Huang, Josephine F.

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.

Abstract We present the case of a 61-year-old woman with a history of orthotopic heart transplant who was hospitalized with new-onset headache. Magnetic resonance imaging (MRI) of the brain revealed T2 hyperintense signal involving the left occipital lobe with leptomeningeal enhancement and mild vasogenic edema. Initial neurologic examination was normal; however, after 7 days she developed imbalance, visual disturbances, night sweats, bradyphrenia, alexia without agraphia, and right hemianopsia. Brain MRI showed enlargement of the left occipital mass and worsening edema. Stereotactic needle biopsy showed nondiagnostic necrosis. The patient continued to deteriorate despite dexamethasone. Cerebrospinal fluid (CSF) suggested infection, and cytomegalovirus CSF polymerase chain reaction (PCR) was positive. The patient received vancomycin, imipenem, and ganciclovir. After obtaining a positive serum beta-D-glucan (Fungitell), amphotericin was added. Despite best medical efforts, the patient died. Postmortem broad-range PCR sequencing of the brain tissue was positive for rare amoeba Balamuthia mandrillaris.

Background: Migraine is associated with neuroimaging differences in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). However, it is unknown if migraine-related disability (MRD) or if calcitonin gene-related peptide (CGRP), a vasoactive peptide important in migraine pathology, have radiographic implications. The aims of this study were to identify whether MRD or interictal serum CGRP levels impacted neuroimaging findings for those with CADASIL. Materials and Methods: A cross-sectional analysis was performed. The primary outcomes were neuroimaging differences associated with MRD among those with migraine or interictal serum CGRP levels of those with and without migraine. MRD was defined by 2 migraine disability scales (Migraine Disability Assessment, Headache Impact Test-6). Retrospective brain magnetic resonance imaging was reviewed (average 1.7 ± 2.0 y before enrollment). Rank-sum and χ2 tests were used. Results: Those with migraine (n=25, vs. n=14 without) were younger [median 49 (25 to 82) y vs. 60 (31 to 82) y, P<0.007], had fewer cerebral microbleeds (0 to 31 vs. 0 to 50, P=0.02) and less frequently had anterior temporal lobe T2 hyperintensities [68% (17/25) vs 100% (14/14), P=0.02]. MRD scale outcomes had no significant radiographic associations. Interictal serum CGRP did not differ (migraine: n=18, 27.0±9.6 pg/mL vs. no migraine: n=10, 26.8±15.7 pg/mL, P=0.965). Conclusions: Migraine may forestall microangiopathy in CADASIL, though possibly independent of severity as measured by MRD. Interictal serum CGRP did not differ in our cohort suggesting CGRP may not be vital to migraine pathophysiology in CADASIL. Larger studies are needed to account for age differences.

Introduction: Collateral circulation plays a crucial role in determining the extent of brain tissue ischemia and functional outcome in large vessel occlusive (LVO) stroke. Heart failure (HF) is known to cause cerebral hypoperfusion, yet the relationship between HF and robustness of collateral flow has not been well described. Here we hypothesized that HF is associated with poor collateral flow and functional outcome in patients presenting with LVO treated with mechanical thrombectomy (MT). Methods: A single center retrospective study of patients presenting with LVO ischemic stroke who underwent MT between 2012-2020 was done. Single-phase CTA of head prior to MT was used to assess collateral status with poor status defined as ≤ 50% filling and good status as >50% filling. Classification of HF by left ventricular ejection fraction (LVEF) on echocardiogram was used where HF with reduced ejection fraction (HFrEF) had LVEF ≤40%, HF with preserved EF (HFpEF) had LVEF ≥50% with evidence of structural heart disease, and no HF was LVEF≥50% without structural heart disease. Functional outcome was modified Rankin scale (mRS) at 90 days with scores of 0-2 representing good outcome and 3-6 representing poor outcome. Multivariable logistic regression analyses were performed to evaluate the association between HF and poor collaterals after adjusting for vascular risk factors. Results: We identified 235 patients, mean age was 69 ±15 years, median NIHSS was 18, and 45.5% had HF (HFrEF 12.8%, HFmrEF 4.7%, HFpEF 28.1%) while 54.5% had no HF. Poor collaterals were seen in 47.7%, and those with HF were likely to have poor collaterals compared to those without HF (56.1% vs 35.1%, P=.001). There was a dose-dependent relationship between severity of HF and poor collaterals: adjusted odds of poor collaterals were 1.63 and 2.45 in HFpEF and HFrEF, compared to those without HF (trend p=.018). Patients with poor collaterals were likely to have poor outcome at 3 months compared to those with good collaterals (75.0% vs 57.8%; p=.015). Conclusion: Patients with HFrEF were twice as likely to have poor collaterals. This study demonstrated a likely mechanism for poor outcomes seen in ischemic stroke with HF, future studies may explore whether optimization of HF may augment collaterals to improve outcomes.

