1. Happi Ngankou E, Gory B, Marnat G, et al. Thrombectomy complications in large vessel occlusions: incidence, predictors, and clinical impact in the ETIS Registry. Stroke 2021;52:e764–68
This study is a retrospective analysis of 4029 stroke patients with anterior large vessel occlusions treated with thrombectomy between January 2015 and May 2020 in 18 centers. The authors systematically collected procedural data, incidence of embolic complications, perforations and dissections, clinical outcome at 90 days, and hemorrhagic complications.
Procedural complications occurred in 7.99%, and embolus to a new territory (ENT) was the most frequent (5.2%). Predictors of embolus to a new territory were terminal carotid/tandem occlusion and an increased total number of passes. ENTs were associated to worse clinical outcomes, increased mortality, and symptomatic intracerebral hemorrhage. Perforations occurred in 1.69%. Predictors of perforations were terminal carotid/tandem occlusions (39.7% versus 27.6%). 40.7% of patients died at 90 days, and the overall rate of poor outcome was 74.6% in case of perforation. Dissections occurred in 1.46% and were more common in younger patients. Dissections did not affect the clinical outcome at 90 days. Besides dissection, complications were independent of the thrombectomy technique.
Whereas dissection did not affect clinical outcome, embolus to a new territory and perforations have a substantial negative clinical effect. ENTs and perforations were related to terminal carotid/tandem occlusions and an increased number of passes for ENTs, but the thrombectomy technique had no impact on procedural complications.
2 tables, 1 figure, no imaging
2. Visser MJ, Yang JY-M, Calamante F, et al. Automated perfusion-diffusion magnetic resonance imaging in childhood arterial ischemic stroke. Stroke 2021;52:3296–3304
Recent studies using automated perfusion imaging software have identified adults most likely to benefit from reperfusion therapies in extended time windows. The time course of penumbral tissue is poorly characterized in childhood arterial ischemic stroke (AIS). The authors explored the feasibility of using automated perfusion-diffusion imaging software to characterize penumbra in childhood AIS.
Diffusion-weighted imaging and dynamic susceptibility contrast perfusion magnetic resonance imaging performed within 72 hours of symptom onset were acquired in 29 children in this cohort study. Perfusion-diffusion mismatch was estimated using RAPID software. Ischemic core was defined as ADC <620×10−6 mm2/s and hypoperfusion as Tmax >6 seconds. Favorable mismatch profile was defined as core volume <70 mL, mismatch volume ≥15 mL, and a mismatch ratio ≥1.8. Patients had 26 unilateral middle cerebral artery and 3 unilateral cerebellar infarcts.
Most cases had cryptogenic (n=11) or focal cerebral arteriopathy (n=9) causes. Median time-to-imaging was 13.7 hours. RAPID detected an ischemic core in 19 (66%) patients. In the remaining cases, the mean apparent diffusion coefficient values were mostly higher than the threshold as the majority of these presentations were delayed (median >21 hours) and infarct volumes were small (<3.5 mL). Overall, 3 children, imaged at 3.75, 11, and 23.5 hours had favorable mismatch profiles.
The majority of children had unilateral subcortical middle cerebral artery infarcts. Twelve children had vascular occlusion on MR angiography, which included 5 with large anterior vessel occlusion (internal carotid artery or M1), 5 children with M2 occlusions, and 2 children with posterior circulation occlusions. All 3 children who had mismatch had a large vessel occlusion, one of whom received intravenous alteplase. A further 9 children had vascular stenoses and 8 had normal vascular imaging. Focal cerebral arteriopathy was the most common identifiable cause (31%). The cause of stroke was undetermined in 41%. The median stroke volume for the entire sample was 12.6 mL. Eighteen participants required general anesthetic before their imaging scans.
This study demonstrates it is feasible to rapidly assess perfusion-diffusion mismatch in childhood AIS using automated software. Favorable mismatch profiles, using adult-based parameters, persisted beyond the standard 4.5 hours window for thrombolysis, suggesting potential therapeutic benefit of RAPID use.
3 figures, 2 tables
3. van der Kamp LT, Rinkel GJE, Verbaan D, et al. Risk of rupture after intracranial aneurysm growth. JAMA Neurol 2021;78:1228–35
To determine the absolute risk of rupture of an aneurysm after detection of growth during follow-up and to develop a prediction model for rupture. Individual patient data were obtained from 15 international cohorts. Patients 18 years and older who had follow-up imaging for at least 1 untreated unruptured intracranial aneurysm with growth detected at follow-up imaging and with 1 day or longer of follow-up after growth were included. Fusiform or arteriovenous malformation-related aneurysms were excluded. Of the 5166 eligible patients who had follow-up imaging for intracranial aneurysms, 4827 were excluded because no aneurysm growth was detected, and 27 were excluded because they had less than 1 day follow-up after detection of growth. All included aneurysms had growth, defined as 1mm or greater increase in 1 direction at follow-up imaging.
