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Brain-injured Patients (brain-injured + patient)
Selected AbstractsActive cooling in traumatic brain-injured patients: a questionable therapy?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 10 2009P.-O. GRÄNDE Hypothermia is shown to be beneficial for the outcome after a transient global brain ischaemia through its neuroprotective effect. Whether this is also the case after focal ischaemia, such as following a severe traumatic brain injury (TBI), has been investigated in numerous studies, some of which have shown a tendency towards an improved outcome, whereas others have not been able to demonstrate any beneficial effect. A Cochrane report concluded that the majority of the trials that have already been published have been of low quality, with unclear allocation concealment. If only high-quality trials are considered, TBI patients treated with active cooling were more likely to die, a conclusion supported by a recent high-quality Canadian trial on children. Still, there is a belief that a modified protocol with a shorter time from the accident to the start of active cooling, longer cooling and rewarming time and better control of blood pressure and intracranial pressure would be beneficial for TBI patients. This belief has led to the instigation of new trials in adults and in children, including these types of protocol adjustments. The present review provides a short summary of our present knowledge of the use of active cooling in TBI patients, and presents some tentative explanations as to why active cooling has not been shown to be effective for outcome after TBI. We focus particularly on the compromised circulation of the penumbra zone, which may be further reduced by the stress caused by the difference in thermostat and body temperature and by the hypothermia-induced more frequent use of vasoconstrictors, and by the increased risk of contusional bleedings under hypothermia. We suggest that high fever should be reduced pharmacologically. [source] Mechanisms of motor-evoked potential facilitation following prolonged dual peripheral and central stimulation in humansTHE JOURNAL OF PHYSIOLOGY, Issue 2 2001M. C. Ridding 1Repetitive electrical peripheral nerve or muscle stimulation can induce a lasting increase in the excitability of the corticomotor projection. By pairing peripheral stimulation with transcranial magnetic brain stimulation it is possible to shorten the duration of stimulation needed to induce this effect. This ability to induce excitability changes in the motor cortex may be of significance for the rehabilitation of brain-injured patients. The mechanisms responsible for the increases in excitability have not been investigated thoroughly. 2Using two paired transcranial magnetic stimuli protocols we investigated the excitability of intracortical inhibitory and excitatory systems before and following a period of repetitive dual muscle and brain stimulation. The dual stimulation consisted of motor point stimulation of first dorsal interosseous (FDI; 10 Hz trains of 1 ms square waves for 500 ms) delivered at one train every 10 s, paired with single transcranial magnetic stimulation given 25 ms after the onset of the train. 3Following 30 min of dual stimulation, motor-evoked potentials (MEPs) were significantly increased in amplitude. During this period of MEP facilitation there was no significant difference in the level of intracortical inhibition. There was, however, a significant increase in the intracortical facilitation demonstrated with paired magnetic stimuli. The increase in facilitation was seen only at short interstimulus intervals (0.8-2.0 ms). These intervals comprised a peak in the time course of facilitation, which is thought to reflect I wave interaction within the motor cortex. 4The relevance of this finding to the MEP facilitation seen following dual peripheral and central stimulation is discussed. [source] Functional and proteomic analysis of serum and cerebrospinal fluid derived from patients with traumatic brain injury: a pilot studyANZ JOURNAL OF SURGERY, Issue 7-8 2010Dieter Cadosch Abstract Background:, An enhanced fracture healing response has been reported in patients with traumatic brain injury (TBI). This has been attributed to circulating humoral factors that are thought to be proteins produced and released by the injured brain. However, these factors remain unknown. The aim of this study was to identify osteogenic factors in serum and cerebrospinal fluid (CSF) from TBI patients. This was carried out using in vitro proliferation assays with the human foetal osteoblastic 1.19 cell line (hFOB) combined with a novel proteomic approach. Methods:, Serum was collected from brain-injured (n = 12) and non-brain-injured (n = 9) patients with a comorbid femur shaft fracture. Similarly, CSF was obtained from TBI (n = 7) and non-TBI (n = 9) patients. The osteoinductive potential of these samples was determined by measuring the in vitro proliferation rate of hFOB cells. Highly osteogenic serum and CSF samples of TBI patients were chosen for protein analysis and were compared to those of non-brain-injured patients. A new hFOB cell-based method was used to enrich the proteins in these samples, which had a functional affinity for these osteoprogenitor cells. These enriched protein fractions were mapped using two-dimensional gel electrophoresis and protein imaging methods displaying serum and CSF proteins of brain-injured and control subjects that had an affinity for human osteoprogenitor cells. Results:, Serum and CSF derived from brain-injured patients demonstrated a greater osteoinductive potential (P < 0.05) than their non-brain-injured counterparts. Clear-cut differences in the pattern of proteins in two-dimensional gels were detected between TBI and control patients. Fourteen proteins were exclusively present in the serum of TBI patients, while other proteins were either up- or downregulated in samples collected from TBI patients (P < 0.05). Conclusion:, Osteoinductive factors are present in the serum and CSF of brain-injured patients. These may include one or more of those proteins identified as having an affinity for osteoprogenitor cells that are either exclusively present or up- or downregulated in the serum and CSF of brain-injured patients. [source] Serum-mediated osteogenic effect in traumatic brain-injured patientsANZ JOURNAL OF SURGERY, Issue 6 2009Oliver P. Gautschi Abstract Background:, Patients with a traumatic brain injury (TBI) and bone fractures often show an enhanced fracture healing, as well as an increased incidence of heterotopic ossifications (HO). It has been suggested that unknown osteoinductive factors may be released by the injured brain into the systemic blood circulation and act peripherally on the affected tissues. The aim of this study was to investigate whether serum from TBI patients is osteoinductive. Methods:, Sixty-one consecutive patients were classified into four groups: TBI and long-bone fracture (group I, n = 12), isolated severe TBI (group II, n = 21), isolated long-bone fracture (group III, n = 19) and controls (group IV, n = 9). Blood samples were collected at 6, 24, 72 and 168 h post-injury. The osteogenic potential was determined by measuring the in vitro proliferation rate of the human fetal osteoblastic cell line hFOB1.19, and primary human osteoblasts. Additionally, serum induced osteoblastic differentiation was assessed by measuring the mRNA expression of specific osteoblastic markers, including alkaline phosphatase, runt-related transcription factor 2, cathepsin K and serine protease 7. Results:, The sera of group I induced a higher mean proliferation rate of primary human osteoblasts at all time points of sampling than group III (P < 0.05). Group I had a higher mean proliferation rate of hFOB1.19 cells than all other groups at 6, 24 and 72 h post-injury (P < 0.05). The expression of alkaline phosphatase, cathepsin K and runt-related transcription factor 2 mRNA was increased in group I compared with group III and serine protease 7 was exclusively expressed in group I. Conclusion:, The study results strongly support a humoral mechanism in enhanced fracture healing and the induction of HO after TBI. Increased proliferation of osteoblastic cells and an accelerated differentiation of osteoprogenitor cells may be responsible for increased osteogenesis in TBI. [source] | ||||||||||