Severe traumatic brain injury (TBI) is one of the major causes of death in younger age groups. In Umeå, Sweden, an intracranial pressure (ICP) targeted therapy protocol, the Lund concept, has been used in treatment of severe TBI since 1994. Decompressive craniectomy is used as a protocolguided treatment step. The primary aim of the investigation was to study the effect of craniectomy on ICP changes over time in patients with severe TBI treated by an ICP-targeted protocol. In this retrospective study, all patients treated for severe TBI during 1998-2001 who fulfilled the following inclusion criteria were studied: GCS Յ 8 at intubation and sedation, first recorded cerebral perfusion pressure (CPP) of Ͼ10 mm Hg, arrival within 24 h of trauma, and need of intensive care for Ͼ72 h. Craniectomy was performed when the ICP could not be controlled by evacuation of hematomas, sedation, ventriculostomy, or low-dose pentothal infusion. Ninety-three patients met the inclusion criteria. Mean age was 37.6 years. Twenty-one patients underwent craniectomy as a treatment step. We found a significant reduction of the ICP directly after craniectomy, from 36.4 mm Hg (range, 18-80 mm Hg) to 12.6 mm Hg (range, 2-51 mm Hg). During the following 72 h, we observed an increase in ICP during the first 8-12 h after craniectomy, reaching approximately 20 mm Hg, and later levelling out at approximately 25 mm Hg. The reduction of ICP was statistically significant during the 72 h. The outcome as measured by Glasgow Outcome Scale (GOS) did not significantly differ between the craniectomized group (DC) and the non-craniectomized group (NDC). The outcome was favorable (GOS 5-4) in 71% in the craniectomized group, and in 61% in the noncraniectomized group. Craniectomy is a useful tool in achieving a significant reduction of ICP over time in TBI patients with progressive intracranial hypertension refractory to medical therapy. The procedure seems to have a satisfactory effect on the outcome, as demonstrated by a high rate of favorable outcome and low mortality in the craniectomized group, which did not significantly differ compared with the non-craniectomized group.

In this series we report on surgical and hardware complications from our 16 years of experience with VNS treatment. Infection following insertion of the VNS device and vocal cord palsy due to damage to the vagus nerve are the most serious complications related to the surgery. Avoiding unnecessary reoperations in order to reduce the appearances of these complications are of great importance. It is therefore essential to minimize technical malfunctions that will lead to additional surgery. Further studies are needed to evaluate the possible superiority of the modified leads.

The outcome results from previous studies using the Lund therapy were reproduced, and no adverse side-effects of low-dose prostacyclin were observed.

In our hands, the CMS device is reliable and easy to use. The ICP recordings are stable over time, and there is only a minor zero drift. The device is today our standard method for ICP measurements.

Removal of the anterior clinoid process (ACP) facilitates radical removal of tumors or radical neck clipping of aneurysms in the supra- and parasellar regions by providing a wide operative exposure of the internal carotid artery (ICA) and the optic nerve and by reducing the need for brain retraction. Over a period of 3 years, anterior clinoidectomy was performed in 40 patients, 30 of whom harbored aneurysms (18 of the ICA and 13 of the basilar artery [one patient had two aneurysms]) and 10 of whom had tumors (four large pituitary tumors, four craniopharyngiomas, and two sphenoid ridge meningiomas). The ACP was removed extradurally in 31 cases and intradurally in nine cases. Extradural clinoidectomy was performed in all cases of pituitary adenoma and craniopharyngioma and in most cases of basilar artery aneurysm. Intradural clinoidectomy was performed in two cases of ICA-ophthalmic artery aneurysm, two cases of ICA-posterior communicating artery aneurysm, two cases of ICA cavernous aneurysm, one case of basilar artery aneurysm, and two cases of sphenoid ridge meningioma. The outcome was satisfactory in all patients, except for one patient who underwent clipping of a basilar tip aneurysm and suffered a thalamic and midbrain infarction. Three patients who underwent extradural clinoidectomy suffered a postoperative diminution of visual acuity or a visual field defect on the side of the clinoidectomy. These deficits may have been caused either by drilling of the ACP or by other operative manipulation of the optic nerve. Cerebrospinal fluid rhinorrhea, which required reoperation, occurred in one patient. The authors' experience suggests that the extradural technique of ACP removal is easier and less time consuming than the intradural one and provides better operative exposure. It can be used routinely in treating lesions in the supra- and parasellar regions.

