F.-C. Chang

Monitoring Peri-Therapeutic Cerebral Circulation Time: A Feasibility Study Using Color-Coded Quantitative DSA in Patients with Steno-Occlusive Arterial Disease

BACKGROUND AND PURPOSE: Intracranial hemodynamics are important for management of SOAD. This study aimed to monitor peri-stent placement intracranial CirT of patients with SOAD. MATERIALS AND METHODS: Twenty-five patients received stent placement for extracranial ICA stenosis, and 34 patients with normal CirT were recruited as controls. Their color-coded DSAs were used to define the Tmax of selected intravascular ROI. A total of 20 ROIs of the ICA, OphA, ACA, MCA, FV, PV, OV, SSS, SS, IJV, and MCV were selected. rTmax was defined as the Tmax at the selected region of interest minus Tmax at the cervical segment of the ICA (I1 on AP view and IA on lateral view). rTmax of the PV was defined as intracranial CirT. Intergroup and intragroup longitudinal comparisons of rTmax were performed. RESULTS: rTmax values of the normal cohorts were as follows: ICA-AP, 0.12; ICA-LAT, 0.10; A1, 0.28; A2, 0.53; A3, 0.81; M1, 0.40; M2, 0.80; M3, 0.95; OphA, 0.35; FV, 4.83; PV, 5.11; OV, 5.17; SSS, 6.16; SS, 6.51; IJV, 6.81; and MCV, 3.86 seconds. Before stent placement, the rTmax values of arterial ROIs, except A3 and M3, were prolonged compared with values from control subjects (P < .05). None of the rTmax of any venous ROIs in the stenotic group was prolonged with significance. After stent placement, the rTmax of all arterial ROIs shortened significantly, except A1and M3. Poststenting rTmax was not different from the control group. CONCLUSIONS: Without extra contrast medium and radiation dosages, color-coded quantitative DSA enables real-time monitoring of peri-therapeutic intracranial CirT in patients with SOAD .

Stent Management of Coil Herniation in Embolization of Internal Carotid Aneurysms

BACKGROUND AND PURPOSE: Coil herniation into the parent artery after detachment is an uncommon complication of embolization of the intracranial aneurysm. We report our experience with stent reconstruction of the lumen and flow of the internal carotid artery (ICA) after coil herniation during embolization for intracranial ICA aneurysms and the possible mechanisms of coil herniation. MATERIALS AND METHODS: A series of 216 consecutive patients was treated by endovascular coil embolizations for intracranial aneurysms. Of these patients, there were 9 (4 men, 5 women; 32–68 years of age) complicating with coil herniation into the ICA and undergoing stent deployment to reconstruct the ICA lumen (n = 8) or both lumen and flow (n = 1). Wide-neck aneurysms were found in 8 and narrow-neck, in 1. Aneurysms were in the posterior communicating artery (n = 5) and the paraophthalmic (n = 3) and cavernous portions (n = 1) of the ICA. Self-expandable stents were deployed in the ICA in 6; balloon-mounted stents were selected in 3. RESULTS: The causes of coil herniation appeared to be coil instability after detachment (n = 6), excessive embolization (n = 1), microcatheter-related problems (n = 1), or being pushed by subsequent coil embolization (n = 1). Endovascular stent placement to reconstruct the lumen and/or flow of the ICA was technically successful in all 9 patients; 1 needed a second stent due to further coil migration. No significant procedure-related complications were found. Clinical follow-up was 8–35 months. CONCLUSION: Coil herniation occasionally occurs during endovascular embolization of ICA aneurysms because of coil instability after detachment, excessive embolization, microcatheter-related problems, or pushing by subsequent coil embolization. In this small series, stent placement was safe and effective in the reconstruction of the arterial lumen and/or restoration of flow past a herniated coil mass.

Dynamic MR Imaging Patterns of Cerebral Fat Embolism: A Systematic Review with Illustrative Cases

SUMMARY: Different MR imaging patterns of cerebral fat embolism have been reported in the literature without a systematic review. Our goal was to describe the patterns, explore the relationship between disease course and the imaging patterns, and discuss the underlying mechanism. We reveal 5 distinctive MR imaging patterns: 1) scattered embolic ischemia occurring dominantly at the acute stage; 2) confluent symmetric cytotoxic edema located at the cerebral white matter, which mainly occurs at the subacute stage; 3) vasogenic edematous lesions also occurring at the subacute stage; 4) petechial hemorrhage, which persists from the acute to the chronic stage; and 5) chronic sequelae, occurring at late stage, including cerebral atrophy, demyelinating change, and sequelae of infarction or necrosis. Underlying mechanisms of these imaging patterns are further discussed. Recognition of the 5 evolving MR imaging patterns of cerebral fat embolism may result in adjustment of the appropriate management and improve the outcome.

