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Results for “Craniocerebral Trauma”

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At least 19 recordsLinked to original sources
PubMed2007

The potential of melatonin in reducing morbidity-mortality after craniocerebral trauma.

Craniocerebral trauma (CCT) is the most frequent cause of morbidity-mortality as a result of an accident. The probable origins and etiologies are multifactorial and include free radical formation and oxidative stress, the suppression of nonspecific resistance, lymphocytopenia (disorder in the adhesion and activation of cells), opportunistic infections, regional macro and microcirculatory alterations, disruptive sleep-wake cycles and toxicity caused by therapeutic agents. These pathogenic factors contribute to the unfavorable development of clinical symptoms as the disease progresses. Melatonin (N-acetyl-5-methoxytryptamine) is an indoleamine endogenously produced in the pineal gland and in other organs and it is protective agent against damage following CCT. Some of the actions of melatonin that support its pharmacological use after CCT include its role as a scavenger of both oxygen and nitrogen-based reactants, stimulation of the activities of a variety of antioxidative enzymes (e.g. superoxide dismutase, glutathione peroxidase, glutathione reductase and catalase), inhibition of pro-inflammatory cytokines and activation-adhesion molecules which consequently reduces lymphocytopenia and infections by opportunistic organisms. The chronobiotic capacity of melatonin may also reset the natural circadian rhythm of sleep and wakefulness. Melatonin reduces the toxicity of the drugs used in the treatment of CCT and increases their efficacy. Finally, melatonin crosses the blood-brain barrier and reduces contusion volume and stabilizes cellular membranes preventing vasospasm and apoptosis of endothelial cells that occurs as a result of CCT.

Craniocerebral Trauma↗
PubMedDate not supplied

[A macro- and microscopic study of the status of the deep and median structures of the lymph circulatory system in craniocerebral trauma].

Craniocerebral injuries involve changes in the vascular plexuses and ependyma of the ventricles, and the severity of these changes varies, depending on the duration of the posttraumatic period and severity of the injury. Analysis of the time course of pathomorphological changes in the cerebral ventricular structures extend our notions on the role and impact of liquor circulation in the pathogenesis of craniocerebral injury. Structural changes in the vascular plexuses may disorder the function of the blood-liquor barrier and promote the development of hydrocephalus. Changes in the structure of the ependymal membrane may involve dysfunction of the liquor-encephalic barrier of the inner surface of the brain and promote the development of brain edema.

Adolescent↗
PubMed2001

[Multiple trauma with craniocerebral trauma. Early definitive surgical management of long bone fractures?].

Head injuries are found in 17.6% of all trauma in-patients and are the most common cause of death after injury (26.6%) in Germany. Main factors for the initial and follow up assessment are the Glasgow Coma Scale (GCS) and pupil reaction. These are of a very predictive value for the outcome and are essential for the emergency crew to choose the adequat trauma hospital. Secondary transport to a higher level trauma center is affected by additional risk factors and a delay in diagnosis resp. treatment. This will increase mortality and must be strictly avoided. Sufficient oxygenation and circulation prevent the patient from secondary brain damage. A low GCS (< or = 8 p.) or specific additional injuries are an indication for immediate intubation. The outcome in patients with a systolic blood pressure below 90 mmHg on arrival is worse: The longer the time of correction the lower the rate of survival. After resuscitation early fracture treatment depends on hemoglobin concentration, hemostasis, oxygenation, body temperature, injury pattern and on the initial cranial CT scan. Cerebral swelling, seen or expected, is a contraindication for definitive fracture stabilization. After resuscitation reassessment should be done including a second CT scan. Cerebral monitoring is best performed by continuous measuring of the intracranial and the arterial pressure. Their difference determines the cerebral perfusion pressure which should be 60 mmHg at least. Intracranial pressure rates below 20 mmHg are favourable. Optimal management within the first days is essential for good outcome.

Adolescent↗
PubMed1987

Contractures. A major complication of craniocerebral trauma.

Contractures in craniocerebral trauma patients are a common problem noted during inpatient rehabilitation. Many factors influence this complication. Seventy-five consecutive cases of craniocerebral trauma observed during a one-year period were evaluated as to the duration of coma, degree of paralysis, treatment facility, and presence of fractures including their relation to contractures. Contractures measured by standard goniometric techniques were defined as loss of range of motion in a joint to a degree that impedes activities of daily living. The incidence of contractures was 84%. The most commonly affected joints were the hips (81%), shoulders (76%), ankles (76%), and elbows (44%). There was a statistically significant increase in the presence of contractures with prolonged duration of coma. Patients with contractures that developed independently of the facility where treated were examined for the presence of fractures. The emphasis after acute craniocerebral trauma is on life preservation. Limb positioning and maintenance of joint motion, which are imperative for the functional activity, have not received the attention necessary for the long-range welfare of the patient.

