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22 results of 7 texts with exact phrase : 'traumatic brain injury'.

1. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, Vol. 1, 2005 , , ,

Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain Injury.
Lang EW, Czosnyka M, Mehdorn HM. Tissue oxygen reactivity and cerebral autoregulation after severe traumatic brain Injury.
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Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: Validation and utility.
Lang EW, Lagopoulos J, Griffith J, Yip K, Mudaliar Y, Mehdorn M, Dorsch NW. Noninvasive cerebrovascular autoregulation assessment in traumatic brain injury: Validation and utility.
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2. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 8, 2012, No. 1 , , ,

Benzodiazepines and antipsychotics appear to slow recovery after traumatic brain injury and stroke.
combined with a therapy program. Dopaminergic and acetylcholinesterase inhibitors improve memory. Benzodiazepines and antipsychotics appear to slow recovery after traumatic brain injury and stroke. Modern neuroimaging technologies allow monitoring of neurophysiologic changes and expand the knowledge about the factors affecting the rehabilitation processes [4].
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It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke.
It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke. The combined use of transcranial magnetic stimulation improves cortical activation and may be a useful therapy adjunct [27]. Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3). An important fact is that general aerobic exercise programs stimulate CNS plasticity. Functional electrical stimulation enhances somatosensory input to the brain. Continued activity and training after formal therapy is necessary to preserve functional gains [17].
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Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3).
It has been shown that reduced activation of the ipsilateral hemisphere improves motor function in both healthy individuals and those with traumatic brain injury or stroke. The combined use of transcranial magnetic stimulation improves cortical activation and may be a useful therapy adjunct [27]. Robot-assisted practice may be helpful by implementation of repetitive training tasks; body weight-supported treadmill training promotes gait improvement after traumatic brain injury, stroke or partial spinal cord injury (fig. 3). An important fact is that general aerobic exercise programs stimulate CNS plasticity. Functional electrical stimulation enhances somatosensory input to the brain. Continued activity and training after formal therapy is necessary to preserve functional gains [17].
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Treatment is directed towards reduction of complications following traumatic brain injury (TBI).
Treatment is directed towards reduction of complications following traumatic brain injury (TBI). The recovery prognosis correlates with the duration of posttraumatic amnesia [43]. Cognitive and behavioral changes and disorders of executive functions are common in traumatic injuries of the frontal lobe [37], which may cause mental retardation in children. Impaired social functions of patients worsen the long-term family relations. Cognitive and behavioral deficits prevent returning to school or work environment. Even though the sequence of recovery after TBI follows a certain model, it is a heterogeneous disorder and rehabilitation programs must be adapted to patient’s individual needs – change of environment, training of relatives.
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Neurobehavioral management of traumatic brain injury in the critical care setting.
Arciniegas DB, McAllister TW. Neurobehavioral management of traumatic brain injury in the critical care setting.
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Medication in the treatment of the behavioural sequelae of traumatic brain injury.
Bates G. Medication in the treatment of the behavioural sequelae of traumatic brain injury.
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Relation of executive functioning to pragmatic outcome following severe traumatic brain injury.
Douglas JM. Relation of executive functioning to pragmatic outcome following severe traumatic brain injury.
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Neurologic examination of the patient with traumatic brain injury.
Gelber DA, Callahan CD. Neurologic examination of the patient with traumatic brain injury. In: Ashley MJ, editor. Traumatic brain injury: rehabilitation, treatment, and case management. 3rd ed. Boca Raton, FL, CRC Press, 2010, 3-27.
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Traumatic brain injury: rehabilitation, treatment, and case management.
Gelber DA, Callahan CD. Neurologic examination of the patient with traumatic brain injury. In: Ashley MJ, editor. Traumatic brain injury: rehabilitation, treatment, and case management. 3rd ed. Boca Raton, FL, CRC Press, 2010, 3-27.
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Aging with traumatic brain injury: cross-sectional follow-up of people receiving inpatient rehabilitation over more than 3 decades.
Sendroy-Terrill M, Whiteneck GG, Brooks CA. Aging with traumatic brain injury: cross-sectional follow-up of people receiving inpatient rehabilitation over more than 3 decades.
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Traumatic brain injury in the United States: assessing outcomes in children,
Traumatic brain injury in the United States: assessing outcomes in children,
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3. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 2, 2012, No. 2 , , ,