A total of 312 patients were included (71% women; mean age,61 years) with 329 aneurysms with growth. During 864 aneurysm-years of follow-up, 25 (7.6%) of these aneurysms ruptured. The absolute risk of rupture after growth was 2.9% at 6 months, 4.3% at 1 year, and 6.0% at 2 years. In multivariable analyses, predictors of rupture were size (7mm or larger), shape (irregular), and site (middle cerebral artery; anterior cerebral artery, posterior communicating artery, or posterior circulation). In the triple-S prediction model based on 3 independent predictors of rupture (size, site, and shape), the 1-year risk of rupture ranged from 2.1% to 10.6%.
The authors state that the implications for clinical practice from the study are that preventive endovascular or neurosurgical aneurysm treatment should be reconsidered as soon as aneurysm growth is detected. In such instances of aneurysm growth, the triple-S prediction model can be used by physicians and patients as a starting point for discussing the pros and cons of preventive aneurysm treatment. If it is decided to continue follow-up imaging, it seems reasonable to repeat imaging at a short interval, but actual data on the optimal time interval are lacking and should be gathered in future studies.
4. Liotta EM. Management of cerebral edema, brain compression, and intracranial pressure. Continuum (Minneap Minn) 2021;27:1172–1200
Cerebral edema and brain compression should be treated in a tiered approach after the patient demonstrates a symptomatic indication to start treatment. All patients with acute brain injury should be treated with standard measures to optimize intracranial compliance and minimize risk of ICP elevation. When ICP monitors are used, therapies should target maintaining ICP at 22 mm Hg or less. Evidence exists that serial clinical examination and neuroimaging may be a reasonable alternative to ICP monitoring; however, clinical trials in progress may demonstrate advantages to advanced monitoring techniques. Early decompressive craniectomy and hypothermia are not neuroprotective in traumatic brain injury and should be reserved for situations refractory to initial medical interventions. Medical therapies that acutely lower plasma osmolality may lead to neurologic deterioration from osmotic cerebral edema, and patients with acute brain injury and renal or liver failure are at elevated risk.
This is an extensive review, and appropriately clinical in orientation, with some minor imaging examples. However, the section on potential new therapies was also interesting, particularly the section on the glymphatic system.
The precise processes by which glymphatic function might contribute to cerebral edema formation are yet to be fully delineated, but several lines of evidence suggest a critical role. Recently, CSF was demonstrated to be the source of fluid influx responsible for early brain swelling after ischemic stroke. In a mouse model of ischemic stroke, accelerated CSF influx into the brain parenchyma along perivascular spaces was observed within minutes of stroke. This CSF influx followed the wave of spreading depolarization that occurred with the loss of ionic gradients during cellular death and appeared to be the result of parenchymal and pial arteriole vasoconstriction precipitated by the spreading depolarization. Interestingly, the magnitude of CSF influx was reduced in AQP4-deficient mice. The authors acknowledged that this process would not completely explain cerebral edema formation after ischemic stroke but proposed that it could also contribute to cerebral edema formation in other diseases in which spreading depolarizations have been observed, such as subarachnoid hemorrhage, intracerebral hemorrhage, and TBI. Glymphatic dysfunction in clearing toxic substances, such as reactive oxygen and nitrogen species and inflammatory cytokines, could also contribute to cerebral edema. For example, reactive oxygen and nitrogen species might lead to cerebral edema through activation of ionic transporters (ie, the Na-K-Cl cotransporter 1), activation of intracellular protein kinase signaling cascades, blood-brain barrier disruption by activation of matrix metalloproteinases, or failure of oxidative phosphorylation through mitochondrial membrane pore formation and depolarization.
Given its prominent role in facilitating fluid movement through the brain, AQP4 might be an intuitive target for developing new cerebral edema therapies. AQP4 membrane expression is increased after hypoxic central nervous system injury.
However, although AQP4-deficient mice demonstrate reduced cerebral edema in models of cytotoxic edema (cerebral ischemia and acute liver failure), cerebral edema is worse in AQP4-deficient models of vasogenic edema (tumors, subarachnoid hemorrhage, and abscesses). Since most acute brain injury involves a mixture of cerebral edema types that evolve at different points in the disease, the pathophysiology around AQP4 and cerebral edema evolution will likely need greater clarification before AQP4 is an actionable therapeutic target.
