Citations

Objective Cervical artery dissection (CeAD) may be limited to the extracranial extradural space or extend to the intradural space. Intradural extension can potentially increase the risk of stroke and subarachnoid hemorrhage. However, the factors associated with intradural extension and its impact on clinical outcome remain unclear. Methods This was a secondary analysis of the STOP‐CAD observational, multi‐center study. Patients with CeAD and intradural extension (CeADid) were compared with those with pure CeAD extradural dissections (CeADed) using multiple regression analyses. Results Of 4,023 patients with CeAD, 534 (13.3%) had CeADid. In comparison to patients with CeADed, those with CeADid more often had clinical overt stroke or transient ischemic attack (TIA) at presentation, acute infarcts on imaging, a vertebral artery affected, and severe stenosis of the involved vessel ( p < 0.001 for all). In contrast, carotid involvement and complete occlusions were more frequent in patients with CeADed ( p < 0.001 for both). CeADid was associated with a shift in the distribution of scores on the modified Rankin Scale (mRS) toward worse functional outcome (odds ratio [OR] = 0.76, 95% confidence interval [CI] = 0.62–0.92) but the odds for favorable outcomes (mRS = 0–2) did not differ between the groups after appropriate adjustments on multivariate analysis. CeADid was independently associated with higher mortality at 180 days on multivariate analysis (adjusted OR = 2.84, 95% CI = 1.50–5.38). Interpretation CeADid is associated with more severe clinical presentation, a shift toward less favorable outcomes, and higher mortality rates. These findings suggest that CeADid may represent a high‐risk type of CeAD. ANN NEUROL 2026;99:1189–1197

Introduction/Purpose Vertebral artery dissection is a recognized cause of ischemic stroke in young and middle‐aged adults, often presenting with headache, neck pain, and focal neurologic deficits. Minor trauma, including neck manipulation, is a statistically significant risk factor for cervical artery dissection, with several case‐control and cohort studies demonstrating an association, particularly in younger patients. The vertebral arteries ascend through the transverse foramina of the cervical vertebrae, making them susceptible to mechanical stress from abnormal spinal curvature. Cervical scoliosis alters the bony alignment and curvature, causing the vertebral artery pathway to be elongated, kinked, or compressed, especially at the apex of the spinal curve. We suspect in patients with abnormal cervical biomechanisms the vertebral arteries are more vulnerable to injury during high velocity cervical manipulation. This case aims to highlight the risk of arterial dissection in a patient with scoliosis after undergoing neck manipulation. Materials/Methods A 37‐year‐old right‐handed male with a history of migraine headaches presented with acute onset diplopia and vertigo accompanied by nausea, vomiting, and right facial sensory loss on awakening. The patient reported recent chiropractic cervical manipulation days prior to symptom onset. Neurological examination revealed right‐sided facial sensory deficits, multidirectional nystagmus, and right homonymous hemianopia. CT angiography demonstrated right vertebral artery dissection in V2 and V3 and subtle luminal changes over the left V2 segment with scoliotic curve of the cervical spine and upper thoracic spine. MRI and MR angiography demonstrated multifocal acute infarcts in the posterior circulation and evidence of vertebral artery dissection. Additional workup included a lipid panel which showing an LDL of 137 mg/dL and a transthoracic echocardiogram revealing a bicuspid aortic valve. Results The patient was initiated on dual antiplatelet therapy with aspirin and clopidogrel for secondary prevention, consistent with American Heart Association guidance for extracranial cervical artery dissection, with plans to transition to single antiplatelet therapy after 3 months, assuming no recurrent events and stable follow up imaging. Ultimately, the patient had improvement in his visual symptoms including complete resolution of right homonymous hemianopia during his hospitalization. Given his elevated LDL, the patient was started on a high intensity statin therapy. Secondary prevention strategies included aggressive vascular risk factor modification, avoidance of further neck manipulation or trauma, and close outpatient follow‐up with repeat vascular imaging in 3 months. The patient was also referred to medical genetics to further evaluate possible underlying connective tissue disorders. He was counseled regarding the statistical association between cervical manipulative therapy and vertebral artery dissection, and the importance of prompt medical evaluation for any future neurological symptoms. Conclusions Cervical scoliosis is not a well‐established independent risk factor for vertebral artery dissection. However, when combined with cervical high velocity manipulations, the vertebral arteries are likely to be more vulnerable to injury and lead to dissections and strokes. Further research is warranted on this topic. Finally, early recognition and evidence‐based antithrombotic therapy are critical to optimizing outcomes in patients with arterial dissection.

