Cerebral Palsy

OBJECTIVE: The diagnosis and management of mild traumatic brain injury continues to be a subject of debate, with varying opinions regarding the extent to which organically based impairments vs the impact of other stressors cause ongoing disability. The aim of this study was to elucidate the possible abnormalities in benzodiazepine receptor uptake in the brains of patients with mild traumatic brain injury. Nine unmedicated patients with mild traumatic brain injury were investigated using 123I-iomazenil single photon emission computerized tomography (SPECT). DESIGN: A descriptive study comparing patients after mild traumatic brain injury with matched control subjects. SUBJECTS: Nine patients with mild traumatic brain injury and 5 controls. METHODS: The SPECT scan was taken 180 min after injection of tracer. Results and conclusion: All 9 patients had a significant increase (> 2 standard deviations higher than the mean of controls) in benzodiazepine receptor uptake in the prefrontal cortex and significantly higher frontal association cortex-to-average global brain activity ratios than in controls. This SPECT study demonstrated focally altered benzodiazepine receptor uptake in the prefrontal cortices in patients with mild traumatic brain injury.

SUMMARY: Radiation therapy, a mainstay in the treatment of many brain tumors, results in a variety of well-documented acute and chronic complications. Isolated cortical damage following irradiation represents an extremely rare delayed therapeutic complication, described only twice in the medical literature. We report this rare delayed complication in a patient following treatment of a right frontal anaplastic oligodendroglioma.

Recombinant tissue-type plasminogen activator (tPA) is the fibrinolytic drug of choice to treat stroke patients. However, a growing body of evidence indicates that besides its beneficial thrombolytic role, tPA can also have a deleterious effect on the ischaemic brain. Although ageing influences stroke incidence, complications and outcome, age-dependent relationships between endogenous tPA and stroke injuries have not been investigated yet. Here, we report that ageing is associated with a selective lowering of brain tPA expression in the murine brain. Moreover, our results show that albumin D site-binding protein (DBP) as a key age-associated regulator of the neuronal transcription of tPA. Additionally, inhibition of DBP-mediated tPA expression confers in vitro neuroprotection. Accordingly, reduced levels of tPA in old mice are associated with smaller excitotoxic/ischaemic injuries and protection of the permeability of the neurovascular unit during cerebral ischaemia. Likewise, we provide neuroradiological evidence indicating the existence of an inverse relationship between age and the volume of the ischaemic lesion in patients with acute ischaemic stroke. Together, these results indicate that the relationship among DBP, tPA and ageing play an important role in the outcome of cerebral ischaemia.

Aging has a striking impact on the arterial structure and function. The principal structural change with age is medial degeneration that leads to a progressive stiffening of the large elastic arteries. Large artery stiffening increases aortic systolic and pulse pressures through an increase in the forward incident wave and an early return of the backward reflected wave. Peripheral muscular arteries/arterioles are only minimally affected in structure by aging itself, but impaired vasomotor function can alter their impedance properties and thereby increase reflection magnitude. An augmented aortic pressure due to enhanced wave reflection increases wasted left ventricular effort and causes cardiac hypertrophy. Increased pulsatile pressure and flow stresses extend to the vulnerable microcirculation of vasodilated organs such as the brain and kidneys, and can predispose to cerebral lacunar infarction and albuminuria. Although most currently available vasodilators appear to have little direct effect on degenerated elastic arteries, they can act instead on less-degenerated muscular arteries to markedly reduce peripheral wave reflection magnitude and central aortic pressure, and thus contribute to the regression of left ventricular hypertrophy. Further studies are necessary to examine whether the effect of vasodilator therapy on reducing wave reflection contributes similarly to the prevention of microvascular damage in the brain and kidneys.

Blank firing pistols are generally considered to be harmless and these guns are not accepted as being firearms in most countries. Due to lack of legal regulations these guns are easily purchased by anyone aged over 18years. Reports of serious injuries and even fatalities due to these guns are increasing in the literature. These guns when modified or even unmodified can cause serious and potentially fatal injuries. Without doing any changes to the barrel, using blank or tear gas cartridges, firing at contact range can cause penetration of gas into the body including bone originated from gunpowder. We report two suicide cases shooting themselves at temporal region with a blank cartridge gun at contact range. There was no foreign body on radiological examination and there was no trajectory of a bullet inside the brain. In both cases the wound was at the right temporal region and there was defect at temporal bone. There was circular soot around this bone defect. The injury of the brain tissue was localized at the level of the defect but there was widespread subarachnoidal bleeding. We discussed the potential danger of these guns and stressed the need of legal regulations concerning these guns.

Goldenberg (Defective imitation of gestures in patients with damage in the left or right hemisphere. Journal of Neurology, Neurosurgery, and Psychiatry, 61, 176-180; 1996) proposed that the vulnerability of the imitation of meaningless gestures to right or left brain damage depends on the body parts that are involved in the gestures. Whereas imitation of hand postures was disturbed only in patients with left brain damage, imitation of finger postures was affected to similar degrees in left and right brain damage. Subsequent studies confirmed the selective vulnerability of hand postures to LBD but failed to replicate the severe disturbance of finger postures in RBD. In contrast to Goldenberg’s studies, these studies excluded RBD patients with neglect. The present investigation aimed to explore the relationship between spatial neglect and imitation of finger postures in RBD patients. Presence and severity of spatial neglect and accuracy of imitation of hand and finger postures were tested in 50 RBD patients. Disturbance of imitation was much more severe for finger than hand postures and was tightly correlated with severity of neglect. The number of errors was higher for fingers which from the patient’s perspective were located on the left side of the examiner’s demonstrating hand but this spatial bias was not sufficient to explain all errors. Possible causes for non-lateralized errors could be a general narrowing of the focus of attention and reduced capacity for processing of information which have been postulated to be regular companions of the lateral displacement of attention in spatial neglect.