Brain Injuries↗
PubMed2002

[Minor craniocerebral trauma].

Mild craniocerebral injury or mild traumatic brain injury (MTBI) predominates, occurring with an 80% frequency. A 1997 publication by the American Academy of Neurology clearly defines MTBI as a transient alteration of mental status, without any neurological deficit, that may or may not involve loss of consciousness or amnesia. On the Glasgow Coma Scale (GCS), mild craniocerebral injury corresponds to a score of 14 and 15. The GCS must be taken immediately. Advanced trauma life support follows primary survey methodology and ABCDE protocol. The prognosis in MTBI is significantly worse when the patient suffers from intercurrent hypotension and hypoxia. In smaller hospitals, 24-hour monitoring is imperative. Wherever computerized tomography (CT) is available, a CT examination is broadly indicated. There is no knowledge of any adverse effects on patients whose GCS worsened when the CT revealed normal findings.

Brain Concussion↗
PubMedDate not supplied

[Brain monoamine oxidase in craniocerebral trauma].

Effect of craniocerebral trauma on monoamine oxidase (MAO) activity was studied. The activity of MAO with monoamines as substrates was shown to decrease. In this case transformation of MAO properties was observed: the enzyme exhibited an ability to deaminate di- and polyamines.

Animals↗
PubMedDate not supplied

[The effect of substances with nootropic activity on oxidative phosphorylation in brain mitochondria in acute craniocerebral trauma].

An open craniocerebral trauma was simulated in rat experiments. Oxidative phosphorylation in the brain mitochondria was studied by polygraphy 24 h after the trauma. It was found that trauma to the brain leads to inhibition of respiration in mitochondria in various metabolic states. Nooglutil in a dose of 50 mg/kg prevents these changes. Nooglutil is more effective than picamilon (500 mg/kg) and piriditol (100 mg/kg).

Acute Disease↗
PubMed1983

Rehabilitation of craniocerebral trauma.

Rehabilitation of the craniocerebral trauma patient is an increasing challenge worldwide. The return of these individuals to society requires the foresight to begin rehabilitation efforts as soon as the patient receives medical attention. This article reviews the spectrum of medical, physical, and social problems associated with craniocerebral trauma and provides guidelines for the rehabilitation process.

Brain Injuries↗
PubMed1999

[The activity of free-radical lipid-peroxidative reactions in the acute and late periods of severe craniocerebral trauma].

Severe craniocerebral injury is shown to result in intensification of processes of lipid peroxidation (LPO), decline in activity of the antioxidant system, which facts lead to further damage to the injured brain caused by products of LPO processes. Activity of LPO processes is recordable as is decline in activity of the antioxidant system after the treatment administered and in 12 and 24 months following the injury sustained as well. The authors recommend that natural and synthetic antioxidants be included into a complex of measures designed to treat severe craniocerebral injury.

Acute Disease↗
PubMed2003

The risk factors of nosocomial infection in severe craniocerebral trauma.

OBJECTIVE: To explore the risk factors of nosocomial infection in severe craniocerebral trauma and the way of prevention. METHODS: The clinical data of 387 patients with severe craniocerebral trauma were reviewed. RESULTS: The total nosocomial infection rate of this study was 22.99%. Pulmonary nosocomial infection presented most frequently. The G-bacilli were the most common infectious bacteria. The mortality rate of the infection group was 38.20%. CONCLUSIONS: Complications of nosocomial infection affect the prognosis of craniocerebral trauma patients. Nosocomial infection is related to the age of the patients, craniocerebral trauma severity, unreasonable utilization of antibiotics and invasive operations, such as tracheal cannula, mechanical ventilation, urethral catheterization and deep venous catheterization. Patients with severe craniocerebral trauma should be carefully treated and nursed to avoid nosocomial infection. In order to reduce the rate of nosocomial infection, intensive measurement should be adopted.

Adolescent↗
PubMedDate not supplied

[The possibility of developing shock in craniocerebral trauma].

It was established in acute experiments on dogs and rabbits that craniocerebral trauma does not lead to the development of torpid shock. In combination of craniocerebral trauma with severe mechanical injury to the thigh or acute massive extracranial blood loss a typical torpid shock develops with death of the animals in the immediate hours. Infusion therapy relieves shock but fails to prevent the development of brain edema. Intravenous injections of procaine hydrochloride have a positive effect in craniocerebral trauma and shock. It is concluded that craniocerebral trauma does not disturb the mechanisms of shock formation and the process takes a course independently of the process of brain edema development.

Acute Disease↗
PubMed1991

Endocrine abnormalities in severe traumatic brain injury--a cue to prognosis in severe craniocerebral trauma?

