Mechanical thrombectomy in patients with acute vertebrobasilar occlusion using the Trevo device: a single-centre experience

Introduction

The purpose of this study is to investigate the efficacy and safety of mechanical thrombectomy in patients with acute vertebrobasilar artery occlusion (VBAO) using the Trevo Stentriever? device.

Methods

Twenty patients diagnosed with VBAO underwent digital subtraction angiography (DSA) with the intention to perform mechanical thrombectomy with stent-retrievers between August 2011 and October 2013. Two patients were excluded because another device was primarily used; in two other patients, thrombectomy was not possible.

Results

Thrombectomy with the Trevo device was performed in 16 patients. The Stentriever? was used either as the sole device (56.3 %) or in conjunction with up to four additional devices or techniques. Thirty-three clot retrieval manoeuvres were performed (mean 2.1?±?1.3, range 1–5); the device could be deployed and retrieved in all manoeuvres (100 %). No device-related complications occurred. Mean duration of the endovascular intervention was 71.8 min (±39.9; range 22–144). Complete or near complete recanalization (thrombolysis in cerebral infarction (TICI) ≥2b) was achieved in 13 patients (81.3 %). Eleven patients (68.8 %) survived and seven patients (43.8 %) showed a good clinical outcome at discharge, defined as modified Rankin Scale (mRS) 0–2 or National Institute of Health Stroke Scale (NIHSS) improvement ≥10 points. Including the two patients in whom thrombectomy was not possible, successful recanalization, good clinical outcome and survival were achieved in 72.2, 38.9 and 61.1 %, respectively.

Conclusions

Thrombectomy in patients with acute VBAO using the Trevo Stentriever?—either as the sole device or in conjunction with other devices—is feasible and seems to be similarly effective and safe as in the anterior circulation compared to reported data in the literature.     

Time course of embryonic midbrain and thalamic auditory connection development in mice as revealed by carbocyanine dye tracing

Central auditory connections develop in mice before the onset of hearing, around postnatal day 7. Two previous studies have investigated the development of auditory nuclei projections and lateral lemniscal nuclear projections in embryonic rats, respectively. Here, we provide detail for the first time of the initiation and progression of projections from the inferior colliculus (IC) to the medial geniculate body (MGB) and from the MGB to the auditory cortex (AC). Overall, the developmental progression of projections follows that of terminal mitoses in various nuclei, suggesting the consistent use of a developmental timetable at a given nucleus, independent of that of other nuclei. Our data further suggest that neurons project specifically and reciprocally from the MGB to the AC as early as embryonic day 14.5. These projections develop approximately a day before the reciprocal connections between the MGB and IC and before development of projections from the auditory nuclei to the IC. The development of IC projections is prolonged and progresses from rostral to caudal areas. Brainstem nuclear projections to the IC arrive first from the lateral lemniscus nuclei then the superior olive and finally the cochlear nuclei. Overall, the auditory connection development strongly suggests that most of the overall specificity of nuclear connections is set up at least 2 weeks before the onset of sound-mediated cochlea responses in mice and, thus, is likely governed predominantly by molecular genetic clues.     

Partial behavioral compensation is revealed in balance tasked mutant mice lacking otoconia

We describe for the first time behavioral tests which show that mammals with congenital absence of otoconia can learn a motor task that normally relies on gravity perception. The mouse mutation tilted (tlt) occurs in the otopetrin 1 gene (Otop1^tlt/tlt) and eliminates an essential component necessary for the formation of otoconia. Our data show that even in the absence of otoconia, tlt mutant mice, like normal mice, learn to cross a bar suspended between two boxes and, with practice, improve their speed of crossing. Despite this learned compensatory skills, tlt mutant mice show balance impairments, such as falling from the bar, not observed in wild type (WT) or heterozygous (het) Otop1^+/tlt littermates. The tlt mutant mice also use their tail as additional support, a behavior that is rarely exhibited in the control littermates. Interestingly, the Otop1^+/tlt heterozygous littermates show in many aspects an intermediate phenotype between wild type and tlt mutant mice, suggestive of a gene dosage effect. Overall, these data support the notion that mammals can use other otic and extraotic receptors such as semicircular canals and limb proprioreceptors, respectively, to compensate for the absence of otoconia-mediated gravity perception in a balance task.     

Improved reproducibility of contrast echocardiography by SH U 454. Experimental studies using digital subtraction echocardiography

The right heart chambers of 10 animals were contrasted by conventional (NaCl, CO2, H2O2, indocyanine green (ICG), haemaccel) and a newly developed echo-contrast medium (SH U 454) and studied by 2-D echocardiography. By means of digital subtraction echocardiography (DSE) endocardial borders were defined automatically and the results were compared with the manual input of endocardial borders of original and contrast echocardiograms. The area enclosed by these borders served as basis for the calculation of reproducibility (in %) and correlations. The following correlation coefficients (r) and SEE were calculated between the areas defined by the different contrast media and DSE and manually derived borders: r = 0.85, 3.98 cm2 (ICG), and 0.89, 1.00 cm2 (haemaccel). The best calculations were found using SH U 454 in concentrations between 100 and 300 mg/ml. The correlation coefficients were in the range of r = 0.95 and 0.98 with an SEE of 0.21 to 0.56 cm2 between manually and automatically derived contours. Comparing the reproducibility of data between the different evaluation methods we found the following results: manual input of endocardial borders in original echocardiograms 12.3%-16.9%; manual definition of endocardial borders in contrast echocardiograms 2.0% (SH U 454) - 15.7% (CO2); automatic contour finding in original echocardiograms 8.6%-28.9% (mean 21.6%); automatic definition of endocardium by DSE in contrast echocardiograms 7.6% (ICG) - 0.9% (SH U 454, 300 mg/ml). Our results demonstrate that digital subtraction echocardiography is a simple an safe procedure to define endocardial contours if echo contrast media lead to a uniform and homogeneous opacification of the left and right cardiac cavities.(ABSTRACT TRUNCATED AT 250 WORDS)     

Development of inner ear afferent connections: forming primary neurons and connecting them to the developing sensory epithelia

The molecular and cellular origin of the primary neurons of the inner ear, the vestibular and spiral neurons, is reviewed including how they connect to the specific sensory epithelia and what the molecular nature of their survival is. Primary neurons of the ear depend on a single basic Helix-Loop-Helix (bHLH) protein for their formation, neurogenin 1 (ngn1). An immediate downstream gene is the bHLH gene neuronal differentiation (NeuroD). Targeted null mutations of ngn1 results in absence of primary neuron formation; targeted null mutation of NeuroD results in loss of almost all spiral and many vestibular neurons. NeuroD and a later expressed gene, Brn3a, play a role in pathfinding to and within sensory epithelia. The molecular nature of this pathfinding property is unknown. Reduction of hair cells in ngn1 null mutations suggests a clonal relationship with primary neurons. This relationship may play some role in specifying the identity of hair cells and the primary neurons that connect with them. Primary neuron neurites growth to sensory epithelia is initially independent of trophic factors released from developing sensory epithelia, but becomes rapidly dependent on those factors. Null mutations of specific neurotrophic factors lose distinct primary neuron populations which undergo rapid embryonic cell death.