Introduction/Purpose Diabetic striatopathy (DS) is a rare neurologic complication of poorly controlled diabetes mellitus characterized by hemichorea/hemiballism and distinctive basal ganglia imaging abnormalities, most commonly T1 hyperintensity in the putamen or caudate nucleus. Emerging evidence suggests that DS may coexist with acute ischemic stroke, particularly in the context of intracranial atherosclerotic disease (ICAS), complicating both diagnosis and management. The pathophysiological interplay between chronic hyperglycemia and impaired regional perfusion is postulated to increase basal ganglia vulnerability to metabolic and ischemic injury, leading to the characteristic clinical and radiological features of DS. This case report aims to highlight the clinical course, diagnostic evaluation, and management of a patient presenting with DS and stroke secondary to ICAS. Materials/Methods A 68‐year‐old female with hypertension, hyperlipidemia, and newly diagnosed diabetes presented with a one‐month history of left arm choreiform movements, episodic dizziness, and blurred vision. Movements correlated with hyperglycemia (home blood glucose in the 400s) and resolved with dietary modification and improved glycemic control. Initial MRI revealed right M1 segment MCA occlusion with multiple subacute‐chronic infarcts in the right MCA territory and T1 hyperintensity in the right putamen, suggestive of DS. CT angiography head and neck demonstrated distal right M1 severe stenosis vs occlusion with distal reconstitution, atherosclerotic calcification in the right carotid siphon, and severe stenosis in the right V4 segment and left AICA. Laboratory evaluation showed LDL 103 mg/dL and HbA1c 10.7%. Cardioembolic evaluation with echocardiography, transcranial doppler, and prolonged cardiac monitoring was unremarkable. The patient was managed with dual antiplatelet therapy (aspirin and clopidogrel for 90 days, then aspirin monotherapy), high‐intensity statin, and intensive glycemic control per current consensus guidelines for ICAS and DS. Results The patient's involuntary movements resolved with improved glycemic control, consistent with DS. Follow‐up imaging at three months demonstrated interval resolution of right lentiform nucleus edema and enhancement, with residual mild T1 hyperintensity and curvilinear susceptibility artifact. No new infarcts were identified; prior right MCA territory infarcts appeared subacute/chronic. Persistent right distal M1 MCA stenosis was noted. The cessation of choreiform movements with normalization of blood glucose and the radiological evolution of basal ganglia changes supported the diagnosis of DS in the context of ICAS. Aggressive medical management, including dual antiplatelet therapy and statin, was implemented per American Heart Association (SAMMPRIS) recommendations for symptomatic ICAS. The patient remained neurologically stable without recurrent stroke or movement disorder. Conclusion This case illustrates the complex interplay between chronic hyperglycemia and intracranial atherosclerotic disease in the pathogenesis of both stroke and diabetic striatopathy. The combination of metabolic and vascular insults likely increases basal ganglia susceptibility to injury, manifesting as DS and ischemic stroke. Recognition of this association is critical for accurate diagnosis and optimal management, as DS may herald imminent cerebrovascular events. Aggressive risk factor modification and guideline‐directed medical therapy are essential for secondary prevention in ICAS, while glycemic control remains the cornerstone of DS management. Further research is needed to elucidate the mechanistic links and refine therapeutic strategies for these overlapping entities.

ABSTRACT Systemic lupus erythematosus (SLE) is an enigmatic autoimmune disease with a varied presentation that carries with it an increased risk for many potentially life‐threatening problems. When compared with the general population, the relative risk of ischemic stroke in SLE is more than doubled. Our case report highlights a rare complication of SLE, vasculitis as the cause of stroke. CNS vasculitis secondary to SLE most commonly affects the endothelium of small and medium vessel arteries through perivascular inflammation in a concentric pattern. We present a case of a 46‐year‐old female with a history of hypertension, hyperlipidemia, hypothyroidism, multiple ischemic strokes (residual left sided weakness), and elevated cardiolipin IgM levels (not on anticoagulation) who presented with left facial numbness, dysarthria, and word finding difficulty. The initial CT head revealed chronic appearing hypodensities in the right parietal and occipital lobes without hemorrhage. CT angiogram of the head and neck demonstrated multifocal stenosis in the right MCA and right PCA. She received IV tenecteplase and MRI brain revealed an infarct in the left MCA distribution along with infarcts in the right thalamus, hippocampus, and cerebellum. Transesophageal echocardiogram was negative for Libman‐Sacks endocarditis. Given concerns for an underlying vasculitis process, an MRA vessel wall imaging was obtained which demonstrated concentric enhancement and persistent vessel narrowing in the left MCA M2 along with symmetric concentric enhancement of vaso vasorum of intracranial vertebral arteries. Lumbar puncture revealed CSF protein 60, culture negative, glucose 61, white blood cells 3, IgG index 0.5, ACE negative, and no oligoclonal bands. Her ESR was 43 and CRP < 0.5. Hypercoagulability workup demonstrated RNP > 8, SSA 6.4, Smith 1.6, +ANA 1:1280, C4 11, cardiolipin IgM 60. Given serum ANA titers and anti‐cardiolipin IgM labs in the setting of intracranial vessel wall enhancement concerning for an inflammatory process, it was believed that this stroke was actually a result of lupus vasculitis. The paucity of literature on the association between SLE vasculitis and cerebrovascular disease presents an important opportunity for more research, and it may be prudent to further investigate the relative risk of stroke in patients with known SLE vasculitis. This is also important because young individuals with SLE are at a higher relative risk of stroke.