Patients with severe craniocerebral trauma (sCCT) display metabolic and endocrine changes. The question is raised whether hormonal patterns give cues to the prognosis of outcome or not. In 21 patients the function of the adrenocortical, gonadal, thyroid and human growth hormone (hGH)-insulin system was assessed. LH, FSH, TSH, prolactin and hGH were stimulated. 3 groups of patients were formed. Group I: patients in acute phase with a Glasgow Coma Score (GCS) more than 6 (group Ia) and less than 6 (group Ib). Group II: patients in transition to traumatic apallic syndrome (TAS). Group III: patients with full-blown or resolving TAS. The values of group Ia comprised low T3, T4 and testosterone, elevated insulin, normal hGH. Group Ib had hypothyroid T3 and T4 and an attenuated response of LH, TSH, prolactin and hGH to stimulation. Group III: there was seen an endocrine normalisation with elevated T4 and TBG and an altered response of hGH and prolactin to stimulation. Endocrine abnormalities were not helpful in predicting which course, either to better or to worse, a given patient would follow.

Adolescent↗
PubMed2003

[Craniocerebral trauma].

In cases of craniocerebral trauma there may be primary and secondary cerebral lesions. The principal goal of treatment is to minimize secondary cerebral trauma by optimized therapy. In the primary treatment phase monitoring of vital signs (blood pressure and respiration) is of crucial importance. CT diagnosis is followed by treatment of any increase in intracranial pressure by relief of hematomas, CSF drainage and appropriate intensive care measures.

Abbreviated Injury Scale↗
PubMed1989

[Ca2+-phospholipid-dependent phosphorylation of cytosol and membrane proteins of the brain in light craniocerebral trauma].

Immediately after light craniocerebral trauma (LCCT) the system of Ca2+, phospholipid-dependent phosphorylation of cytosol and microsomes of diencephalic-brainstem regions was impaired. The system of regulation of activity of C-kinase by phosphatidylserine was upset in the course of posttraumatic period and was different for cytosol and hemispheres. The increase in phosphorylation upon addition of exogenic C-kinase to incubation medium was evident only with stimulation of endogenic phosphorylation by phosphatidylserine. The decrease in Ca2+, phospholipid-dependent phosphorylation was characteristic of all fractions studied 1 day after trauma. After 14 days, the enzyme activity did not return to baseline. The authors suggest that C-kinase participates in trigger mechanisms of posttraumatic disease.

Animals↗
PubMed1988

[Treatment and results in severe craniocerebral trauma].

Treatment of severe craniocerebral traumas in medium and major hospitals not provided with special neurosurgical equipment requires particularly close interdisciplinary cooperation between surgeons, neurologists and anaesthesiologists. CT facilities are an essential prerequisite for best possible patient care. Patient safety during the posttraumatic and postoperative phases is improved by measuring the intracranial pressure. Whereas corticosteroid treatment may be arguable, barbiturate treatment should presently not be a routine procedure because of its side effects and high rate of complications.

Brain Concussion↗
PubMedDate not supplied

Trauma radiology: Part IV. Imaging of acute craniocerebral trauma.

Diagnostic imaging has a key role in diagnosis and management of patients sustaining craniocerebral injuries from trauma. We review the current role of skull radiography, computed tomography (CT), and magnetic resonance (MR) in imaging patients sustaining craniocerebral trauma, and we describe the appearance of major forms of pathology as depicted by each modality. CT scan is used to assess quickly the extent of injury and to triage patients to observation, medical, or neurosurgical management. CT findings can be divided into primary craniocerebral injuries, including skull fractures; extraaxial hematomas (subdural and epidural); intraparenchymal injury, such as hematoma, contusion, and diffuse axonal shearing; and intraventricular or subarachnoid hemorrhage. Secondary manifestations of injury, such as cerebral edema and herniation, are also identified, and their course can be followed by serial CT. CT is crucial in assessing the outcome of surgical intervention and in identifying potential delayed complications of either head trauma or surgical intervention, including infection, delayed hemorrhage, cerebral infarction, and tension pneumocephalus. In recent years, MRI has been shown to be valuable in diagnosing cerebral injury. MRI has generally been shown to have greater overall accuracy than CT in identifying and characterizing most forms of traumatic cerebral pathology, but it is less accurate at demonstrating subarachnoid hemorrhage acutely, pneumocephalus, and calvarial fractures, particularly those involving the skull base. Moreover, MRI is still more difficult to perform than CT in critically ill patients, and it is generally far more time-consuming. However, MRI is unequivocally more accurate than CT at revealing certain lesions, particularly brainstem contusion, diffuse axonal shearing, predominantly nonhemorrhagic contusions, and thin collections of blood adjacent to bone, and it should be used selectively when these injuries are suspected.

Craniocerebral Trauma↗