Hypotermia therapy after traumatic brain injury in children.
Hutchison E, Ward R, Lacroix J, Hebert P, Barnes M, bohn D, Dorks P. Hypotermia therapy after traumatic brain injury in children.
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4. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 9, 2013, No. 2 , , ,

Specific TCD Clinical Applications for Patients with Traumatic Brain Injury.
Specific TCD Clinical Applications for Patients with Traumatic Brain Injury.
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Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
TCD findings compatible with the diagnosis of brain death include systolic spikes without diastolic flow or with diastolic reversed flow, and no demonstrable flow in a patient in who flow had been clearly documented on a previous examination. Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
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SPECIFIC TCD CLINICAL APPLICATIONS FOR PATIENTS WITH TRAUMATIC BRAIN INJURY
SPECIFIC TCD CLINICAL APPLICATIONS FOR PATIENTS WITH TRAUMATIC BRAIN INJURY
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Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances.
Critical care management of patients with traumatic brain injury (TBI) has undergone tremendous advances. Neurosurgeons, neurologists and neurointensivists, including military, have a large armamentarium of invasive monitoring modalities available to detect secondary brain injury and guide therapy. The primary goal monitoring is to prevent secondary insults to the brain, primarily cerebral ischemia due to the posttraumatic vasospasm (PTV), and intracranial hypertension (ICH). This lecture summarizes the advantages and the specific roles of transcranial Doppler (TCD) ultrasound to establish and monitor the presence of PTV and ICH.
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intracranial hypertension, posttraumatic vasospasm, transcranial Doppler ultrasound, traumatic brain injury.
intracranial hypertension, posttraumatic vasospasm, transcranial Doppler ultrasound, traumatic brain injury.
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5. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 1 , , ,

Quality of life after hemicraniectomy for traumatic brain injury in adults.
Danish SF, Barone D, Lega BC, Stein SC. Quality of life after hemicraniectomy for traumatic brain injury in adults. A review of the literature.
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6. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 10, 2014, No. 2 , , ,

Sometimes its application could induce heterogenic reaction, especially in traumatic brain injury.
The test with breath-holding for 30 sec, where the induced hypercapnia causes vasodilatation is easy to perform and suitable for screening. The test could be expanded with applying of hyperventilation (hypocapnia) and consequent calculation of the index of total vasomotor reactivity and the vasomotor range. The hypocapnia exerts vasoconstrictive effect and it has been used for mapping of the cerebral VMR. Sometimes its application could induce heterogenic reaction, especially in traumatic brain injury. The disadvantage of the breath-holding test is the inability to control the lung ventilation [5].
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7. NEUROSONOLOGY AND CEREBRAL HEMODYNAMICS, vol. 12, 2016, No. 2 , , ,

Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury.
It has been frequently employed for the clinical evaluation of cerebral vasospasm following subarachnoid hemorrhage (SAH). To a lesser degree, TCD has also been used to evaluate cerebral autoregulatory capacity, monitor cerebral circulation during cardiopulmonary bypass and carotid endarterectomy, to diagnose brain death and for monitoring of cerebral hemodynamics in neurotrauma. TCD is a suitable bedside method for daily assessment of the changes of intracranial pressure (ICP) by continuous monitoring of the changes of blood flow velocities and pulsatility index (PI), reflecting decreases in cerebral perfusion pressure due to increases in ICP. Growing body of literature demonstrates the usefulness of transbulbar B-mode sonography of the optic nerve for detecting increased ICP in patients requiring neurocritical care. TCD findings compatible with the diagnosis of brain death include systolic spikes without diastolic flow or with diastolic reversed flow, and no demonstrable flow in a patient in who flow had been clearly documented on a previous examination. Assessment of cerebral autoregulation using TCD blood flow velocity has been previously validated to be predictive of outcome following traumatic brain injury. The commonly used bedside methods of determining the status of autoregulation include the transient hyperemic response test, the leg-cuff deflation test and reaction to spontaneous blood pressure fluctuations. TCD PI has emerged as a surrogate marker for ICP. The measurement of PI is also an useful adjunct to guide the use of hyperosmolar therapy in various conditions with intracranial hypertension.
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