was a remarkable increase in the neuronal damage of the THH-10 group (29.88 50 +/- 8.20/hpf). However, hypothermia provided nearly complete protection against secondary insults, and neuronal damage was equal to that of the trauma alone group (p = 0.42). The results of this study confirm that hypothermia provides remarkable protection against the adverse effects of neuronal damage exacerbated by secondary injury. This study also presents a new model of secondary insult, which can be used experimentally to further define the mechanism of increased vulnerability of the injured brain.

Objective: A combination of CT and MRI is recommended for radiotherapy planning of head and neck cancers, and optimal spatial co-registration is achieved by imaging in the treatment position using the necessary immobilisation devices on both occasions, something which requires wide-bore scanners. Quality assurance experiments were carried out to commission a newly installed 1.5-T widebore MRI scanner and a dedicated, flexible six-channel phased array head and neck coil. Methods: Signal-to-noise ratio (SNR) and spatial signal uniformity were quantified using a homogeneous aqueous phantom, and geometric distortion was quantified using a phantom with water-filled fiducials in a grid pattern. Volunteer scans were also used to determine the in vivo image quality. Clinically relevant T 1 weighted and T 2 weighted fat-suppressed sequences were assessed in multiple scan planes (both sequences fast spin echo based). The performance of two online signal uniformity correction schemes, one utilising low-resolution reference scans and the other not utilising low-resolution reference scans, was compared. Results: Geometric distortions, for a 635-kHz bandwidth, were ,1 mm for locations within 10 cm of the isocentre rising to 1.8 mm at 18 cm away. SNR was above 50, and uniformity in the axial plane was 71% and 95% before and after uniformity correction, respectively. Conclusion: The combined performance of the wide-bore scanner and the dedicated coil was adjudged adequate, although superior-inferior spatial coverage was slightly limited in the lower neck. Advances in knowledge: These results will be of interest to the increasing number of oncology centres that are seeking to incorporate MRI into planning practice using dedicated equipment.

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This study examines neuropsychological dysfunction after varying severities of the Impact Acceleration Model of diffuse traumatic brain injury. Adult rats (340 g-400 g) were divided into five groups, and exposed to varying degrees of Impact Acceleration Injury (1 m, 2 m, 2.1 m/500 g and second insult). After injury, animals were allowed to recover; acute neurological reflexes, beam walk score, beam balance score, inclined plane score, and Morris Water Maze score were then assessed at multiple time points. Injury of all severities caused significant motor and cognitive deficits. With milder injuries these effects were transient; however, with more severe injuries no recovery in function was seen. The addition of hypoxia and hypotension made a moderate injury worse than a severe injury. The acute neurological reflexes, the beam balance test and the inclined plane test distinguished between the more severely injured groups, but were affected less by mild injury. The beam walk test was sensitive to mild injury, but appeared unable to distinguish between the severe groups. The Morris Water Maze was sensitive for all injury groups, but appeared to adopt a different response profile with secondary insult. This study has for the first time characterized the degree of motor and cognitive deficits in rodents exposed to differing severities of Impact Acceleration Injury. These data confirm that the tests considered, and the Injury Model used, provide a useful system for the consideration of potential therapies which might ameliorate neuropsychological deficits in diffuse brain injury.