Comparison of the effect of decompressive craniectomy on different neurosurgical diseases.

BACKGROUND: Many previous studies have reported that decompressive craniectomy has improved clinical outcomes in patients with intractable increased intracranial pressure (ICP) caused by various neurosurgical diseases. However there is no report that compares the effectiveness of the procedure in the different conditions. The authors performed decompressive craniectomy following a constant surgical indication and compared the clinical outcomes in different neurosurgical diseases. MATERIALS AND METHODS: Seventy five patients who underwent decompressive craniectomy were analysed retrospectively. There were 28 with severe traumatic brain injury (TBI), 24 cases with massive intracerebral haemorrhage (ICH), and 23 cases with major infarction (MI). The surgical indications were GCS score less than 8 and/or a midline shift more than 6 mm on CT. The clinical outcomes were assessed on the basis of mortality and Glasgow Outcome Scale (GOS) scores. The changes of ventricular pressure related to the surgical intervention were also compared between the different disease groups. FINDINGS: Clinical outcomes were evaluated 6 months after decompressive craniectomy. The mortality was 21.4% in patients with TBI, 25% in those with ICH and 60.9% in MI. A favourable outcome, i.e. GOS 4-5 (moderate disability or better) was observed in 16 (57.1%) patients with TBI, 12 (50%) with ICH and 7 (30.4%) with MI. The change of ventricular pressure after craniectomy and was 53.2 (reductions of 17.4%) and further reduced by 14.9% (with dural opening) and (24.8%) after returning to its recovery room, regardless of the diseases group. CONCLUSIONS: According to the mortality and GOS scores, decompressive craniectomy with dural expansion was found to be more effective in patients with ICH or TBI than in the MI group. However, the ventricular pressure change during the decompressive craniectomy was similar in the different disease groups. The authors thought that decompressive craniectomy should be performed earlier for the major infarction patients.

Cranioplasty effect on the cerebral hemodynamics and cardiac function.

BACKGROUND: Cranioplasty is usually performed for aesthetic, protective and patient comfort reasons. The objective of this study is to examine the effects of cranioplasty on the cerebral hemodynamics and cardiovascular system. METHODS: Twenty-seven patients who had undergone cranioplasty after extensive skull bone removal to prevent uncontrollable intracranial hypertension were included in this study. Arterial blood flow velocities in the middle cerebral artery (MCA) and internal carotid artery (ICA) were assessed by transcranial doppler (TCD). The cardiac functions were evaluated using the echocardiogram. And cerebral blood flow were measured by perfusion CT. FINDINGS: The blood flow velocity at the MCA ipsilateral to the cranioplasty was decreased from 50.5 +/- 15.4 cm/s preoperative to 38.1 +/- 13.9 cm/s following cranioplasty (p < 0.001) and from 33.1 +/- 8.3 cm/s to 26.4 +/- 6.6 cm/s at the ICA (p < 0.001). The stroke volume was increased from 64.7 +/- 18.3 ml/beat, to 73.3 +/- 20.4 ml/beat (p < 0.001), while the cardiac output and mean arterial blood pressure were unchanged. The cerebral blood flow was increased from 39.1 +/- 7.2 ml/100g/min to 44.7 +/- 8.9 ml/100g/min on the cranioplasty side (P = 0.05). CONCLUSIONS: Cranioplasty can get rid of the atmospheric pressure on the brain and increase the cerebral blood flow as well as improve the cardiovascular functions. A skull defect should be corrected, because cranioplasty has not only aesthetic or protective effects but also improves the cardiovascular functions.

A molecular basis for the efficacy of magnesium treatment following traumatic brain injury in rats.

Magnesium ions have been shown to be a promising treatment for brain lesions caused by traumatic brain injury (TBI), as well as for the associated acute neurodegeneration and progressive functional deficits. This study investigated the effects of magnesium on the expression of the cell death/survival related proteins following TBI. Male Sprague-Dawley (SD) rats (n = 66, 280-320 g body weight) were subjected to sham surgery alone (n = 14), or to the surgery followed by a lateral fluid percussion brain injury of moderate severity (n = 52, 2.4-2.7 atm). The injured rats were randomly treated with an intravenous bolus of magnesium chloride (n = 26, 125 micromol) or saline vehicle (n = 26). The coronal brain sections were quantitatively analyzed for cell apoptosis and the expression of p53-related proteins, Bcl-2, cyclin D1 and PCNA at 1, 2, and 4 days post-injury by immunohistochemistry or in situ hybridization. Tissue damage was observed primarily in the ipsilateral cortex of the injured region with the induction of apoptosis and p53 mRNA level at 2 days after TBI. The expression of p53 and responding proteins (p21(WAF1/CIP1), Mdm2 and Bax) showed a temporal pattern similar to the apoptotic events in the time course experiments. They were induced in the early time points of days 1-2, decreasing by day 4 after TBI. In contrast, the expression of the cell survival related proteins - Bcl-2, cyclin D1, and PCNA - was most significant at day 4 post-injury, when the rate of apoptosis decreased. Magnesium treatment resulted in a reduction in apoptosis and expression of p53-related proteins. However, it had only a slight additive effect on the expression of the survival related proteins in the same time-course. These results provide a molecular basis for the efficiency of magnesium in treating TBI-induced tissue damage.