The clinical presentation of traumatic brain injury (TBI) involves either mild, moderate, or severe injury to the head resulting in long-term and even permanent disability. The recapitulation of this clinical scenario in animal models should allow examination of the pathophysiology of the trauma and its treatment. To date, only a few studies have demonstrated TBI animal models encompassing the three levels of trauma severity. Thus, in the present study we characterized in mice and rats both brain histopathologic and behavioral alterations across a range of injury magnitudes arising from mild, moderate, and severe TBI produced by controlled cortical impact injury technique. Here, we replicated the previously observed TBI severity-dependent brain damage as revealed by 2,3,5-triphenyltetrazolium chloride staining (severe>moderate>mild) in rats, but also extended this pattern of histopathologic changes in mice. Moreover, we showed severity-dependent abnormalities in locomotor and cognitive behaviors in TBI-exposed rats and mice. Taken together, these results support the use of rodent models of TBI as a sensitive platform for investigations of the injury-induced neurostructural and behavioral deficits, which should serve as key outcome parameters for testing experimental therapeutics.

A mAb targeting the CD11d subunit of the leukocyte integrin CD11d/CD18 decreases intraspinal inflammation and oxidative damage leading to improved neurological outcomes in rodent models of SCI. CD11d/CD18 is the fourth member of the beta2-integrin family. Current evidence indicates that CD11d/CD18 is regulated differently than other beta2-integrins, suggesting that CD11d(+) leukocytes play a distinct role in inflammation. Although the transcriptional control of CD11d expression has been evaluated, control of the intracellular distribution of CD11d has not been addressed. For this reason and as a result of the potential of CD11d as a therapeutic target for SCI and possibly other CNS injuries, we investigated the intracellular localization and surface expression of CD11d in cultured cells. CD11d and CD18 were fused at their C-termini with YFP and mRFP, respectively. Flow cytometry and confocal microscopy demonstrated that rCD11d-YFP is expressed on the cell surface of leukocyte cell lines expressing CD18. In contrast, in heterologous cell lines, CD11d-YFP is retained intracellularly in the TGN. Coexpression of CD11d-YFP and CD18-mRFP relieves this intracellular restriction and allows the CD11d/CD18 heterodimer to be surface-expressed. Based on domain-swapping experiments with CD25, the extracellular domain of CD11d is required and sufficient for the observed intracellular retention in heterologous cells. Furthermore, the transmembrane and C-terminus are also required for proper heterodimerization with CD18 and localization to the plasma membrane. These findings suggest that multiple CD11d domains play a role in controlling intracellular location and association with CD18.

Evidence suggests that recovery from stroke damage results from the production of new synaptic pathways within surviving brain regions over weeks. To address whether brain function might redistribute more rapidly through preexisting pathways, we examined patterns of sensory-evoked depolarization in mouse somatosensory cortex within hours after targeted stroke to a subset of the forelimb sensory map. Brain activity was mapped with voltage-sensitive dye imaging allowing millisecond time resolution over 9 mm(2) of brain. Before targeted stroke, we report rapid activation of the forelimb area within 10 ms of contralateral forelimb stimulation and more delayed activation of related areas of cortex such as the hindlimb sensory and motor cortices. After stroke to a subset of the forelimb somatosensory cortex map, function was lost in ischemic areas within the forelimb map center, but maintained in regions 200-500 mum from blood flow deficits indicating the size of a perfused, but nonfunctional, penumbra. In many cases, stroke led to only partial loss of the forelimb map, indicating that a subset of a somatosensory domain can function on its own. Within the forelimb map spared by stroke, forelimb-stimulated responses became delayed in kinetics, and their center of activity shifted into adjacent hindlimb and posterior-lateral sensory areas. We conclude that the focus of forelimb-specific somatosensory cortex activity can be rapidly redistributed after ischemic damage. Given that redistribution occurs within an hour, the effect is likely to involve surviving accessory pathways and could potentially contribute to rapid behavioral compensation or direct future circuit rewiring.

INTRODUCTION: Trauma patients in an unresponsive state upon presentation to the Emergency Department have a poor prognosis. Rapid assessment of injuries combined with life-preserving therapy is required but defining the optimal strategy can be complicated when multiple organ systems are involved. This study analysed various categories of trauma patients with a Glasgow Coma Scale (GCS) of 3 on admission and evaluated the relation between injuries, clinical condition, treatment and outcome. PATIENTS AND METHODS: A retrospective cohort-study, performed at a level 1 Trauma Center from 2002 to 2005. Trauma patients of all ages with GCS of 3 (without sedation) and Injury Severity Score (ISS) >/=16 were included. The collected patient data comprised data on demographics, mechanism of injury, physiological condition on admission, diagnosis, ISS, treatment, admission to Intensive Care Unit, complications and outcome. RESULTS: Ninety-seven patients were included and divided into three groups based on the pathology that caused the GCS of 3: traumatic brain injury N=48 (49%), anoxic brain injury N=27 (28%) and haemorrhagic shock N=22 (23%). The overall mortality was 81%; 91% of the haemorrhagic shock patients, 81% of the ABI patients and 77% of the TBI patients died. Eighteen patients survived of whom five patients (5%) made a good recovery. The pupillary light response and pH on admission were related to mortality. No relation with ISS, age or hypothermia was found. DISCUSSION: Distinguishing salvageable patients from those beyond salvation remains problematic. This study illustrated the diversity of patients, their injuries and their condition upon presentation to the hospital as well as the limitations of therapy. CONCLUSION: Trauma patients with a GCS of 3 have a poor outcome. Despite aggressive treatment only 5% of the patients made a good recovery. Pupil reactivity and the pH on admission were found to be related to mortality.