Border Zone Infarcts Research Articles

The Relationship between Neurological Worsening and Lesion Patterns in Patients with Acute Middle Cerebral Artery Stenosis

Background: Intracranial atherosclerotic disease is one of the most common causes of ischemic stroke especially in Asians, Hispanics and blacks. Although middle cerebral artery (MCA) stenosis is increasingly being recognized with the advent of magnetic resonance angiography (MRA) or transcranial Doppler ultrasonography, few studies have focused on acute neurological worsening (NW) in patients with MCA stenosis. We investigated the relationship between NW and lesion patterns detected by diffusion-weighted imaging (DWI). Methods: We studied 44 consecutive patients out of a total of 2,863 consecutive patients who had symptomatic lesions in the territory of the MCA and in whom MRA and/or conventional angiography showed isolated MCA stenosis ≥50% in the MCA trunk. Acute DWI lesion patterns were classified as follows: (1) pial artery territory infarcts (PAI); (2) small cortical and/or subcortical infarcts (SCS); (3) deep penetrating artery territory infarcts (DPI); (4) cortical border zone infarcts (CBZ), and (5) internal border zone infarcts (IBZ). NW was defined as worsening by ≥2 points on the National Institutes of Health Stroke Scale (NIHSS) during the first 7 days. Functional outcome was assessed by the modified Rankin Scale (mRS) at 3 months after stroke onset. Poor outcome was defined as ≥3 on the mRS. The severity of MCA stenosis on MRA was further categorized as 50-75% (moderate) and >75% or focal signal loss with the presence of distal MCA signal (severe). Results: There were 14 patients (31.8%) who showed NW and 16 patients (36.3%) who showed poor outcomes. Nine of the 14 patients with NW showed poor outcomes (64.2%). The most frequent lesions in the present study were SCS (n = 16, 36.3%), followed by IBZ (n = 12, 27.2%) and DPI (n = 11, 25.0%). Prevalence of IBZ was significantly higher in the group with NW compared to that without NW (p = 0.0081), while the prevalence of SCS, DPI, PAI and CBZ did not differ between the two groups. Logistic regression analysis showed significantly high age- and sex-adjusted odds ratios (ORs) for NW only for IBZ (OR 10.9, p = 0.0051). The degree of stenosis did not correlate with NW and lesion patterns. Conclusions: Only IBZ among various lesion patterns correlated strongly with NW. IBZ are considered to be more associated with hemodynamic compromise, while embolic pathogeneses contribute more to CBZ or SCS. Early interventional medical treatments such as thrombolytic or anti-platelet therapy or stenting should be considered in cases of IBZ in MCA stenosis.

Prognostic Value of Preoperative Border-zone (Watershed) Infarcts on the Early Postoperative Outcomes of Carotid Endarterectomy after Acute Ischemic Stroke

Prognostic Value of Preoperative Border-zone (Watershed) Infarcts on the Early Postoperative Outcomes of Carotid Endarterectomy after Acute Ischemic Stroke

Prognostic Value of Preoperative Border-zone (Watershed) Infarcts on the Early Postoperative Outcomes of Carotid Endarterectomy after Acute Ischemic Stroke