BACKGROUND: Small, randomized trials of patients with cervical artery dissection showed conflicting results regarding optimal stroke prevention strategies. We aimed to compare outcomes in patients with cervical artery dissection treated with antiplatelets versus anticoagulation. METHODS: This is a multicenter observational retrospective international study (16 countries, 63 sites) that included patients with cervical artery dissection without major trauma. The exposure was antithrombotic treatment type (anticoagulation versus antiplatelets), and outcomes were subsequent ischemic stroke and major hemorrhage (intracranial or extracranial hemorrhage). We used adjusted Cox regression with inverse probability of treatment weighting to determine associations between anticoagulation and study outcomes within 30 and 180 days. The main analysis used an as-treated crossover approach and only included outcomes occurring with the above treatments. RESULTS: The study included 3636 patients (402 [11.1%] received exclusively anticoagulation and 2453 [67.5%] received exclusively antiplatelets). By day 180, there were 162 new ischemic strokes (4.4%) and 28 major hemorrhages (0.8%); 87.0% of ischemic strokes occurred by day 30. In adjusted Cox regression with inverse probability of treatment weighting, compared with antiplatelet therapy, anticoagulation was associated with a nonsignificantly lower risk of subsequent ischemic stroke by day 30 (adjusted hazard ratio [HR], 0.71 [95% CI, 0.45–1.12]; P =0.145) and by day 180 (adjusted HR, 0.80 [95% CI, 0.28–2.24]; P =0.670). Anticoagulation therapy was not associated with a higher risk of major hemorrhage by day 30 (adjusted HR, 1.39 [95% CI, 0.35–5.45]; P =0.637) but was by day 180 (adjusted HR, 5.56 [95% CI, 1.53–20.13]; P =0.009). In interaction analyses, patients with occlusive dissection had significantly lower ischemic stroke risk with anticoagulation (adjusted HR, 0.40 [95% CI, 0.18–0.88]; P interaction =0.009). CONCLUSIONS: Our study does not rule out the benefit of anticoagulation in reducing ischemic stroke risk, particularly in patients with occlusive dissection. If anticoagulation is chosen, it seems reasonable to switch to antiplatelet therapy before 180 days to lower the risk of major bleeding. Large prospective studies are needed to validate our findings.

BACKGROUND: Patients presenting with cervical artery dissection (CAD) are at risk for subsequent ischemic events. We aimed to identify characteristics that are associated with increased risk of ischemic stroke after initial presentation of CAD and to evaluate the differential impact of anticoagulant versus antiplatelet therapy in these high-risk individuals. METHODS: This was a preplanned secondary analysis of the STOP-CAD study (Antithrombotic Treatment for Stroke Prevention in Cervical Artery Dissection), a multicenter international retrospective observational study (63 sites from 16 countries in North America, South America, Europe, Asia, and Africa) that included patients with CAD predominantly between January 2015 and June 2022. The primary outcome was subsequent ischemic stroke by day 180 after diagnosis. Clinical and imaging variables were compared between those with versus without subsequent ischemic stroke. Significant factors associated with subsequent stroke risk were identified using stepwise Cox regression. Associations between subsequent ischemic stroke risk and antithrombotic therapy type (anticoagulation versus antiplatelets) among patients with identified risk factors were explored using adjusted Cox regression. RESULTS: In all, 4023 patients (mean age was 47.4 years; 44.5% were women) were included. By day 180, subsequent ischemic stroke occurred in 5.3% of the cohort. In adjusted Cox regression, factors associated with increased risk of subsequent ischemic stroke were prior history of ischemic stroke (adjusted hazard ratio [aHR], 7.31 [95% CI, 1.61–33.13]; P =0.010), presentation within 7 days from first symptoms (aHR, 3.04 [95% CI, 1.04–8.91]; P =0.043), infarct on baseline imaging (aHR, 9.85 [95% CI, 3.65–26.58]; P <0.001), and occlusive dissection (aHR, 2.34 [95% CI, 1.03–5.34]; P =0.043). Only patients with occlusive dissection demonstrated a reduced risk of subsequent ischemic stroke when treated with anticoagulation versus antiplatelets (aHR, 0.36 [95% CI, 0.16–0.80]; P =0.01). CONCLUSIONS: In this post hoc analysis of the STOP-CAD study, several factors associated with subsequent ischemic stroke were identified among patients with CAD. Furthermore, we identified a potential benefit of anticoagulation in patients with CAD with occlusive dissection. These findings require validation by meta-analyses of prior studies to formulate optimal treatment strategies for specific high-risk CAD subgroups.