Acta neurochirurgica. Supplement
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Acta Neurochir. Suppl. · Jan 1997
Mannitol decreases ICP but does not improve brain-tissue pO2 in severely head-injured patients with intracranial hypertension.
Little is known about the effect of post-traumatic mannitol infusion on cerebral metabolism and oxygenation. The purpose of this study was to investigate the effects of mannitol in comatose patients on PtiO2, PtiCO2 and brain tissue pH using Clark-type electrodes implanted into cerebral white matter. In the neurosurgical intensive care unit PtiO2, PtiCO2, brain tissue pH, arterial blood pressure, intracranial pressure (ICP), cerebral perfusion pressure (CPP) and jugular bulb oxygen saturation (SjvO2) were prospectively studied in eleven patients with severe traumatic brain injury (TBI) during a total of 30 mannitol administrations (125 ml of 20% Mannitol infused over 30 min through a central vein). ⋯ These effects were not reflected in PtiO2 or SjvO2, which were 29 +/- 4 mmHg and 61 +/- 3%, respectively, at the beginning of mannitol injection and remained unchanged during the observation period. PtiCO2 and brain tissue pH were not affected by mannitol infusion. Future studies should focus on the identification of ICP or CPP thresholds where infusion of mannitol may actually improve O2-supply to the brain.
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Acta Neurochir. Suppl. · Jan 1997
Clinical TrialHypertonic/hyperoncotic saline reliably reduces ICP in severely head-injured patients with intracranial hypertension.
Hypertonic saline (HS) has been shown to decrease intracranial pressure (ICP) and cerebral water content in experimental models of traumatic brain injury (TBI). The purpose of the present study was to test the efficacy of administration of HS (7.5%) combined with 6% hydroxyethyl starch (molecular weight 200.000/0.60-0.66; HHES) for the treatment of therapy-resistant intracranial hypertension in patients with severe TBI. Six patients with severe TBI (GCS < 8) who met the inclusion criteria (therapy resistant ICP > 25 mmHg, cerebral perfusion pressure (CPP) < 60 mmHg, plasma-Na+ < 150 mOsm and > 4 hours since the last HS/HHES treatment) were prospectively enrolled in the study and received between one and ten bolus infusions of maximal 250 ml HS/HHES at a rate of 20 ml/min. ⋯ Plasma sodium normalized within 30 min. Experimental studies from our laboratory indicate that the ICP lowering effect is primarily due to dehydration of brain tissue and that cerebral blood volume remains largely unaffected by HS. In summary, HS/HHES reduces otherwise therapy-resistant intracranial hypertension and improves cerebral perfusion even after repeated administration without negatively affecting blood pressure or causing a rebound ICP increase.
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Acta Neurochir. Suppl. · Jan 1997
Clinical TrialNear infrared spectroscopy (NIRS) in patients with severe brain injury and elevated intracranial pressure. A pilot study.
Near infrared spectroscopy (NIRS) was used to asses changes in regional cerebral oxygen saturation (rSO2) in 8 head injured patients with an intracranial pressure (ICP) higher or lower than 25 mmHg (n = 4 for each group). NIRS values in the high ICP group (> 25 mmHg) were significantly lower than in the low ICP group (< 25 mmHg). In contrast, arterial pO2, pCO2, peripheral oxygen saturation and transcranial Doppler sonography (TCD) values were similar in both groups. ⋯ However, rSO2 values in patients with an ICP > 25 mmHg were significant lower than in patients with an ICP < 25 mmHg after the hyperoxygenation period. In addition, patients with an ICP < 25 mmHg revealed a significant increase in rSO2 values at the end of the hyperoxygenation period, not detectable in patients with an ICP > 25 mmHg. Our results suggest that NIRS may be an additional diagnostic tool in the non-invasive evaluation of impaired cerebral microcirculation in patients with increased intracranial pressure.
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Acta Neurochir. Suppl. · Jan 1997
Treatment of deafferentation pain by chronic stimulation of the motor cortex: report of a series of 20 cases.
Twenty patients with deafferentation pain were treated by chronic stimulation of the motor cortex. The central fissure was localized using stereotactic MRI and the motor cortex was mapped using intra-operative somatosensory evoked potentials. Seven patients with trigeminal neuropathic pain experienced definite pain relief varying between 40 and 100%. ⋯ One patient developed a small extradural haematoma which resolved spontaneously. None of the patients developed seizure activity. This study confirms the potential value of motor cortex stimulation in the treatment of certain forms of intractable pain, especially in cases with trigeminal neuropathic pain.
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Acta Neurochir. Suppl. · Jan 1997
Biphasic pathophysiological response of vasogenic and cellular edema in traumatic brain swelling.
The objective of this study was to quantify the temporal water content changes and document the type of edema (cellular versus vasogenic) that is occurring during both the acute and the late stages of edema development following closed head injury. Adult Sprague rats (n = 50) were separated into two groups: Group I: Sham (n = 8), Group II: Trauma (n = 42). The measurement of brain water content (BWC) was based on T1, whereas the differentiation of edema on the measurement of the random, translational motion of water protons (apparent diffusion coefficients-ADC) by MRI. ⋯ This transient increase; however, was followed by a continuing decrease in ADC beginning at 45 minutes post injury and reaching a minimum at days 7-14 (-103%). Since the BWC continued to increase during the next day (10.3%), it is suggested cellular edema formation started to develop soon after injury and became dominant between 1-2 weeks post injury. In conclusion we may consider, that there is a predominantly vasogenic edema formation immediately after injury and later a more widespread and slower edema formation due to a predominantly cellular swelling.