Giant paleo-seafloor craters and mass wasting associated with magma-induced uplift of the upper crust.

Giant seafloor craters are known along many a continental margin with recurrent mass-wasting deposits. However, the impact of breakup-related magmatism on the evolution of such craters is barely understood. Using high-quality geophysical datasets, this work examines the genetic relationship among the location of magmatic sills, forced folds and the formation of giant paleo-seafloor craters underneath an ancient mass-transport complex in the Møre and Vøring basins, offshore Norway. The data reveal that forced folding of near-seafloor strata occurred because of the intrusion of several interconnected magmatic sills. Estimates of 1-dimensional uplift based on well data show that uplift occurred due to the intrusion of magma in Upper Cretaceous to Lower Eocene strata. Our findings also prove that subsurface fluid plumbing associated with the magmatic sills was prolonged in time and led to the development of several vertical fluid flow conduits, some of which triggered mass wasting in Neogene to Recent times. The repeated vertical expulsion of subsurface fluids weakened the strata on the continental slope, thereby promoting mass wasting, the selective cannibalization of the paleo-seafloor, and the formation of elongated craters at the basal shear zone of the mass-transport complex. Significantly, the model presented here proves a close link between subsurface magmatic plumbing systems and mass wasting on continental margins.

Retinal neurovascular coupling in patients with glaucoma and ocular hypertension and its association with the level of glaucomatous damage.

PURPOSE: To analyze neurovascular coupling in the retina of untreated primary open-angle glaucoma (POAG) and ocular hypertension (OHT) patients. PATIENTS AND METHODS: Maximal vessel dilation in response to flicker light was analyzed with Retinal Vessel Analyzer (RVA) in temporal superior/inferior arterioles and veins in 51 POAG patients, 46 OHT and 59 control subjects. RVA parameters were compared between groups, between contralateral POAG eyes, and correlated to intraocular pressure, visual field mean defect and retinal nerve fiber layer thickness. RESULTS: POAG eyes demonstrated generally smaller response of all vessels to flicker light than the other two groups (ANOVA p=0.026; mean arterial flicker response in percent of baseline, averaged superior and inferior was 3.48 ± 2.22 % for controls , 2.35 ± 2.06 % for POAG patients , and 2.97 ± 2.35 % for OHT patients; corresponding values for venules were 3.88 ± 1.98 %, 2.89 ± 1.72 %, 3.45 ± 2.77 %). There was no difference in flicker response between the eye with more and less advanced damage in each patient of the POAG group (ANOVA p=0.79). Correlation of flicker response to intraocular pressure (IOP) was borderline at best, correlations to the level of glaucomatous damage were not significant. Correlation of flicker response of superior and inferior vessels of the same eye was significant for the arteries (Pearson r=0.23, p=0.004), as well as venules (r=0.52, p<0.001). CONCLUSION: General vessel response to flicker light was decreased in POAG patients, compared to normal controls and OHT patients. In contrast to significant correlation between the two contralateral eyes of the flicker response itself, only its borderline correlation to IOP was seen. There was no correlation to the level of damage, altogether indicating a systemic dysregulation phenomenon. GRANTS: Swiss National Foundation Grant 3200B0-113685, Velux Stiftung Grant, Freie Akademische Gesellschaft (FAG) Grant, Pfizer Inc. Grant CLINICAL TRIAL REGISTRATION REFERENCE NUMBER: ClinicalTrials.gov NCT00430209.

Dynamics of retinal vessel response to flicker light in glaucoma patients and ocular hypertensives.

PURPOSE: To analyze dynamics of retinal vessel dilation response to flicker light in patients with glaucoma and ocular hypertension. PATIENTS AND METHODS: Response to flicker light was measured in retinal vessels by means of Retinal Vessel Analyzer. After the baseline 50 seconds long diameter recording of inferior and superior temporal artery and vein, three flicker stimulations of 20 seconds duration was applied, with a 80 seconds break in between. Area under the curve of the vessel diameter (AUC) was compared during 3 flicker periods in the open angle glaucoma patients group (POAG, n = 47) and ocular hypertensives (OHT, n = 46) and age-matched healthy controls (n = 56) RESULTS: POAG eyes demonstrated smaller response of all vessels to flicker light in general than the other two groups (p = 0.0008), but the response dynamics was significantly different between the groups (p = 0.038), showing in three flicker periods a delayed increasing response in the POAG and OHT groups, and remaining stable in healthy subjects. CONCLUSION: General vessel response to flicker light was decreased in POAG patients despite the slow improvement in repeated flicker stimulation, indicating an altered response pattern.

Increased prevalence of obstructive sleep apnoea in patients with Charcot-Marie-Tooth disease: a case control study.

Obstructive sleep apnoea (OSA) has previously been described in a large family suffering from Charcot-Marie-Tooth disease type 1 (CMT1). In the present study, we used a case control design to establish whether this suggested link between OSA and CMT1 may also be found when studying genetically non-related patients. 12 patients with CMT1 and 24 control patients matched for age, sex and body mass index (BMI) were included in the study. Neurological disability was graded with a previously established 6 point score. All patients underwent overnight polysomnography. The mean apnoea-hypopnoea index (AHI) of patients with CMT1 was 10.5 (16.3) which was significantly higher than that of the control group (1.5 (1.3)). Five out of 12 patients with CMT1 had an AHI > or =10/h compared with 1 of 24 control patients (p<0.01). In patients with CMT1, a significant correlation between AHI and neurological disability was found (Spearman r = 0.62; p = 0.031) while BMI and age were not related to AHI. CMT1, in particular CMT1A, predisposes with disease progression to the development of OSA. Pathophysiologically, one may assume that CMT1 related pharyngeal neuropathy increases the collapsibility of the upper airway which in turn leads to recurring obstructive respiratory events.