Object Recent years have been marked by efforts to improve the quality and safety of pedicle screw placement in spinal instrumentation. The aim of the present study is to compare the accuracy of the SpineAssist robot system with conventional fluoroscopy-guided pedicle screw placement. Methods Ninety-five patients suffering from degenerative disease and requiring elective lumbar instrumentation were included in the study. The robot cohort (Group I; 55 patients, 244 screws) consisted of an initial open robot-assisted subgroup (Subgroup IA; 17 patients, 83 screws) and a percutaneous cohort (Subgroup IB, 38 patients, 161 screws). In these groups, pedicle screws were placed under robotic guidance and lateral fluoroscopic control. In the fluoroscopy-guided cohort (Group II; 40 patients, 163 screws) screws were inserted using anatomical landmarks and lateral fluoroscopic guidance. The primary outcome measure was accuracy of screw placement on the Gertzbein-Robbins scale (Grade A to E and R [revised]). Secondary parameters were duration of surgery, blood loss, cumulative morphine, and length of stay. Results In the robot group (Group I), a perfect trajectory (A) was observed in 204 screws (83.6%). The remaining screws were graded B (n = 19 [7.8%]), C (n = 9 [3.7%]), D (n = 4 [1.6%]), E (n = 2 [0.8%]), and R (n = 6 [2.5%]). In the fluoroscopy-guided group (Group II), a completely intrapedicular course graded A was found in 79.8% (n = 130). The remaining screws were graded B (n = 12 [7.4%]), C (n = 10 [6.1%]), D (n = 6 [3.7%]), and E (n = 5 [3.1%]). The comparison of “clinically acceptable” (that is, A and B screws) was neither different between groups (I vs II [p = 0.19]) nor subgroups (Subgroup IA vs IB [p = 0.81]; Subgroup IA vs Group II [p = 0.53]; Subgroup IB vs Group II [p = 0.20]). Blood loss was lower in the robot-assisted group than in the fluoroscopy-guided group, while duration of surgery, length of stay, and cumulative morphine dose were not statistically different. Conclusions Robot-guided pedicle screw placement is a safe and useful tool for assisting spine surgeons in degenerative spine cases. Nonetheless, technical difficulties remain and fluoroscopy backup is advocated.

SUMMARY:Our aim was to review the etiologic background of isolated acute nontraumatic cSAH. While SAH located in the basal cisterns originates from a ruptured aneurysm in approximately 85% of cases, a broad spectrum of vascular and even nonvascular pathologies can cause acute nontraumatic SAH along the convexity. Arteriovenous malformations or fistulas, cortical venous and/or dural sinus thrombosis, and distal and proximal arteriopathies (RCVS, vasculitides, mycotic aneurysms, Moyamoya, or severe atherosclerotic carotid disease) should be sought by noninvasive imaging methods or/and conventional angiography. Additionally, PRES may also be a source of acute cSAH. In elderly patients, cSAH might be attributed to CAA if numerous hemorrhages are demonstrated by GRE T2 images. Finally, cSAH is rarely observed in nonvascular disorders, such as abscess and primitive or secondary brain tumors.ABBREVIATIONS: CAA ϭ cerebral amyloid angiopathy; cSAH ϭ cortical subarachnoid hemorrhage; CTA ϭ CT angiography; CTV ϭ CT venography; CVT ϭ cerebral venous thrombosis; DSA ϭ digital subtraction angiography; DWI ϭ diffusion-weighted imaging; FLAIR ϭ fluid-attenuated inversion recovery; Gd ϭ gadolinium; GRE T2 ϭ gradient echo T2-weighted imaging; MRA ϭ MR angiography; MRV ϭ MR venography; PRES ϭ posterior reversible encephalopathy syndrome; RCVS ϭ reversible cerebral vasoconstriction syndrome; SAH ϭ subarachnoid hemorrhage; SWI ϭ susceptibility-weighted imaging; TIA ϭ transient ischemic attack; TOF ϭ time of flight N ontraumatic (spontaneous) SAH arises in approximately 85% of cases from rupture of a saccular aneurysm at the base of the brain. Nonaneurysmal perimesencephalic hemorrhages account for another 10%.

Our findings suggest that CAA could be a common cause of cSAH in the elderly with a fairly uniform clinical presentation. In addition to prior cortical bleeding (ICH, MBs), most patients from the present series had evidence of focal cortical hemosiderosis likely corresponding with prior unrecognized cSAH and suggesting that cSAH was a recurrent event.

This article reviews the most relevant state-of-the-art magnetic resonance (MR) techniques, which are clinically available to investigate brain diseases. MR acquisition techniques addressed include notably diffusion imaging (diffusion-weighted imaging (DWI), diffusion tensor imaging (DTI), and diffusion kurtosis imaging (DKI)) as well as perfusion imaging (dynamic susceptibility contrast (DSC), arterial spin labeling (ASL), and dynamic contrast enhanced (DCE)). The underlying models used to process these images are described, as well as the theoretic underpinnings of quantitative diffusion and perfusion MR imaging-based methods. The technical requirements and how they may help to understand, classify, or follow-up neurological pathologies are briefly summarized. Techniques, principles, advantages but also intrinsic limitations, typical artifacts, and alternative solutions developed to overcome them are discussed. In this article, we also review routinely available three-dimensional (3D) techniques in neuro MRI, including state-of-the-art and emerging angiography sequences, and briefly introduce more recently proposed 3D quantitative neuro-anatomy sequences, and new technology, such as multi-slice and multi-transmit imaging.

BackgroundWhite matter hyperintensities (WMH) lesions on T2/FLAIR brain MRI are frequently seen in healthy elderly people. Whether these radiological lesions correspond to irreversible histological changes is still a matter of debate. We report the radiologic-histopathologic concordance between T2/FLAIR WMHs and neuropathologically confirmed demyelination in the periventricular, perivascular and deep white matter (WM) areas.ResultsInter-rater reliability was substantial-almost perfect between neuropathologists (kappa 0.71 - 0.79) and fair-moderate between radiologists (kappa 0.34 - 0.42). Discriminating low versus high lesion scores, radiologic compared to neuropathologic evaluation had sensitivity / specificity of 0.83 / 0.47 for periventricular and 0.44 / 0.88 for deep white matter lesions. T2/FLAIR WMHs overestimate neuropathologically confirmed demyelination in the periventricular (p < 0.001) areas but underestimates it in the deep WM (0 < 0.05). In a subset of 14 cases with prominent perivascular WMH, no corresponding demyelination was found in 12 cases.ConclusionsMRI T2/FLAIR overestimates periventricular and perivascular lesions compared to histopathologically confirmed demyelination. The relatively high concentration of interstitial water in the periventricular / perivascular regions due to increasing blood–brain-barrier permeability and plasma leakage in brain aging may evoke T2/FLAIR WMH despite relatively mild demyelination.