Middlebrooks, Erik H

The craniovertebral junction (CVJ) is a complex transition area between the skull and cervical spine. Pathologies such as chordoma, chondrosarcoma and aneurysmal bone cysts may be encountered in this anatomical area and may predispose individuals to joint instability. An adequate clinical and radiological assessment is mandatory to predict any postoperative instability and the need for fixation. There is no common consensus on the need for, timing and setting of craniovertebral fixation techniques after a craniovertebral oncological surgery. The aim of the present review is to summarize the anatomy, biomechanics and pathology of the craniovertebral junction and to describe the available surgical approaches to and considerations of joint instability after craniovertebral tumor resections. Although a one-size-fits-all approach cannot encompass the extremely challenging pathologies encountered in the CVJ area, including the possible mechanical instability that is a consequence of oncological resections, the optimal surgical strategy (anterior vs posterior vs posterolateral) tailored to the patient’s needs can be assessed preoperatively in many instances. Preserving the intrinsic and extrinsic ligaments, principally the transverse ligament, and the bony structures, namely the C1 anterior arch and occipital condyle, ensures spinal stability in most of the cases. Conversely, in situations that require the removal of those structures, or in cases where they are disrupted by the tumor, a thorough clinical and radiological assessment is needed to timely detect any instability and to plan a surgical stabilization procedure. We hope that this review will help shed light on the current evidence and pave the way for future studies on this topic.

Summary: The responsive neurostimulator continuously monitors the electrocorticogram. It delivers short bursts of high-frequency electrical stimulation when personalized patterns are detected. Intracranial EEG recording including electrocorticography is susceptible to artifacts, albeit at a lesser frequency compared with scalp recording. The authors describe a novel case of a patient with focal epilepsy, bitemporal responsive neurostimulation, and seizures without self-awareness manifest as focal impaired awareness seizures adversely affecting memory. At follow-up evaluation, the patient reported being clinically seizure-free although a single long episode was detected using the Patient Data Management System over the course of 3 years. Initial review identified a left-sided rhythmic discharge with a bilateral spatial field of involvement. In response to detection, the responsive neurostimulation delivered a series of five electrical stimulations. On further review, the patient recalled undergoing cervical radiofrequency ablation, which coincided with the appearance of the “electrographic seizure.” Extrinsic electrical artifact involving monomorphic nonevolving waveforms confirmed electrical artifact identified and treated by responsive neurostimulation as an epileptic seizure. On rare occasion, implanted electrical devices may lead to misdiagnosis and mistreatment of patients because of intracranial artifact.

There are many lesions that cause compression of nerves and vessels in the head and neck, and they can often be overlooked in the absence of adequate history or if not suspected by the radiologist. Many of these lesions require a high index of suspicion and optimal positioning for imaging. While a multimodality approach is critical in the evaluation of compressive lesions, an MRI utilizing high-resolution (heavily weighted) T2-weighted sequence is extremely useful as a starting point. In this review, we aim to discuss the radiological features of the common and uncommon compressive lesions of the head and neck which are broadly categorized into vascular, osseous, and miscellaneous etiologies.

Transient ischemic attack (TIA) has gained significant attention recently due to the increased incidence of subsequent stroke. However, there are many nonvascular clinical mimics of TIA, creating a need for improved biomarkers to identify a vascular origin. Following the recent approval of ultra-high field (UHF) 7T MRI in clinical practice, several clinical studies have highlighted its added utility in neuroimaging compared to lower-field 1.5T and 3T MRI, particularly in epilepsy and multiple sclerosis. Our case series of three patients with TIA illustrates that 7T MRI can depict small areas of intracortical microhemorrhages and microinfarctions, which could not be resolved with 3T or 1.5T MRI. There are currently no reports of intracortical localization of microhemorrhages in patients with TIA. This discovery may enhance our understanding and characterization of cerebrovascular abnormalities in TIAs. In addition, UHF imaging could potentially be utilized to distinguish transient neurological episodes secondary to cerebrovascular events from other differential considerations. Our cases highlight the underestimation of imaging abnormalities in cases of TIA and support the potential expanded application of clinical 7T to assess patients with TIA. Future studies are necessary at 7T redundant to determine the true incidence of such lesions in TIA and to examine the correlation between cortical microhemorrhages and subsequent ischemic stroke, hemorrhagic events, and neurocognitive impairment.

AbstractNeuromodulation in epilepsy is a proven treatment for people with drug‐resistant focal epilepsy. Dual device therapies are increasingly utilized in people with drug‐resistant epilepsy. Vagus nerve stimulation (VNS) and deep brain stimulation (DBS) target the thalamus involving the primary neurobiological network in patients with genetic generalized epilepsy (GGE). We report a novel case of combined neuromodulation in a patient with drug‐resistant GGE who achieved a partial response with seizure reduction after VNS implantation yet following VNS‐DBS polyneurostimulation gradually achieved prolonged seizure freedom. We speculate that by combining the indirect activating effects of VNS with the direct inhibitory effects of DBS, this may provide synergy to thalamic modulated networks. We hypothesize a “rational polytherapy” may exist in some patients with GGE undergoing dual neuromodulation.

Introduction: Carotid revascularization is known to prevent stroke in patients with high-grade carotid stenosis, but whether carotid revascularization may slow the progression of hemispheric WMD in patients with carotid stenosis to prevent cognitive decline have not been well described. Methods: We conducted a longitudinal study involving patients age ≥40 years with carotid stenosis on ultrasound from 2011-2015 with serial brain MRI scans at least 1 year apart followed for radiographic and clinical outcomes to 2020. Severity of carotid stenosis was defined as moderate 50-69%, high-grade 70-99%, or occluded. Hemispheric WMD volume was quantified from axial T2 FLAIR images. Patients were stratified by revascularization status. Primary outcome was change in WMD volume per year ipsilateral or contralateral to the index carotid. Hemispheric differences in the annual rate of WMD progression (cc/yr) were compared between revascularized vs not revascularized using multivariable linear regression analysis adjusted for variables that differed between revascularization status. Results: Of the 150 patients, moderate stenosis was present in 37.3%, high-grade stenosis in 42.0%, and carotid occlusion in 20.7%. Mean age was 71±10 years, 36.7% were female. Seventy-three (48.7%) had carotid revascularization with a median follow-up of 5.1 years. Baseline WMD volume was 4.86cc ipsilateral and 4.39cc contralateral to the index carotid. Patients who underwent revascularization trended to have slower WMD progression in the hemisphere ipsilateral to the index carotid compared to those not revascularized (0.32cc/yr vs 0.63 cc/yr, p=0.340). The same trend was not observed in the contralateral hemisphere. In adjusted models, carotid revascularization was associated with a 0.33 cc per year decrease in WMD progression between hemispheres compared to those not revascularized (β= -0.33, p=0.070). Conclusions: In this study with a median follow-up of 5 years, we found that carotid revascularization resulted in a 50% reduction in the annual rate of WMD progression. Intervention trials should test whether carotid revascularization slows WMD progression in patients with cognitive impairment to prevent further cerebrovascular events and cognitive decline.