To evaluate the prognostic value of cerebral border-zone infarctions (watershed infarctions) on the early postoperative outcomes of patients undergoing carotid endarterectomy (CEA) after acute ischemic stroke (AIS). Sixty-six (66) patients with symptomatic carotid stenosis (SCS) that underwent ipsilateral CEA after AIS from January 2007 to March 2012 were included in this study. They were divided into two groups according to the topographic patterns of the stroke: group 1, Territorial Cerebral Ischemic Strokes (TCIS) caused by emboli of carotid origin; group 2, cerebral border-zone infarctions (CBZI) related to an SCS associated with hemodynamic impairment. All data was collected in a prospective database and analyzed. Outcome measures included postoperative neurological morbidity and 30-day mortality. Forty-three (43) patients (65.15%) experienced TCIS and were included in group 1, 23 patients (34.85%) had a CBZI and were included in group 2. There were no postoperative deaths. The postoperative neurologic morbidity rate was significantly higher in the CBZI group (22% vs. 2%, p = 0.02). Multivariate analysis demonstrates that CBZI was the only independent predictive factor of neurologic morbidity after CEA for AIS related to an SCS. Furthermore, the risk of postoperative neurologic morbidity remained significantly higher for patients with CBZI after adjustment for age, sex, initial NHISS scores, and associated contralateral carotid occlusion (HR: 0.059, 95% CI 0.004-0.85; p = 0.03). CBZIs, compared to TCIS, were associated with a higher neurological complication rate during the postoperative period after CEA for SCS in cases of AIS. Further studies are required to better define the timing and the best treatment modality for patients with CBZI related to an SCS in order to reduce associated procedural complications.

Embolism and impaired washout: A possible explanation of border zone strokes in hypereosinophilic syndrome

We describe 4 patients with stroke caused by hypereosinophilic syndrome, all of whom presented with border zone infarcts, and discuss the possible underlying mechanism. Cardioembolism (endomiocardial fibrosis) would coexist with impaired washout (perfusion disturbance due to high eosinophil count and/or eosinophil-derived substances), explaining the watershed characteristics of the infarcts.

Reversible cerebral vasoconstriction syndrome（RCVS）による脳梗塞をきたした全身性エリテマトーデス・抗リン脂質抗体陽性患者の1例

A 36-year-old female with systemic lupus erythematosus and antiphospholipid syndrome was referred to our department because of mild weakness of left arm and an episode of right amaurosis fugax for twenty days. Brain MRI showed right ACA/MCA/PCA border zone infarction on DWI/T2WI/FLAIR and MR angiography (MRA) showed multiple segmental stenosis in right internal carotid artery, right and left middle cerebral artery, and bilateral posterior cerebral arteries. Treatment with oral aspirin (100 mg/day) and continuous infusion of heparin kept her neurological symptoms and signs stable. MRA on 28 days revealed complete recovery of multiple stenotic lesions, thus, diagnosis of reversible cerebral vasoconstriction (RCVS) was made. RCVS should be considered as a cause of neurological deficit in patients with SLE regardless of thunderclap headache.

Effect of Statin on Progression of Symptomatic Intracranial Atherosclerosis

Symptomatic intracranial atherosclerosis (ICAS) is a dynamic disease that frequently progresses. Statins have been shown to have anti-atherosclerotic activity. We therefore investigated whether statins could prevent progression of ICAS. This retrospective cohort study assessed 55 patients with acute ischemic stroke and symptomatic ICAS in the middle cerebral or basilar arteries as shown on magnetic resonance angiography (MRA), with follow-up MRA performed more than 1 year after the index stroke. Change in ICAS was classified as progressive, regressive, or stable. Baseline clinical characteristics and risk factor control during follow-up were assessed, and laboratory tests were performed at the time of follow-up MRA. The statin group was defined as patients regularly treated with statins for more than 75% of the follow-up period; the remaining patients were defined as the non-statin group. At a median follow-up time of 21.8 months (range, 11.8-66.1 months), the statin group consisted of 26 (47.3%) patients and the non-statin group of 29 (52.7%). During follow-up, 6 (10.9%) patients progressed, 14 (25.5%) regressed, and 35 (63.6%) remained stable. Statin treatment was significantly associated with non-progression of ICAS (p=0.024). Two patients in the non-statin group had recurrent strokes. Border-zone infarcts were associated with progression of ICAS (3/6, 50%; p=0.007), whereas risk factors and inflammatory biomarkers were not related to progression. Treatment with statins may prevent progression of symptomatic ICAS. Prospective randomized controlled trials are required to confirm that statins protect against such progression.

