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At least 19 recordsLinked to original sources
PubMed1998

Accumulation of passively transferred primed T cells independently of their antigen specificity following central nervous system trauma.

The central nervous system (CNS) enjoys a unique relationship with the immune system. Under non-pathological conditions, T cells move through the CNS but do not accumulate there. CNS trauma has been shown to trigger a response to CNS self-antigens such as myelin basic protein (MBP). Here, we examined whether the injured CNS tissue undergoes changes that permit T cell accumulation. We found that injury to CNS white matter, such as the optic nerve, led to a transiently increased accumulation of T cells (between days 3 and 21). In Lewis rats with unilaterally injured optic nerves, systemic administration of passively transferred T cells recognizing either self-antigen (MBP) or non-self-antigen (ovalbumin) resulted in accumulation of the T cells in injured optic nerve, irrespective of their antigenic specificity. The effect of the T cells on the damaged nerve, the lack of selectivity in T cell accumulation and the mechanism underlying non-selective accumulation are discussed.

Animals↗
PubMed1992

Association of perinatal events, epilepsy, and central nervous system trauma with juvenile delinquency.

The association of perinatal events, childhood epilepsy, and central nervous system trauma with juvenile delinquency was studied prospectively in a geographically defined population of 5966 males in northern Finland. Those who had obtained a criminal record up to the age of 22 years, totalling 355, or 6.0%, were defined as delinquents. The incidence of delinquency was not increased in males with a birth weight less than 2500 g or greater than 4000 g, preterm births < 37 weeks' gestation, or those with perinatal brain damage or having epileptic seizures before 14 years of age. The incidence was increased by 6.8% in the group of males with birth weights less than 3500 g, but not significantly increased after standardisation for a number of social and demographic background variables. The incidence was increased by 10.3% among the males who had had a central nervous system trauma by the age of 14 years, however, and this factor remained significant when social and demographic factors were standardised by regression analysis, with an odds ratio of 1.9 for all males with a criminal record and an odds ratio of 3.15 for those who had committed a violent crime. Previous central nervous system trauma may be a cause of delinquency, or another possibility is that the type of behaviour pursued by males who are likely to commit a violent crime will expose them more often to accidents which can result in central nervous system trauma.

Adolescent↗
PubMed1987

Central nervous system trauma.

Traumatic injury to the central nervous system causes immediate damage and sets in motion a complex series of pathophysiologic events that result in further neuronal injury. This secondary damage seems to be related to changes in blood flow and pressure on a systemic, regional, and microvascular level. Currently, there is evidence that these changes are, in part, mediated by endogenous opioids and arachidonic acid metabolites, namely thromboxane A2. Medical management is generally designed to intervene at one or more stages in this secondary cascade of events. Further research should lead us to better understanding of the mechanisms involved in trauma to the central nervous system and, subsequently, more specific and effective treatments.

Animals↗
PubMed1986

Resuscitation of patients with central nervous system trauma.

The care patients with spinal cord or head injury receive in the acute phase of their injury is critical to outcome. The basics of trauma care are of primary importance to the patient with central nervous system trauma. In the SCI patient, extreme care must be used in establishing an airway. The focus in the head-injured patient is to provide adequate oxygenation and ventilation sufficient to cause hypocarbia. Proper immobilization of the neck is a priority concomitant to establishing an airway in the SCI patient, while control of ICP is a challenge in the head-injured patient. Paramedics, nurses, and physicians who are aware of these important factors in caring for the neurotrauma patient will ensure the patient every chance of functional recovery.

Coma↗
PubMed2001

Protective autoimmunity as a T-cell response to central nervous system trauma: prospects for therapeutic vaccines.

Immune activity in general, and autoimmunity in particular, have long been considered as harmful in the context of central nervous system (CNS) trauma. Increasing evidence suggests, however, that the injured CNS can benefit from autoimmune manipulations. Active or passive immunization with CNS-associated self antigens was shown to promote recovery from a CNS insult. It is now also evident that this beneficial 'autoimmunity' is not solely an outcome of immune manipulation but is also a physiological response, evoked by a non-pathogenic insult and apparently designed to counteract the insult-related toxicity which is induced in part by essential physiological compounds present in excess of their normal levels. It appears that when the buffering capacity of constitutive local mechanisms (transporters, enzymes, etc.) that normally regulate these compounds is exceeded, assistance is recruited from the immune system. Like the overactive physiological compounds themselves, the immune system needs to be rigorously regulated in order to produce adequate phagocytic activity and the required quantity of cytokines and growth factors at the right time and place. Boosting of this autoimmune response is potentially a powerful strategy for neuroprotective therapy.

Animals↗
PubMed1995

Neurotrophic factors in central nervous system trauma.