Endovascular treatment of intracranial high-flow arteriovenous fistulas by Guglielmi detachable coils.

Background: This study reports our experience in performing transarterial Guglielmi detachable coil (GDC) embolization for intracranial high‐flow arteriovenous fistulas (AVFs) and evaluates its efficacy and safety. Methods: Over 3 years, 13 patients with 14 intracranial high‐flow AVFs had been managed by transarterial GDC embolization in our institution. There were 6 men and 7 women, with a mean age of 27 years. Of these 14 AVFs, 8 were traumatic carotid‐cavernous fistulas (TCCFs); 5 were AVFs at the frontal, temporal, parieto‐occipital lobes, or associated with arteriovenous malformation (n = 3); 1 was a tentorium AVF. Results: All of these high‐flow AVFs were successfully occluded by a single session of transarterial GDC embolization. In 8 patients with TCCFs, the nearby parent arteries were preserved. The average number of coils was 8 and the average length was 126 cm. All AVF‐related symptoms resolved immediately or gradually on clinical follow‐up. No significant procedure‐related neurologic complication or recurrent AVF was seen. All 13 patients were followed up clinically for an average of 16 months (range, 6–25 months). Conclusion: Transarterial GDC embolization is a useful method in the treatment of intracranial high‐flow AVFs. GDC affords more control in the placement of coils and proved both efficient and safe in the management of intracranial high‐flow AVFs.

Role of CT and endovascular embolization in managing pseudoaneurysms of the internal maxillary artery.

Background: The purpose of this study was to evaluate the role of computed tomography (CT) and endovascular embolization in managing 10 patients with 11 internal maxillary arterial pseudoaneurysms (IMPAs) with acute oronasal hemorrhage. Methods: A series of 10 patients with 11 IMPAs presenting with profuse oronasal hemorrhage, all treated with endovas‐cular embolization, were reviewed. There were 9 males and 1 female ranging in age from 10 to 56 years (mean, 38 years). The predisposing factors of IMPA were trauma (n = 6) or head and neck carcinomas (HNCs) after surgical treatment and/or postradiation therapy (n = 5). Before embolization, all patients had CT of maxillofacial regions to evaluate the extension of trauma or to evaluate the treatment outcome for HNCs. Endovascular embolization was employed to occlude the IMPAs by delivering the embolic agents of liquid adhesives (n = 9) or microcoils (n = 2) to the IMPAs. Results: On the lesion side, CT revealed maxillofacial fractures in all 5 trauma patients and recurrent or residual tumors in 3 patients with HNCs. In the other 2 patients with HNCs, CT showed no significant finding and contributed little to the catheter angiography in detecting the IMPAs. Endovascular treatment was technically successful in all 11 IMPAs, ceasing hemorrhage immediately after embolization. No recurrence of bleeding was observed. No patient developed neurologic deficit, skin, or mucosal necrosis at the maxillofacial region. Clinical follow‐up was 2‐36 months (mean, 14 months). Two patients with advanced carcinoma died during follow‐up because of disease progression. Conclusion: CT is a useful tool for guiding catheter angiography to localize the majority of IMPAs. Endovascular embolization can succeed in managing IMPAs, and should be performed as soon as the IMPA is depicted.

Stenotic transverse sinus predisposes to poststenting hyperperfusion syndrome as evidenced by quantitative analysis of peritherapeutic cerebral circulation time.