Stroke Radiology and Distinguishing Characteristics of Intracranial Atherosclerotic Disease in Native South Asian Pakistanis

There are no descriptions of stroke mechanisms from intracranial atherosclerotic disease in native South Asian Pakistanis. Men and women aged ≥ 18 years with acute stroke presenting to four tertiary care hospitals in Karachi, Pakistan were screened using magnetic resonance angiography/transcranial Doppler scans. Trial of ORG 10172 in Acute Stroke Treatment criteria were applied to identify strokes from intracranial atherosclerotic disease. We studied 245 patients with acute stroke due to intracranial atherosclerotic disease. Two hundred thirty scans were reviewed. Also, 206/230 (89.0%) showed acute ischaemia. The most frequent presentation was with cortically based strokes in 42.2% (87/206) followed by border-zone infarcts (52/206, 25.2%). Increasing degrees of stenosis correlated with the development of both cortical and border-zone strokes (P = 0.002). Important associated findings were frequent atrophy (166/230, 72.2%), silent brain infarcts (66/230, 28%) and a marked lack of severe leukoaraiosis identified in only 68/230 (29.6%). A total of 1870 arteries were studied individually. Middle cerebral artery was the symptomatic stroke vessel in half, presenting with complete occlusion in 66%. Evidence of biological disease, symptomatic or asymptomatic was identified in 753 (40.2%) vessels of which 543 (72%) were significantly (>50%) stenosed at presentation. Intracranial atherosclerotic disease is a diffuse process in Pakistani south Asians, with involvement of multiple vessels in addition to the symptomatic vessel. The middle cerebral artery is the most frequent symptomatic vessel presenting with cortical embolic infarcts. There is a relative lack of leukoaraiosis. Concomitant atrophy, silent brain infarcts and recent ischaemia in the symptomatic territory are all frequently associated findings.

Cortical border-zone infarcts: clinical features, causes and outcome

ObjectiveTo report the clinical features, causes and outcome of cerebral cortical border-zone infarcts BZI (C-BZI).MethodsThe authors prospectively included patients with MRI-confirmed C-BZI among individuals consecutively admitted in Stroke Unit.ResultsForty-five patients...

Revascularization of Collaterals for Hemodynamic Stroke

Carotid atherosclerosis accounts for up to 15% of all strokes1 and approximately 15 000 to 20 000 have symptomatic carotid occlusions in the United States each year.2 Furthermore, recurrent ipsilateral stroke in unselected patients with carotid occlusion affects 2.1% to 3.8% on an annual basis.3–5 The pathophysiology of stroke due to atherosclerotic plaque of the internal carotid artery may be distinct once the stenotic or narrowed vessel progresses to occlusion. Various mechanisms for cerebral ischemia in carotid occlusion have been described, including downstream clot propagation and stump embolism6,7; however, impaired perfusion plays a major role, particularly once the distal stump of the occlusion develops mature endothelium. A combined effect of hypoperfusion and poor clearance of embolic material has also been described.8 Perfusion through collaterals to downstream territories of the brain is therefore pivotal. In fact, collaterals largely determine recurrence of symptomatic ischemia after hemodynamic stroke in carotid occlusion. The clinical observation of stereotypical events and those that occur with hypotension and initiation of antihypertensive agents, after a hot bath, or even with the upright position, support a hemodynamic process. Imaging reveals a hemodynamic pattern of ischemia with border zone infarcts as an initial presentation of carotid occlusion in 5% to 13% and in 44% to 72% of recurrent strokes.4,9 As perfusion pressure is reduced, cerebral blood flow determined by collaterals is maintained by dilatation of the resistance arterioles (Stage 1 hemodynamic impairment). Further reduction of perfusion pressure may exhaust this autoregulatory capacity and blood flow decreases proportionally to the perfusion pressure. Initially, increased oxygen extraction fraction (OEF) will maintain tissue metabolism (Stage 2 hemodynamic impairment). Thereafter, insufficient flow and oxygen delivery may result in energetic failure and infarction.10 The Carotid Occlusion Surgery Study (COSS)11 provides …