AbstractThe authors illustrate the use of through-and-through brachio/radio-femoral access technique in two patients who presented with subclavian steal syndrome. This is an additional tool in the armamentarium of the endovascular specialist to improve management of complex cases with subclavian steal syndrome. This technique provides several advantages to improve efficiency and precision of the procedure while reserving the open surgical bypass option if needed.

INTRODUCTION: Studies suggest 8%-28% of ischemic strokes present as wake-up strokes (WUS). The unknown time of symptom onset precludes these patients from approved treatments for acute ischemic stroke, but a substantial proportion of patients may be deemed candidates for treatment if other factors are considered. The aim of this study was to identify characteristics associated with clinical outcomes of WUS patients. METHODS: We retrospectively reviewed the medical record of patients with ischemic stroke admitted to a large academic medical center between January 2011 and May 2012. We identified patients with stroke symptoms upon awakening or those who were found with stroke symptoms with an unknown time of onset. Baseline demographics, stroke mechanism, presenting NIHSS, Alberta Stroke Program Early Computed Tomography Score (ASPECTS), and modified Rankin Scale (mRS) scores on discharge and at 3-month follow-up were obtained. A good outcome was defined as mRS 0-2. RESULTS: WUS patients comprised 22% (162/731) of all patients with ischemic stroke at our institution during this time period. Median age was 74 years (range 15-100), median presenting NIHSS was 5 (range 0-28), and median initial ASPECTS 10 (range 0-10). A cardioembolic mechanism was identified in 68 patients (42%). Predictors of good outcome at hospital discharge were lower initial NIHSS (3.5 versus 12.0, p<0.0001) and higher ASPECTS (9.8 versus 8.1, p=0.0002). The predictors of good outcomes at 3 months were younger age (69.1 versus 75.8, p=0.009), lower initial NIHSS (5.0 versus 12.6, p<0.0001), and higher ASPECTS (9.5 versus 8.1, p=0.0006). One hundred and eleven patients (68.5%) had initial ASPECTS of 10. Of those, 19 had NIHSS≥10 and 7 were treated with acute recanalization therapies. Four of the 7 treated patients had good outcomes, and 2 of the 12 untreated patients had good outcomes. CONCLUSIONS: Few patients with strokes of unknown onset and severe deficits have good outcomes without acute stroke treatment. Patients with NIHSS≥10 and ASPECTS 10 may be candidates for acute recanalization therapy.

Introduction: Cilostazol has promise as an alternative to aspirin for secondary stroke prevention given its vasodilatory and anti-inflammatory properties in addition to platelet aggregation inhibition. We conducted a systematic review and meta-analysis to estimate the comparative effectiveness and safety of cilostazol compared to aspirin for stroke prevention in patients with previous stroke or TIA. Hypothesis: Cilostazol is more effective than aspirin in preventing recurrent ischemic stroke with lower risk of intracranial hemorrhage and bleeding. Methods: We searched PubMed and the Cochrane Central Register of Controlled Trials from inception to 2019. Randomized clinical trials that compared cilostazol vs aspirin and reported the endpoints of ischemic stroke, intracranial hemorrhage and bleeding were included. A random-effects estimate was computed based on Mantel-Haenszel methods. The pooled estimates with 95% confidence intervals were compared between cilostazol and aspirin and displayed as forest plots (Figure). Results: The search identified 5 randomized clinical trials comparing cilostazol vs aspirin for secondary stroke prevention that enrolled 7,240 patients from primarily Asian countries (3,615 received cilostazol and 3,625 received aspirin). The pooled results from the random-effects model showed that cilostazol was associated with significantly lower risk of recurrent ischemic stroke (Hazard ratio [HR] 0.70; 95%CI, 0.54-0.89), intracranial hemorrhage (HR 0.41; 95%CI, 0.25-0.65) and bleeding (HR 0.71; 95%CI, 0.55-0.91). See forest plots. Conclusion: This meta-analysis suggests cilostazol is more effective than aspirin in the prevention of recurrent ischemic stroke with lower risk of intracranial hemorrhage and bleeding. Confirmatory randomized trials of cilostazol for secondary stroke prevention to be performed in more generalizable populations are needed.