Although regeneration of injured neurons does not occur after trauma in the central nervous system (CNS), there is often significant recovery of functional capacity with time. Little is currently known about the molecular basis for such recovery, but the increased trophic activity in injured CNS tissue and the known properties of neurotrophic factors in neuronal growth and maintenance suggest that these polypeptides are probably involved in recovery of function. Members of the neurotrophin family, including nerve growth factor (NGF), brain-derived neurotrophic factors (BDNF), and neurotrophin 3 (NT-3), are capable of supporting survival of injured CNS neurons both in vitro and in vivo. They also stimulate neurite outgrowth, needed for reorganization of the injured CNS, and the expression of key enzymes for neurotransmitter synthesis that may need to be upregulated to compensate for reduced innervation. The effects of the neurotrophins are mediated through specific high affinity trk receptors (trk A, B, C) as well as a common low affinity receptor designated p75NGFR. Another class of neurotrophic polypeptides also provides candidate recovery-promoting molecules, the heparin-binding growth factors' acidic and basic fibroblast growth factor (aFGF, bFGF). FGFs not only sustain survival of injured neurons but also stimulate revascularization and certain glial responses to injury. Both the neurotrophins and the FGFs, as well as their respective receptors, have been shown to be upregulated after experimental CNS injury. Further, administration of neurotrophins or FGF has been shown to reduce the effects of experimental injury induced by axotomy, excitotoxins, and certain other neurotoxins. The cellular basis for the potential therapeutic use of neurotrophic molecules is discussed as well as new strategies to increase neurotrophic activity after CNS trauma based on the recently obtained information on pharmacological and molecular control of the expression of these genes.

Animals↗
PubMed1986

Pathophysiology of cerebrospinal fluid in head injury: Part 2. Biochemical markers for central nervous system trauma.

Many substances are released into the cerebrospinal fluid after head injury. The study of these substances and their relationship to the severity and outcome of head trauma has lead to the search for biochemical markers to aid in the quantification of the severity of the lesion and serve as a prognostic guide. The authors review the potential usefulness of biochemical markers, qualities of an ideal marker, and several potential enzymes that may be utilized as markers in central nervous system trauma.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1997

Magnetic resonance imaging: utilization in the management of central nervous system trauma.

OBJECTIVE: To determine the availability, use, and perceived value of magnetic resonance imaging (MR) in the management of acute central nervous system (CNS) trauma in United States Level I (or equivalent) trauma centers (TCs). DESIGN, MATERIALS, AND METHODS: One hundred sixty-nine American College of Surgeons, state or locally designated Level I (or equivalent) TCs were identified using compiled lists and telephone contacts. Surveys about MR use in CNS trauma were mailed to each institution. Follow-up telephone calls were made to nonresponding institutions. Data were analyzed using frequency distribution. MEASUREMENTS: Using returned questionnaires from trauma directors and follow-up telephone contacts, data on the physical location, technologist availability, and patient monitoring capabilities were accrued. The questionnaire addressed the perceived value and cost-effectiveness of MR for acute CNS trauma in general, distinguishing between spinal cord and traumatic brain injury, using a Likert-type rating scale. MAIN RESULTS: One hundred nine (65%) of identified TCs responded by mail. Sixty (33%) required contact by telephone. One hundred fifty-two (93%) reported MR scanners "on site." Five of seven TCs without on-site MR had facilities within 5 miles. No TC reported the inability to obtain MR scans. Seventy-four percent of TCs reported MR angiography capabilities. Ninety-seven percent of MR facilities were staffed 24 hours per day, 83% by on-call, out-of-hospital technologists at night and on weekends. TCs reported patient monitoring capabilities including cardiac monitoring (83%) and pulse oximetry (91%). Seventy-one percent reported the ability to scan intubated patients. Forty-five percent of TCs "rarely" use MR, 51% report "occasional" use, and 4% "frequently" use MR for acute trauma. Ninety-four percent of trauma directors agreed or strongly agreed that MR directed management and was cost-effective for spinal cord trauma. Fifty-four percent agreed or strongly agreed that MR directed management and was cost-effective for traumatic brain injury. No correlation existed between perceptions of MR applicability in CNS trauma and the number of trauma admissions or on-site availability. CONCLUSIONS: Most trauma directors consider MR important in the acute evaluation of spinal trauma and, to a lesser extent, for traumatic brain injury. Despite these opinions, the vast majority of these centers reported only "rare" to "occasional" use of MR in the setting of acute CNS trauma. Our results show that most TCs have on-site and continuously available MR facilities capable of cardiac and pulmonary monitoring. Other factors such as the higher relative cost of MR may be responsible for the discrepancy between the perceived value and the actual utilization of MR imaging in the setting of CNS trauma.

Brain Injuries↗
PubMed1979

An injury severity scale for comprehensive management of central nervous system trauma.

The Glasgow Coma Scale (GCS) is used in central Virginia by emergency medical technicians (EMT's), emergency department personnel and neurosurgical staff to evaluate patients with central nervous system (CNS) trauma. In a series of 406 patients admitted to the neurosurgical services at the University of Virgina Hospital between October 1977 and February 1978, a GCS score was recorded by the neurosurgeon, nurse, and EMT. All 250 data points, including clinical diagnosis and incidence of associated injuries were entered into our information system analysis. The scale can be easily mastered by all members of the emergency medical team giving reproducible results. It also appears to be a valid predictor of the ultimate outcomes of head injury. The GCS has substantial clinical value in the management of the nuerotrauma patient. It is presently being employed in all phases of the emergency medical system to monitor the progression of the neurologic injury. Ultimately, this injury severity scoring system will be used to standardize patient populations in well controlled clinical studies in which different treatment parameters will be assessed.