8 figures, 3 clinical cases, 2 tables
5. Scheuren PS, David G, Kramer JLK, et al. Combined neurophysiologic and neuroimaging approach to reveal the structure-function paradox in cervical myelopathy. Neurology 2021;97:e1512–22
The clinical phenotype of cervical myelopathy is often dissociated from structural damage evidenced by neuroimaging of the spinal cord. This clinicoradiologic paradox seen with conventional measures warrants the integration of physiologic assessments of somatosensory pathways in cervical myelopathy. Here, lesion progression is usually characterized by neuronal loss and atrophy of the anterior horn expanding into lateral and posterior funiculi and eventually leading to degeneration of the entire gray matter. Based on this pathoanatomic concept of lesion progression, spinothalamic damage can occur in the dorsal horn, the anterior commissure, or the anterolateral quadrant. Spinal cord lesion topography can be scrutinized by means of atlas-based lesion mapping. Electrophysiologic measures, such as contact heat–evoked potentials (CHEPs), are highly sensitive to capture such centromedullary damage often affecting decussating fibers bound for the spinothalamic tract (STT). Moreover, multimodal evoked potentials (EPs) such as cold-evoked potentials (CEPs) and pinprick-evoked potentials (PEPs) have been reported in cases of spinal pathology and can be used to objectively characterize sub-modality-specific spinothalamic pathways. Combining electrophysiologic measures of somatosensory integrity, anatomical lesion extent, and ultimately changes in the clinical presentation is essential to improve our understanding of structure-function relationships and may provide a conceptual foundation for the prospective monitoring of myelopathic progression.
The aim of this study was to disentangle structure-function associations in focal cervical myelopathies using a multimodal phenotyping approach. Tract-specific structural impairments were assessed with atlas-based MRI of the cervical cord and related to electrophysiologic and clinical correlates of functional somatosensory impairments.
Sixteen individuals (mean age 61 years) with either degenerative (n = 13) or posttraumatic (n = 3) cervical myelopathy participated in the study. Most individuals presented with mild myelopathy (modified Japanese Orthopaedic Association score >15; n = 13). A total of 71% of individuals presented with structural damage within spinal nociceptive pathways on MRI. However, 50% of these individuals presented with complete functional sparing (i.e., normal contact heat–, cold-, and pinprick-evoked potentials). The extent of structural damage within spinal nociceptive pathways was not associated with functional integrity of thermal and mechano-nociceptive pathways or with the clinical somatosensory phenotype. The amount of structural damage to the spinothalamic tract did not correlate with spinothalamic conduction velocity.
The authors conclude that the findings provide neurophysiologic evidence to substantiate that structural damage in the spinal cord does not equate to functional somatosensory deficits. This study recognizes the pronounced structure-function paradox in cervical myelopathies and underlines the inevitable need for a multimodal phenotyping approach to reveal the eloquence of lesions within somatosensory pathways. While MRI is highly sensitive to detect structural damage in the spinal cord, it insufficiently portrays the overall consequences with regard to the functional integrity of specific spinal pathways.
4 figures, 3 tables
6. Aunan-Diop JS, Pedersen CB, Halle B, et al. Magnetic resonance elastography in normal pressure hydrocephalus-a scoping review. Neurosurg Rev 2021 Oct 23. [Epub ahead of print]
Normal pressure hydrocephalus is a syndrome characterized by symptoms arising in the triad of dementia, urinary incontinency, and gait disturbance. The condition is accompanied by ventriculomegaly in the setting of normal intracranial pressure (ICP). There are two major motivations for MRE studies of NPH. First, central pathophysiological theories on the disease entity describe increased compliance (ΔV/ΔP) in the ventricles, a property closely related to tissue elasticity. MRE studies performed on other types of dementias show characteristic mechanical changes, as do studies on aging and memory performance. Secondly, NPH is a clinically diverse disease with symptomatology that overlaps with both neurological disorders and common age-related conditions. Supplemental clinical tests such as cerebrospinal fluid (CSF) tap and lumbar infusion test have low sensitivity and are invasive. MRE might provide valuable information about the tissue mechanics that can be utilized clinically to address these challenges and possibly to identify patients most likely to benefit from treatment.
MRE can be described in three stages. First, stress is introduced by mechanical waves that cause tissue excitation (i.e., deformation). Image acquisition applies phase contrast MRI sequences to record the propagation of waves in tissues. Inversion describes a series of complex mathematical operations that extract information about tissue properties.
Image acquisition uses motion encoding gradients (MEG) to encode displacement into the MR phase signal. Images are typically acquired in three directions (x, y, z), to derive the three-dimensional displacement vector, represented by the signal at each pixel. Multiple acquisitions are often made during a phase (phase offsets), and a Fourier transformation is used to extract the motion at the driving frequency. This motion is described by a complex number at each pixel that contains the wave amplitude and phase. The images containing the information about displacement in time are referred to as wave images.
