Prophylactic enlargement of the thecal sac volume by spinal expansion duroplasty in patients with unresectable malignant intramedullary tumors and metastases prior to radiotherapy.

Unresectable malignant intramedullary tumors and metastases usually require radiotherapy which intensifies spinal cord edema and might result in neurological decline. Spinal expansion duroplasty before radiotherapy enlarges the intrathecal volume and might thus prevent neurological deficits. The study aims to evaluate the clinical course of patients undergoing expansion duroplasty. This retrospective analysis (2007-2016) included all patients with unresectable intramedullary tumors who underwent spinal expansion duroplasty. To assess the degree of preoperative cord enlargement, we calculated the "diameter ratio": diameter of the spinal cord below and above the tumor / diameter of the tumor × 2. The presence of perimedullary cerebrospinal fluid (CSF) at the affected levels was analyzed on the preoperative magnetic resonance imaging (MRI). We recorded the occurrence of neurological deficits, wound breakdown, and CSF fistula. We screened 985 patients, 11 of which were included. Eight patients had an intramedullary metastasis, three patients a spinal malignant glioma. A diameter ratio ≤ 0.8 representing a significant preoperative intramedullary enlargement was seen in 10 cases (90.9%). Postoperative imaging was available in 9 patients, demonstrating successful decompression in 8 of the 9 patients (88.9%). The postoperative course was uneventful in 9 patients (81.8%). Mean overall survival was 13.4 (SD 16.2) months. Spinal expansion duroplasty prior to radiotherapy is a previously undescribed concept. Despite neoadjuvant radiation, no wound breakdown or CSF fistula occurred. In unresectable intramedullary tumors and metastases, spinal expansion duroplasty seems to be a safe procedure with the potential to prevent neurological decline due to radiation-induced cord swelling.

Non-assisted versus neuro-navigated and XperCT-guided external ventricular catheter placement: a comparative cadaver study.

BACKGROUND AND PURPOSE: Accurate placement of an external ventricular drain (EVD) for the treatment of hydrocephalus is of paramount importance for its functionality and in order to minimize morbidity and complications. The aim of this study was to compare two different drain insertion assistance tools with the traditional free-hand anatomical landmark method, and to measure efficacy, safety and precision. METHODS: Ten cadaver heads were prepared by opening large bone windows centered on Kocher's points on both sides. Nineteen physicians, divided in two groups (trainees and board certified neurosurgeons) performed EVD insertions. The target for the ventricular drain tip was the ipsilateral foramen of Monro. Each participant inserted the external ventricular catheter in three different ways: 1) free-hand by anatomical landmarks, 2) neuronavigation-assisted (NN), and 3) XperCT-guided (XCT). The number of ventricular hits and dangerous trajectories; time to proceed; radiation exposure of patients and physicians; distance of the catheter tip to target and size of deviations projected in the orthogonal plans were measured and compared. RESULTS: Insertion using XCT increased the probability of ventricular puncture from 69.2 to 90.2 % (p = 0.02). Non-assisted placements were significantly less precise (catheter tip to target distance 14.3 ± 7.4 mm versus 9.6 ± 7.2 mm, p = 0.0003). The insertion time to proceed increased from 3.04 ± 2.06 min. to 7.3 ± 3.6 min. (p < 0.001). The X-ray exposure for XCT was 32.23 mSv, but could be reduced to 13.9 mSv if patients were initially imaged in the hybrid-operating suite. No supplementary radiation exposure is needed for NN if patients are imaged according to a navigation protocol initially. CONCLUSION: This ex vivo study demonstrates a significantly improved accuracy and safety using either NN or XCT-assisted methods. Therefore, efforts should be undertaken to implement these new technologies into daily clinical practice. However, the accuracy versus urgency of an EVD placement has to be balanced, as the image-guided insertion technique will implicate a longer preparation time due to a specific image acquisition and trajectory planning.

Fibrillary structure is key for hemostasis: a similar effect of collagen fleece and oxidized cellulose on experimental hemorrhagic brain injury.

BACKGROUND: The choice of the ideal hemostatic agent for intraoperative cerebral bleeding is under continuous debate. Our aim was to assess the influence of such materials on bleeding time in hemorrhagic cerebral contusions. We compared oxidized regenerated cellulose in fibrillar form (ORC) to microfibrillar collagen fleece (CF) in an experimental study. METHODS: N=50 Sprague Dawley rats underwent a bilateral craniectomy. 3 separate standardized superficial cortical impacts were inflicted using a high-speed drill. Immediately after lesion placement, each of the 3 lesions was covered with (a) nothing (control), (b) ORC, or (c) CF. We observed the 3 lesions with a surgical microscope. The bleeding times were recorded for each cerebral lesion and compared using ANOVA test. RESULTS: All traumatic lesions produced significant bleeding. The statistical analysis showed a clear reduction in bleeding time for groups treated with either ORC or CF compared to the control group. Lesions covered with ORC and CF showed no significant difference with regard to bleeding time. CONCLUSIONS: ORC and CF significantly reduce blood loss from hemorrhagic contusions. Our data suggest that they effectively reduce bleeding time. We advocate the use of hemostatic material for limiting bleeding from superficial cortical lesions.