Introduction: Left atrial enlargement (LAE) is associated with atrial fibrillation, a frequent cause of large vessel occlusion (LVO) leading to ischemic stroke. Leptomeningeal collaterals protect tissue from ischemia, but the association between collaterals and structural heart disease is not well described. We aim to investigate the association between LAE and cerebral collaterals during acute LVO when microvasculature, vasodilation, and chronotropic competence are critically important. Hypothesis: Left atrial enlargement is associated with poor collaterals. Methods: We reviewed consecutive patients presenting with middle cerebral and internal carotid LVO who underwent thrombectomy from 2012 to 2017. Patients with CT angiogram of the head and echocardiogram were included. Poor collaterals were defined as ≤ 50% filling on CT angiogram. LAE was defined as left atrial volume index ≥ 35 mL/m 2 . Multivariate logistic regression analysis was performed to evaluate the relationship between LAE and poor collaterals with adjustment for age and hypertension. Results: There were 128 eligible patients. The mean age was 68± 15 years, median NIHSS was 17, and 51 (39.8%) had LAE. Baseline characteristics are described in the table. Poor collaterals were observed in 50 (39%) patients. Patients with LAE were more likely to have poor collaterals compared to those with normal left atrial size (52.9% vs. 29.9%, p=0.009). After adjusting for age and hypertension, a trend towards association remained (OR 2.00, p=0.089). Conclusion: Our results indicate that patients with LVO and LAE were more likely to have poor collaterals. Further research is warranted to determine the cause of the association. One possibility is shared pathophysiology affecting both cardiac and cerebral vasculature such as microvascular disease or endothelial dysfunction. Alternatively, structural heart disease causing chronotropic incompetence may lead to poor collateral filling.

Objective: To characterize migraine in patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Background: CADASIL serves as a key model of a monoallelic stroke disease. A portion of patients have coexistent migraine with aura, yet the relationship between migraine and the pathophysiology of CADASIL is poorly understood. Design/Methods: We performed a prospective study of adults with a confirmed genetic diagnosis of CADASIL, age-matched controls with migraine with aura (MA), and headache-free controls. The Migraine Disability Assessment Questionnaire (MIDAS) and Headache Impact Test (HIT-6) were used to quantify migraine-related disability. Subjects were followed for one year after enrollment. Results: We enrolled 88 subjects, which included 33 subjects with CADASIL, 32 subjects without CADASIL but with MA, and 23 control subjects without CADASIL or MA. Mean age was 53.6 (range, 22-86), 64.8% (57/88) were females, and 83% (73/88) were white. Of the CADASIL subjects, 61% (20/33) suffered from MA (CAD/+MA). Aura semiology amongst the CAD/+MA and MA patients were as follows: visual (80% vs 81%), sensory (75% vs 81%), speech (75% vs 50%), motor (30% vs 50%), brain stem (60% vs 81%) and retinal (30% vs 25%). Mean MIDAS scores at enrollment were comparable between the CAD/+MA and MA populations (32.3 vs 33.5), as were mean HIT-6 scores (56.3 vs 56.9). Discussion: These preliminary results do not show a significant difference in migraine disability between CADASIL migraineurs and chronic migraineurs. Minor differences were observed in aura distribution between the two groups, although further investigations are needed to better understand the underlying pathology of CADASIL and migraine.