Differential Contribution of ASPECTS Regions to Clinical Outcome after Thrombectomy for Acute Ischemic Stroke.

BACKGROUND AND PURPOSE: Ischemic stroke is the leading cause of long-term disability in adults, but our ability to prognosticate from baseline imaging data is limited. The ASPECTS measures ischemic change in the middle cerebral artery territory on noncontrast CT based on 10 anatomic regions. Here, we investigated whether infarction in particular regions was associated with worse long-term outcome. MATERIALS AND METHODS: We identified consecutive patients receiving mechanical thrombectomy for ICA/MCA occlusion at 2 comprehensive stroke centers. Pretreatment ASPECTS was assessed by 2 blinded reviewers. Clinical data including demographics, baseline NIHSS score, and 90-day mRS were collected. The relationship between individual ASPECTS regions and the mRS score (0-2 versus 3-6) was assessed using multivariable logistic regression. RESULTS: Three hundred fifty-three patients were included (mean age, 70 years; 46% men), of whom 214 had poor outcome (mRS = 3-6). Caudate (OR = 3.26; 95% CI, 1.33-8.82), M4 region (OR = 2.94; 95% CI, 1.09-9.46), and insula (OR = 1.75; 95% CI, 1.08-2.85) infarcts were associated with significantly greater odds of poor outcome, whereas M1 region infarction reduced the odds of poor outcome (OR = 0.38; 95% CI, 0.14-0.99). This finding remained unchanged when restricted to only patients with good recanalization. No significant associations were found by laterality. Similarly, no region was predictive of neurologic improvement during the first 24 hours or of symptomatic intracerebral hemorrhage. CONCLUSIONS: Our results indicate that ASPECTS regions are not equal in their contribution to functional outcome. This finding suggests that patient selection based on total ASPECTS alone might be insufficient, and infarct topography should be considered when deciding eligibility for thrombectomy.

Facial Nerve Arterial Arcade Supply in Dural Arteriovenous Fistulas: Anatomy and Treatment Strategies.

BACKGROUND AND PURPOSE: Endovascular treatment of petrous dural AVFs may carry a risk of iatrogenic facial nerve palsy if the facial nerve arterial arcade, an anastomotic arterial arch that supplies the geniculate ganglion, is not respected or recognized. Our purpose was to demonstrate that the use of a treatment strategy algorithm incorporating detailed angiographic anatomic assessment allows identification of the facial nerve arterial arcade and therefore safe endovascular treatment. MATERIALS AND METHODS: This was a retrospective cohort study of consecutive petrous dural AVF cases managed at Toronto Western Hospital between 2006 and 2018. Our standard of care consists of detailed angiographic assessment followed by multidisciplinary discussion on management. Arterial supply, primary and secondary treatments undertaken, angiographic outcomes, and clinical outcomes were assessed by 2 independent fellowship-trained interventional neuroradiologists. RESULTS: Fifteen patients had 15 fistulas localized over the petrous temporal bone. Fistulas in all 15 patients had direct cortical venous drainage and received at least partial supply from the facial nerve arterial arcade. Following multidisciplinary evaluation, treatment was performed by endovascular embolization in 8 patients (53%) and microsurgical disconnection in 7 patients (47%). All patients had long-term angiographic cure, and none developed iatrogenic facial nerve palsy. CONCLUSIONS: By means of our treatment strategy based on detailed angiographic assessment and multidisciplinary discussion, approximately half of our patients with petrous AVFs were cured by endovascular treatment, half were cured by an operation, and all had preserved facial nerve function.

Diagnostic Impact of Intracranial Vessel Wall MRI in 205 Patients with Ischemic Stroke or TIA.

BACKGROUND AND PURPOSE: Secondary prevention of ischemic stroke depends on determining the cause of the initial ischemic event, but standard investigations often fail to identify a cause or identify multiple potential causes. The purpose of this study was to characterize the impact of intracranial vessel wall MR imaging on the etiologic classification of ischemic stroke. MATERIALS AND METHODS: This was a single-center, retrospective study of 205 consecutive patients who were referred for vessel wall MR imaging to clarify the etiology of an ischemic stroke or TIA. An expert panel classified stroke etiology before and after incorporating vessel wall MR imaging results using a modified Trial of Org 10172 in Acute Stroke Treatment system. We measured the proportion of patients with an altered etiologic classification after vessel wall MR imaging. RESULTS: The median age was 56 years (interquartile range = 44-67 years), and 51% (106/205) of patients were men. Vessel wall MR imaging altered the etiologic classification in 55% (112/205) of patients. The proportion of patients classified as having intracranial arteriopathy not otherwise specified decreased from 31% to 4% (64/205 versus 9/205; P < .001) and the proportion classified as having intracranial atherosclerotic disease increased from 23% to 57% (48/205 versus 116/205; P < .001). Conventional work-up classification as intracranial arteriopathy not otherwise specified was an independent predictor of vessel wall MR imaging impact (OR = 8.9; 95% CI, 3.0-27.2). The time between symptom onset and vessel wall MR imaging was not a predictor of impact. CONCLUSIONS: When vessel wall MR imaging is performed to clarify the etiology of a stroke or TIA, it frequently alters the etiologic classification. This is important because the etiologic classification is the basis for therapeutic decision-making.