Two structurally different T-type Ca 2+ channel inhibitors, mibefradil and pimozide, protect CA1 neurons from delayed death after global ischemia in rats.

Recent in vitro evidence suggests that T-type Ca(2+) channels are implicated in the mechanisms of ischemia-induced delayed neuronal cell death. The aim of this work was to study the neuroprotective potential of mibefradil and pimozide, both T-type Ca(2+) channel inhibitors, in an in vivo rat model of global ischemia. We performed blinded and randomized placebo vs. treatment experiments using 57 animals to test mibefradil and fourteen animals to test pimozide. Each treated animal received a single stereotactic intraventricular injection of mibefradil or intraperitoneal injection of pimozide prior to transient global cerebral ischemia. The primary endpoint was the number of neurons surviving in the CA1 region 72 h after insult as evaluated by NeuN-labeled cell counts. All physiological variables monitored immediately before and after ischemic insult were equivalent between all groups. Surviving neurons in the CA1 region were significantly more frequent in the treated groups compared to the placebo group (mibefradil: 36.8 ± 2.8 cells in a 200 × 100 µm counting area vs. placebo: 25.2 ± 3.2 [P < 0.01]; pimozide: 39.4 ± 1.12 vs. placebo: 27.8 ± 0.7 [P < 0.0001]). Thus, administration of mibefradil or pimozide effectively prevents neuronal death after ischemia in a rat model of global ischemia. This study provides further support for a neuroprotective effect of T-type Ca(2+) current inhibition during ischemia.

Simultaneous bedside assessment of global cerebral blood flow and effective cerebral perfusion pressure in patients with intracranial hypertension.

BACKGROUND: We examined a bedside technique transcerebral double-indicator dilution (TCID) for global cerebral blood flow (CBF) as well as the concept of effective cerebral perfusion pressure (CPP(eff)) during different treatment options for intracranial hypertension, and compared global CBF and CPP(eff) with simultaneously obtained conventional parameters. METHODS: Twenty-six patients developing intracranial hypertension in the course of traumatic brain injury or subarachnoid hemorrhage were prospectively analyzed using a combined assessment during elevated ventilation (n = 15) or osmotherapy (hypertonic saline or mannitol). For calculation of global CBF, injections of ice-cold indocyanine green boluses were performed and temperature and dye concentration changes were monitored in the thoracic aorta and the jugular bulb. CBF was then calculated according to the mean transit time principle. Estimation of CCP, the arterial pressure at which cerebral blood flow becomes zero, was performed by synchronized registration of corresponding values of blood flow velocity in the middle cerebral artery and arterial pressure and extrapolation to zero-flow velocity. CPP(eff) was calculated as mean arterial pressure minus critical closing pressure (CPP(eff) = MAP(c) - CCP). RESULTS: Elevated ventilation causes a decrease in both ICP (P < 0.001) and CBF (P < 0.001). While CPP(conv) increased (P < 0.001), CPP(eff) decreased during this observation (P = 0.002). Administration of osmotherapeutic agents resulted in a decrease of ICP (P < 0.001) and a temporary increase of CBF (P = 0.052). CPP(conv) and CPP(eff) showed no striking difference under osmotherapy. CONCLUSION: TCID allows repeated measurements of global CBF at the bedside. Elevated ventilation lowered and osmotherapy temporarily raised global CBF. In situations of increased vasotonus, CPP(eff) is a better indicator of blood flow changes than conventional CPP.

Correlation of end-tidal CO2 with transcranial Doppler flow velocity is decreased during chemoregulation in delayed cerebral vasospasm after subarachnoid haemorrhage--results of a pilot study.

BACKGROUND: Cerebrovascular responses to variations in blood pressure and CO2 are attenuated during delayed vasospasm after subarachnoid hemorrhage (SAH). Transcranial Doppler sonography (TCD) is routinely used to assess the presence of vasospasm, but cerebral blood flow velocities (CBF-V) measured by TCD do not necessarily reflect cerebral blood flow (CBF) or the severity of vasospasm. We hypothesized that the correlation of end-tidal pCO2 levels with CBF-V and CBF is equally decreased in subjects with cerebral vasospasm during variations in pCO2. METHODS: Four cynomolgus monkeys were assigned to the vasospasm group and eight animals to the control group. The animals in the vasospasm group underwent placement of an autologous subarachnoid blood clot and vasospasm was confirmed by angiography on day 7. In both groups, CBF and CBF-V were measured simultaneously while end-tidal pCO2 was altered. CBF was measured using a thermal probe placed on the cortical surface and CBF-V was measured using a commercial TCD device. RESULTS: Pearson's correlation coefficient between CBF-V values and pCO2 levels in the control group was strong (r = 0.94, p < 0.001) while it was moderate in the vasospasm group (r = 0.54, p = 0.04). The correlation of CBF values with pCO2 in healthy controls was equally strong (r = 0.87, p = 0.005), while there was no correlation in the vasospasm group (r = -0.09, p = 0.83). CONCLUSION: In this pilot study, correlations of CBF-V with pCO2 values during chemoregulation testing were lower in animals with vasospasm than in healthy ones. This correlation coefficient based on modifications in pCO2 may potentially facilitate the non-invasive assessment of vasospasm.