Adolescent↗
PubMed1975

Dimethyl sulfoxide in central nervous system trauma.

Dimethyl sulfoxide has been tested in various experimental injuries of the central nervous system in relation to other therapies. It appears to be a useful drug in acute extradural mass-forming lesions, middle cerebral artery occlusion, respiratory anoxia, and spinal cord injuries, in rhesus and squirrel monkeys, dogs, and rats. The data from these studies suggest that in the experimental models used, DMSO is clearly superior to no treatment, and appears to be more generally effective than other comparable treatments. No satisfactory answer has yet been found to explain the beneficial effects of DMSO, but several hypothetical suggestions are offered; their validation hinges primarily on further confirmatory evidence. Further experiments with our present models and alternative research lines are discussed.

Animals↗
PubMed1989

Central nervous system trauma and stroke. I. Biochemical considerations for oxygen radical formation and lipid peroxidation.

The generation of oxygen radicals and the process of lipid peroxidation have become a focus of attention for investigators in the fields of central nervous system (CNS) trauma and stroke (e.g., ischemia). Considering our level of understanding of free radical and lipid peroxidation chemistry, absolute proof for their involvement in the pathophysiology of traumatic and ischemic damage to the CNS has been meager. While direct, unequivocal evidence for the participation of free radicals and lipid peroxidation as primary contributors to the death of neuronal tissue waits to be established, numerous recent studies have provided considerable support for the occurrence of free radical and lipid peroxidation reactions in the injured or ischemic CNS. In addition, the pharmacological use of antioxidants and free radical scavengers in the treatment of experimental CNS trauma and ischemia has provided convincing, although indirect evidence, for the involvement of oxygen radicals and lipid peroxidation in these conditions. The intent of this and its companion paper is to review: 1) the biochemical processes which may give rise to free radical reactions in the CNS, 2) the environment of the ischemic cell as it may affect the generation of oxygen radicals and the catalysis of lipid peroxidation reactions, 3) the evidence for the involvement of free radical mechanisms in CNS trauma and ischemia, and 4) the pathophysiological consequences of these phenomena.

Animals↗
PubMed1989

Central nervous system trauma and stroke. II. Physiological and pharmacological evidence for involvement of oxygen radicals and lipid peroxidation.

The previous article outlined the biochemical basis and evidence for the occurrence of oxygen radical generation and lipid peroxidation during the acute phase of central nervous system (CNS) trauma or stroke (ischemic and hemorrhagic). The identification of oxygen radicals and lipid peroxidation as important pathophysiological mediators of trauma or stroke-induced neural degeneration, rather than simply epiphenomena, depends upon the successful demonstration of their association with actual secondary physiological and structural degenerative events. Moreover, their significance in the pathophysiology of CNS trauma or stroke must be supported by experimental observations that pharmacological antagonism of either oxygen radical generation and/or lipid peroxidation results in a therapeutic effect (i.e., interruption of secondary nervous tissue degeneration). Indeed, recent investigations have provided compelling evidence for the view that oxygen radical-mediated processes play a key pathophysiological role during the acute phase of CNS trauma or stroke. Furthermore, their pharmacological manipulation may serve as an avenue for therapeutic attempts aimed at limiting neural degeneration and improving neurological recovery.

Animals↗
PubMed1979

The neurologic examination in patients with central nervous system trauma.

The neurological assessment of the head injured patient must be integrated into the emergency management and daily care of the patient. Neurosurgical nurses are in the best position to perform serial neurologic examinations and assess changes in the patient's clinical picture. If this added responsibility is assumed, neurosurgical nurses must take an active role in improving assessment skills. The improved assessment of the head injured patient will result in early intervention in the patient's course to avert potential problems, thus resulting in improved morbidity and eventual outcome. As neurosurgical nurses expand their roles in nursing, improved patient assessments are mandatory to deliver optimal patient care.

Humans↗
PubMed2004

Neuro-ophthalmologic diagnosis and therapy of central nervous system trauma.

Although direct injury to the orbit and globes can easily result in ophthalmologic disorders, it is less appreciated that distant head injury can similarly result in injury to the retrobulbar afferent visual pathways or cranial nerves. The physician must be suspicious of latent and manifest injuries to the neuro-ophthalmologic system after head trauma and maintain an awareness of the need for timely intervention in a subset of these disorders. Even patients with injuries removed from the eyes should be checked for visual problems, and if any are detected, a careful neuro-ophthalmologic examination should be performed. In most cases, examination and judicious use of neuroimaging will help in choosing the appropriate management for injuries to the afferent and efferent visual systems.

Craniocerebral Trauma↗