High-Resolution Vessel Wall Magnetic Resonance Imaging in Angiogram-Negative Non-Perimesencephalic Subarachnoid Hemorrhage.

PURPOSE: Standard magnetic resonance imaging (MRI) rarely identifies the cause of hemorrhage in patients with an angiogram-negative, non-perimesencephalic subarachnoid hemorrhage (SAH). Yet up to 10 % of these patients have recurrent hemorrhage. The aim of the study was to explore the potential role of high-resolution contrast-enhanced 3-Tesla vessel wall-MRI in patients with angiogram-negative SAH. METHODS: We performed intracranial vessel wall-MRI of the circle of Willis using a 3-Tesla scanner in consecutive patients presenting with a spontaneous, angiogram-negative, non-perimesencephalic SAH. Vessel wall-MRI included T1-, T2-, and gadolinium-enhanced T1-weighted two-dimensional black-blood sequences in multiple planes (voxel size 0.4 × 0.4 × 2.0 mm). Two neuroradiologists independently scored abnormalities of the arterial wall. RESULTS: In all, 11 patients (mean age 59 years) underwent vessel wall-MRI. A total of seven patients had vessel wall abnormalities despite normal catheter angiography. Two patients had focal abnormalities contiguous with the outer margin of the basilar artery wall for which we considered a differential of ruptured blood blister aneurysm, thrombosed aneurysm, and loculated extramural blood from elsewhere. Two patients had arterial wall enhancement involving multiple arteries, possibly secondary to SAH. Three patients had arterial wall enhancement at sites of dural penetration, remote from the SAH, likely related to age and atherosclerotic risk factors. Vessel wall-MRI did not alter patient management in this cohort. CONCLUSION: Vessel wall-MRI showed abnormalities in seven patients with angiogram-negative SAH. These findings did not alter patient management, but the findings may be useful for other physicians who choose to perform vessel wall-MRI in this patient population.

Evaluation of the occlusion status of coiled intracranial aneurysms with MR angiography at 3T: is contrast enhancement necessary?

BACKGROUND AND PURPOSE: MR angiography (MRA) is increasingly used as a noninvasive imaging technique for the follow-up of coiled intracranial aneurysms. However, the need for contrast enhancement has not yet been elucidated. We compared 3D time-of-flight MRA (TOF-MRA) and contrast-enhanced MRA (CE-MRA) at 3T with catheter angiography. MATERIALS AND METHODS: Sixty-seven patients with 72 aneurysms underwent TOF-MRA, CE-MRA, and catheter-angiography 6 months after coiling. Occlusion status on MRA was classified as adequate (complete and neck remnant) or incomplete by 2 independent observers. For TOF-MRA and CE-MRA, interobserver agreement, intermodality agreement, and correlation with angiography were assessed by kappa statistics. RESULTS: Catheter-angiography revealed incomplete occlusion in 12 (17%) of the 69 aneurysms; 3 aneurysms were excluded due to MR imaging artifacts. Interobserver agreement was good for CE-MRA (kappa = 0.77; 95% confidence interval [CI], 0.55-0.98) and very good for TOF-MRA (kappa = 0.89; 95% CI, 0.75-1.00). Correlation of TOF-MRA and CE-MRA with angiography was good. The sensitivity of TOF-MRA and CE-MRA was 75% (95% CI, 43%-95%); the specificity of TOF-MRA was 98% (95% CI, 91%-100%) and of CE-MRA, 97% (95% CI, 88%-100%). All 5 incompletely occluded aneurysms, which were additionally treated, were correctly identified with both MRA techniques. Areas under the receiver operating characteristic curve for TOF-MRA and CE-MRA were 0.90 (95% CI, 0.79-1.00) and 0.91 (95% CI, 0.79-1.00). Intermodality agreement between TOF-MRA and CE-MRA was very good (kappa = 0.83; 95% CI, 0.65-1.00), with full agreement in 66 (96%) of the 69 aneurysms. CONCLUSIONS: In this study, TOF-MRA and CE-MRA at 3T were equivalent in evaluating the occlusion status of intracranial aneurysms after coiling. Because TOF-MRA does not involve contrast administration, this method is preferred over CE-MRA.