Removal of the anterior clinoid process (ACP) facilitates radical removal of tumors or radical neck clipping of aneurysms in the supra- and parasellar regions by providing a wide operative exposure of the internal carotid artery (ICA) and the optic nerve and by reducing the need for brain retraction. Over a period of 3 years, anterior clinoidectomy was performed in 40 patients, 30 of whom harbored aneurysms (18 of the ICA and 13 of the basilar artery [one patient had two aneurysms]) and 10 of whom had tumors (four large pituitary tumors, four craniopharyngiomas, and two sphenoid ridge meningiomas). The ACP was removed extradurally in 31 cases and intradurally in nine cases. Extradural clinoidectomy was performed in all cases of pituitary adenoma and craniopharyngioma and in most cases of basilar artery aneurysm. Intradural clinoidectomy was performed in two cases of ICA-ophthalmic artery aneurysm, two cases of ICA-posterior communicating artery aneurysm, two cases of ICA cavernous aneurysm, one case of basilar artery aneurysm, and two cases of sphenoid ridge meningioma. The outcome was satisfactory in all patients, except for one patient who underwent clipping of a basilar tip aneurysm and suffered a thalamic and midbrain infarction. Three patients who underwent extradural clinoidectomy suffered a postoperative diminution of visual acuity or a visual field defect on the side of the clinoidectomy. These deficits may have been caused either by drilling of the ACP or by other operative manipulation of the optic nerve. Cerebrospinal fluid rhinorrhea, which required reoperation, occurred in one patient. The authors' experience suggests that the extradural technique of ACP removal is easier and less time consuming than the intradural one and provides better operative exposure. It can be used routinely in treating lesions in the supra- and parasellar regions.

Objective: This study evaluated the outcome of treatment according to the Lund concept in children with severe traumatic brain injury and investigated whether the preset goals of the protocol were achieved. Design and setting: A twocenter retrospective study in neurointensive care units at university hospitals. Patients: Forty-one children with severe traumatic brain injury from blunt trauma and arriving at hospital within 24 h after injury. Median age was 8.8 years (range 3 months-14.2 years), Glasgow Coma Scale 7 (3-8), and Injury Severity Score 25 (16-75). All children had pathological findings on initial computed tomography. All developed intracranial hypertension, and survivors required intensive care longer than 72 h. Interventions: Treatment according to the principles of the Lund concept. Measurements and results: Neurosurgery was required in 46% of the children. Survival rate was 93% and favorable outcome (Glasgow Outcome Score 4 or 5) was 80% at long-term follow-up (median 12 months postinjury, range 2.5-26). The preset physiological and biochemical goals were achieved in over 90% of observations. Conclusions: Treating pediatric patients with severe traumatic brain injury, according to the Lund concept, results in a favorable outcome when the protocol is followed.

Objective: To prospectively study S-100B and neuron specific enolase (NSE) levels in subjects treated for severe head injury (sTBI), and investigate the prognostic value of these biomarkers. Methods: Subjects included in a prospective double blind randomised study for sTBI. Inclusion criteria: Glasgow Coma Score (GCS) (8, age 15-70 years, first recorded cerebral perfusion pressure of .10 mm Hg and arrival ,24 h after trauma. Subjects were treated with an intracranial pressure (ICP) targeted therapy. Blood samples for S-100B and NSE were drawn immediately after arrival and every 12 h for 5 days. Outcome was evaluated as Glasgow Outcome Scale (GOS) by independent staff at 3 and 12 months. Results: 48 subjects, mean age 35.5 years, and median GCS 6 were included. The first blood sample was drawn at 15.6 (1.4) h after injury. Initial concentration of S-100B was 1.04 (0.21) mg/l and for NSE 18.94 (2.32) mg/l. The biomarkers were significantly higher in subjects with GCS 3 and in those who died compared with those with GCS 4-8 and GOS 2-5, respectively. Receiver operated characteristic curve analyses of the initial S-100B and NSE levels to GOS dichotomised as unfavourable (GOS 1-3) and favourable (GOS 4-5) showed a weak correlation: AUC 0.585 and 0.555, respectively. Using the dichotomisation dead (GOS 1)/alive (GOS 2-5), the AUC values were 0.687 and 0.734, respectively. Furthermore, a correlation was found between the biomarkers themselves and the biomarkers and ICP. Conclusion: At 3 and 12 months after trauma, no differences in prognostic values between the markers were apparent nor was there any clinical significant value of the markers as predictors of clinical outcome.Over the past decades there has been a rising interest in biochemical markers. They are used for diagnosis of many disorders, including: myocardial infarction (troponin), renal failure (creatinine), acute pancreatitis (amylase) and malignant diseases (prostate specific antigen, a-phoeto protein). One of the first substances studied as a biochemical marker of cerebral injury in the clinical setting was CK-BB.1 2 Today, several biochemical markers for brain injury have been evaluated for clinical use. The studies have mostly aimed at finding reliable biochemical markers for brain injury which would allow for discrimination between potentially serious and potentially non-serious head injury, mostly defined as findings on CT scan.3-5 Other studies have focused on the prediction of outcome after head injury. 7Among the recent most intensely studied biochemical markers are S-100B and neuron specific enolase (NSE).S-100B is a small calcium binding protein found in the astroglial cells and in Schwann cells. 8 9 It has been shown that the concentration of this protein increases in CSF and serum after cerebral injuries such as: head injury, meningitis, subarachnoid haemorrhage and stroke.10 11 However, increased levels of S-100B can also be detected after extracranial injuries (eg, coronary bypass surgery and fractures of long bones).12-14 S-100B i...