BACKGROUND AND PURPOSE: Hyperperfusion syndrome is a devastating complication of carotid stent placement. The shortening of cerebral circulation time after stent placement is seen as a good indicator of the development of hyperperfusion syndrome. The purpose of our study was to evaluate whether patients with ipsilateral transverse sinus stenosis are prone to having shortened cerebral circulation time after stent placement, subsequently leading to the possible development of hyperperfusion syndrome. MATERIALS AND METHODS: Forty-nine patients with >70% unilateral carotid stenosis undergoing stent placement were recruited for analysis. Group A consisted of patients with a stenotic ipsilateral transverse sinus >50% greater than the diameter of the contralateral transverse sinus; the remaining patients were in group B. Quantitative DSA was used to calculate cerebral circulation time. Cerebral circulation time was defined as the time difference between the relative time to maximal intensity of ROIs in the proximal internal carotid artery and the internal jugular vein. ΔCCT was defined as cerebral circulation time before stent placement minus cerebral circulation time after stent placement. ΔCCT, white matter hyperintensity signals, and sulcal effacement in MR imaging were compared between the 2 groups. RESULTS: ΔCCT was significantly shorter in group A (0.65 ± 1.3) than in group B (−0.12 ± 1.4). Three patients had white matter hyperintensity signals in group A, and 1 developed hyperperfusion syndrome. Group B showed no MR imaging signs of hyperperfusion syndrome. CONCLUSIONS: Ipsilateral hypoplastic transverse sinus was associated with prolonged cerebral circulation time before stent placement and greatly shortened cerebral circulation time after stent placement. Inadequate venous drainage might play a role in impaired cerebral autoregulation and might influence the development of poststenting hyperperfusion syndrome.

Can iterative reconstruction improve imaging quality for lower radiation CT perfusion? Initial experience.

BACKGROUND AND PURPOSE: Initial results using IR for CT of the head showed satisfactory subjective and objective imaging quality with a 20–40% radiation dose reduction. The aim of our study was to compare the influence of IR and FBP algorithms on perfusion parameters at standard and lowered doses of CTP. MATERIALS AND METHODS: Forty patients with unilateral carotid stenosis post–carotid stent placement referred for follow-up CTP were divided into 2 groups (tube currents were 100 mAs in group A and 80 mAs in group B). Datasets were reconstructed with IR and FBP algorithms; and SNRs of gray matter, white matter, and arterial and venous ROIs were compared. CBF, CBV, and MTT means and SNRs were evaluated by using linear regression, and qualitative imaging scores were compared across the 2 algorithms. RESULTS: The mean effective radiation dose of group B (2.06 mSv) was approximately 20% lower than that of group A (2.56 mSv). SNRs for ROIs in the dynamic contrast-enhanced images were significantly higher than those for the FBP images. Correlations of the SNRs for CBF, CBV, and MTT across the 2 algorithms were moderate (R2 = 0.46, 0.23, and 0.44, respectively). ROIs in gray matter rather than the IR algorithm predicted increasing SNRs in all CBF, CBV, and MTT maps. Two cases of significant restenosis were confirmed in both algorithms. CBV, CBF, and MTT imaging scores did not differ significantly across algorithms or groups. CONCLUSIONS: Lower dose CTP (20% below normal dose) without IR can effectively identify oligemic tissue in poststenting follow-up. IR does not alter the absolute values or increase the SNRs of perfusion parameters. Other methods should be attempted to improve SNRs in settings with low tube currents.

Ipsilateral crural monoparesis in lateral medullary infarction due to vertebral artery dissection

Sir, Vertebral artery (VA) dissection has been much emphasized in brainstem stroke due to its detrimental manifestations and young onset. We describe a VA-dissected patient with an ipsilateral crural monoparesis in addition to a lateral medullary syndrome, i.e. Opalski’s syndrome [1]. A 37-year-old woman of recently noticed hypertension suffered from a sudden-onset occipital headache, severe vertigo, right facial numbness, and right leg monoparesis. She had frequently held the phone between the right cheek and shoulder. Neurologic examinations revealed a left-beating torsional nystagmus, right miosis, right peripheral facial palsy, and an impaired pinprick sensation on the right face and left body. Her right arm was ataxic and normal in strength, but the right lower limb was so weak that she could only raise it up to 30 cm from bed and hold there for 1–2 s. Magnetic resonance imaging (MRI) on the second day of admission revealed a right lateral medullary infarction (LMI) and an aneurismal dilatation in the ipsilateral VA (Fig. 1a–c). Conventional angiography demonstrated a fusiform aneurysm (Fig. 1d). Her weakness recovered almost completely on the seventh day of admission, and she was discharged on the 29th day with the prescription of aspirin 100 mg per day. Opalski first described an LMI case with ipsilateral hemiparesis [1,2]. Although it was thought to be rare, a recent study suggests that ipsilateral hemiparesis appears in as many as 7% of cases of LMI [3]. As VA dissection resulted in as many as 29% of LMI and 21% of medial medullary infarction [3], cases with ipsilateral hemiparesis were not frequently reported [4–6]. In our case, ipsilateral crural monoparesis was evident in addition to right LMI. To our knowledge, only one similar case has been reported [7]. Ipsilateral hemiparesis in medullary infarction may result from compromised medullary-penetrating arteries, which arise from VA or the anterior spinal artery and supply the pyramidal fibers below the decussation. Despite the arguments [8], crural monoparesis in our case supports that pyramidal tract fibers innervating the lower and upper extremities decussate at different levels. They do not mix with each other. Nevertheless, false localization signs from cerebellar infarction [9] or occlusion of both the posterior spinal artery and the posterior inferior cerebellar artery [10] may also mimic Opalski’s syndrome. In conclusion, attention should be paid to the ipsilateral crural or hemiparesis obscuring from limb ataxia in brainstem infarction. Brain MRI or magnetic resonance angiography study is mandatory due to the possibility of VA dissection.