Inversion is the process of extracting material properties from wave images. Many inversion algorithms are based on the Helmholtz equation. This equation is used to extract the complex shear modulus (G*) from the motion at the driving frequency. The shear modulus can be expressed as a complex quantity because energy is lost as the wave propagates. The complex shear modulus (G*) has an elastic part, termed the storage modulus (G′), and a viscous part, termed the loss modulus (G″).
555 non duplicate citations were screened, and 7 papers made the cut. Study designs, technical challenges, regional stiffness in NPH and NPH and brain network structure are discussed. They conclude that MRE studies in NPH are still in the preclinical stage, and the clinical utility remains to be validated. The technical approaches to brain MRE differ widely, reflecting both the challenges but also the diversity of the technique. MRE shows great potential for a number of clinical applications in NPH, including but not limited to diagnosis and prediction of treatment outcomes. Furthermore, MRE can shed light on the complex and poorly understood pathophysiology of NPH and thus inspire novel diagnostic and treatment strategies.
2 figures, 2 tables
7. Herta J, Schmied T, Loidl TB, et al. Microvascular decompression in trigeminal neuralgia: predictors of pain relief, complication avoidance, and lessons learned. Acta Neurochir (Wien) 2021;163:3321–36
One hundred sixty-five patients with TGN underwent 171 MVD surgeries at the authors’ institution. Patient characteristics and MRI datasets were obtained through the hospital’s archiving system. Patients provided information about pre- and post-operative pain characteristics and neurologic outcome.
Definitions: Classical TGN is “a neurovascular compression with morphological changes of the trigeminal root” and idiopathic TGN is a TGN with “no neurovascular contact (NVC) or NVC without morphological changes of the trigeminal root”.
The preoperative MRI scans revealed classical TGN in 67/171 (39.2%) patients and idiopathic TGN in 102/171 (59.7%) patients. Retrospective MRI scans were unavailable in two patients. Two patients suffered from multiple sclerosis but were classified as classical TGN as both MRI scans showed a NVC at the affected side in the absence of multiple sclerosis plaques in the trigeminal nuclei. TGN was classified again by the intraoperative judgment of the treating neurosurgeon. TGN was classified as classical in 129/171 (75.4%) patients and as idiopathic in 41/171 (24%) patients. One patient was not classified by the treating neurosurgeon. Taking these numbers into account, MRI had a detection sensitivity for a NVC of 52% and a specificity of 97.6%, giving a low negative predictive value of 39.6%. Intraoperatively, the NVC was caused by an artery in the majority of cases (49.7%), namely, the superior cerebellar artery (68.9%) followed by a combination of arteries and veins (33.3%) and veins only (13.3%).
It is generally accepted that patients with classical TGN benefit more from MVD than patients with idiopathic TGN, relying on the MRI in counseling patients with regard to the potential MVD outcome may be misleading. In this series, only the intraoperative but not the MRI classification was predictive of pain relief. The results emphasize that the presence of a NVC on MRI is not mandatory to suggest MVD to the patient.
5 tables, 3 figures
8. Boutet A, Loh A, Chow CT, et al. A literature review of magnetic resonance imaging sequence advancements in visualizing functional neurosurgery targets. J Neurosurg 2021;135:1445–58
While direct MRI visualization of the targeted brain structures was used early on, generally it has been insufficient for preoperative planning. Indirect targeting methods, which estimate the location of targets in relation to fixed and identifiable anatomical landmarks on MRI, have traditionally been used because DBS targets could not be visualized on ventriculography and CT. However, indirect targeting fails to account for interindividual variability in the location of target structures. To improve DBS targeting accuracy, indirect targeting methods were coupled with a variety of other techniques, such as intraoperative microelectrode recordings and intraoperative stimulation testing in awake patients. However, these methods are associated with prolonged procedural times and require multiple penetrations of deep brain structures, increasing the risk of intra- and postoperative complications.
Routine brain MRI sequences acquired with standard field strengths and acquisition parameters have shortcomings in visualizing DBS targets. However, with advances in stereotactic frames, MRI hardware, and pulse sequences, direct visualization of certain structures, such as the subthalamic nucleus (STN), is replacing indirect targeting methods for preoperative planning at some institutions. Nonetheless, other structures, including thalamic nuclei, still require indirect targeting, as their direct radiological visualization remains challenging.
The goal of this manuscript was to review the many different MRI techniques that have been developed to date to enhance visualization of the most common gray matter nuclei targeted with DBS while also discussing the relevant anatomy and clinical indications of these structures.
3 figures and 2 tables, with specific listing of optimized MR acquisition parameters
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