Relationship between freezing of gait (FOG) and other features of Parkinson's: FOG is not correlated with bradykinesia.

BACKGROUND: The pathophysiology of freezing of gait (FOG) is unclear. OBJECTIVE: To assess the relationships between FOG and other parkinsonian features in Parkinson's disease (PD), focusing on levodopa effects. METHODS: Nineteen PD patients with significant FOG in "off" were assessed while "off" and "on". Three observers independently viewed videotapes of a 130-m walk and scored FOG frequency. The Unified Parkinson's disease Rating Scale was used to evaluate clinical state. RESULTS: FOG frequency was not correlated with other parkinsonian features in "off" and only with speech and writing in "on". Levodopa significantly decreased FOG frequency (p<0.001). This reduction was strongly correlated with improvement of tremor (R=0.80, p<0.01) and speech (R=0.62, p<0.05), but not with improvement in rigidity, bradykinesia, or balance. CONCLUSION: Levodopa decreases FOG in PD. FOG is apparently an independent motor symptom, caused by a paroxysmal pathology that is different from that responsible for bradykinesia, rigidity or postural instability.

Characterization of freezing of gait subtypes and the response of each to levodopa in Parkinson's disease.

To assess the effect of levodopa on distinct freezing of gait (FOG) subtypes in patients with 'off' FOG. Nineteen patients (12 men, mean age 62.0 +/- 8.4 years) with Parkinson's disease and clinically significant FOG during 'off' states were videotaped whilst walking 130 m during 'off' and 'on' states. Three independent observers characterized the type, duration, and clinical manifestations and quantified FOG by analyzing the videotapes. Their combined mean scores were used for statistical analysis. The intra-class correlation coefficient assessed inter-observer reliability. Wilcoxon and Friedman tests evaluated differences in mean frequencies of FOG characteristics. During 'off' states, FOG was elicited by turns (63%), starts (23%), walking through narrow spaces (12%) and reaching destinations (9%). These respective values were only 14, 4, 2 and 1% during 'on' states (P < 0.011). Moving forward with very small steps and leg trembling in place were the most common manifestations of FOG; total akinesia was rare. Most FOG episodes took <10 s and tended to be shorter during 'on' states. Levodopa significantly decreased FOG frequency (P < 0.0001) and the number of episodes with akinesia (P < 0.001). Distinction amongst FOG subtypes enables evaluation of distinctive therapeutic response. Levodopa helps in reducing the frequency and duration of 'off'-related FOG.

Impaired regulation of stride variability in Parkinson's disease subjects with freezing of gait.

Patients with Parkinson's disease (PD) often experience freezing of gait, a debilitating phenomenon during which the subject suddenly becomes unable to start walking or to continue to move forward. Little is known about the gait of those subjects with PD who experience freezing of gait or the pathophysiology of freezing. One possibility is that freezing of gait is a truly paroxysmal phenomenon and that the usual walking pattern of subjects who experience freezing of gait is not different than that of other patients with PD who do not experience these transient episodes of freezing of gait. On the other hand, a recent study noted gait changes just prior to freezing and concluded that dyscontrol of the cadence of walking contributes to freezing. To address this question, we compared the gait of PD subjects with freezing of gait to PD subjects without freezing of gait. Given the potential importance of the dyscontrol of the cadence of walking in freezing, we focused on two aspects of gait dynamics: the average stride time (the inverse of cadence, a measure of the walking pace or rate) and the variability of the stride time (a measure of "dyscontrol," arrhythmicity and unsteadiness). We found that although the average stride time was similar in subjects with and without freezing, stride-to-stride variability was markedly increased among PD subjects with freezing of gait compared to those without freezing of gait, both while "on" (P<0.020) and "off" (P<0.002) anti-parkinsonian medications. Further, we found that increased gait variability was not related to other measures of motor control (while off medications) and levodopa apparently reduced gait variability, both in subjects with and without freezing. These results suggest that a paradigm shift should take place in our view of freezing of gait. PD subjects with freezing of gait have a continuous gait disturbance: the ability to regulate the stride-to-stride variations in gait timing and maintain a stable walking rhythm is markedly impaired in subjects with freezing of gait. In addition, these findings suggest that the inability to control cadence might play an important role in this debilitating phenomenon and highlight the key role of dopamine-mediated pathways in the stride-to-stride regulation of walking.