Endovascular treatment of ruptured vertebral dissecting aneurysms with electrodetachable coils.

Background: Ruptured intradural vertebral dissecting aneurysm (VDA) is associated with a high risk of rebleeding and a high incidence of mortality if left untreated because of its natural history. We report our experience of endovascular treatment of ruptured VDAs using electrodetachable coils. Methods: Over 7 years, 10 patients with spontaneously ruptured intradural VDAs were managed by endovascular embolization in our institute. All patients received endovascular trapping of the dissecting aneurysm and proximal occlusion by electrodetachable coils. Results: There were 5 men and 5 women, with a mean age of 48 years. Of the 10 VDAs, 8 were located in the supra‐posterior inferior cerebellar artery (PICA) area, and 2 were in the infra‐PICA area. Six affected vertebral arteries were dominant (n = 3) or co‐dominant (n = 3) in the vertebrobasilar system. Nine ruptured VDAs and their parent arteries were successfully occluded by a single session of endovascular embolization by electrodetachable coils. In the tenth patient, the dissecting aneurysm showed subtotal occlusion because of involvement of the vertebrobasilar junction. The mean number and coil length were 7 and 58 cm, respectively. There were no significant periprocedural complications or recurrent bleeding. All patients demonstrated good clinical recovery (n = 9) or improvement (n = 1) after embolization over a mean follow‐up of 15 months (range, 6–24 months). Conclusion: Endovascular embolization is a useful and safe method in the treatment of ruptured VDAs even when the affected vertebral arteries are dominant or co‐dominant in vertebrobasilar flow. Trapping procedures and direct occlusion of the dissecting segment with preservation of the PICA by detachable coils should be performed as early as possible in the management of VDAs.

Internal jugular venous abnormalities in transient monocular blindness

BackgroundThe etiology of transient monocular blindness (TMB) in patients without carotid stenosis has been linked to ocular venous hypertension, for their increased retrobulbar vascular resistance, sustained retinal venule dilatation and higher frequency of jugular venous reflux (JVR). This study aimed to elucidate whether there are anatomical abnormalities at internal jugular vein (IJV) in TMB patients that would contribute to impaired cerebral venous drainage and consequent ocular venous hypertension.MethodsContrast-enhanced axial T1-weighted magnetic resonance imaging (MRI) was performed in 23 TMB patients who had no carotid stenosis and 23 age- and sex-matched controls. The veins were assessed at the upper IJV (at C1–3 level) and the middle IJV (at C3–5 level). Grading of IJV compression/stenosis was determined bilaterally as follows: 0 = normal round or ovoid appearance; 1 = mild flattening; 2 = moderate flattening; and 3 = severe flattening or not visualized.ResultsThere was significantly more moderate or severe IJV compression/stenosis in the TMB patients at the left upper IJV level and the bilateral middle IJV level. Defining venous compression/stenosis scores ≥ 2 as a significant cerebral venous outflow impairment, TMB patients were found to have higher frequency of significant venous outflow impairment at the upper IJV level (56.5% vs. 8.7%, p = 0.0005) and the middle IJV level (69.6% vs. 21.7%, p=0.0011).ConclusionsTMB Patients with the absence of carotid stenosis had higher frequency and greater severity of IJV compression/stenosis which could impair cerebral venous outflow. Our results provide evidence supporting that the cerebral venous outflow abnormality is one of the etiologies of TMB.