Vasculopathy after intracystic bleomycin administration for a recurrent cystic craniopharyngioma

Intracystic bleomycin (ICB) administration is known to be effective in the treatment of cystic craniopharyngiomas (CRPs) and rarely causes serious complications. The authors report a case of vasculopathy after ICB injection for a recurrent cystic CRP. A 5-year-old boy presented with the cystic recurrence of a CRP. A catheter and Ommaya system were inserted into the cyst, followed by a leakage test 2 weeks later. Bleomycin was delivered at 3 mg per week for 14 weeks (total dose 42 mg). Four months later, the patient's activity decreased and right hemiparesis occurred. Magnetic resonance imaging and cerebral angiography demonstrated a recurrent multicystic mass and infarction at the left middle cerebral artery territory with stenosis/occlusion of the left distal internal carotid artery and posterior cerebral artery. During the operation to remove the recurrent cystic mass, fibrotic stenoocclusion of the left intracranial arteries was identified. The cyst was totally removed. However, additional multiple border zone infarctions occurred in the left hemisphere, and the patient became wheelchair bound. Leakage of ICB was considered as the most probable cause of the cerebral vasculopathy and corresponding infarction. A leakage test may not always guarantee a leakage-free status even if the test is negative. Direct bypass surgery should have been considered to prevent a high risk of postoperative infarction in this case of a recurrent CRP with confirmed vasculopathy.

A complex abnormality of the circle of Willis. Case presentation

Objective. We report a case of a patient with medium ACI stenosis and border zone infarct that occurred under normal hemodynamic conditions (normal BP, sinus rhythm), as normal supply mechanisms through the circle of Willis were absent. The circle of Willis was practically absent: the right ICA ramified in right MCA and a single ACA. Left ICA ramified in MCA and PCA. Right PCA was a branch of BA. Case presentation. A 75 year old patient was admitted in emergency with dressing apraxia. CT scan and MRI disclosed a 5/4 cm infarction in the temporo-parieto-occipital junction on the right side. Doppler ultrasonography of the precerebral vessels revealed medium stenosis of right ICA. 3D TOF MRA reconstruction disclosed a complex abnormality of the circle of Willis: absence of A1 and P1 on the left side, absence of PCoA on the right side, a single and fenestrated ACA originating in right ICA. The circle was practically absent; there was no possibility of circulatory supply. The territories of distribution of the precerebral vessels suffered severe modifications: right ICA ramified in MCA and a single ACA, left ICA ramified in MCA and PCA, right PCA was a branch of basilar artery. The infarction occurred between the boundaries of the right ICA (MCA respectively) and the posterior territory (PCA respectively). Conclusion. We report a complex and extremely rare abnormality of the circle of Willis that became clinically manifest because of a severe hemodynamic compromise.

Abstract 2970: Inter-observer Agreement in Diagnosis of “Borderzone” Infarcts On Diffusion Weighted MR Imaging.

Aim: To evaluate consensus in diagnosis of “borderzone” infarcts on diffusion weighted MR imaging (DWI). Methods: DWI of 144 consecutive stroke patients were independently reviewed by blinded Neuroradiologists (n=2) and Vascular Neurologists (n=2) and classified into embolic versus borderzone infarct patterns. CT angiography studies of each of these patients were later reviewed to determine degree of ipsilateral carotid artery stenosis/occlusion by NASCET criteria. Subjects with any MCA occlusion/stenosis on any side were excluded. Results: The agreement between Neuroradiologists was fair (Kappa=0.22, 95% CI 0.089 to 0.351), agreeing on 61.8% as embolic and 7.64% as borderzone infarcts. The agreement between Vascular Neurologists was good (Kappa=0.722, 95% CI 0.55 to 0.893), agreeing on 84.14% as embolic and 9.66% as borderzone infarcts. Inter-rater agreement between Neuroradiologist and Vascular Neurologist pairs varied between fair to moderate (Kappa = 0.22 to 0.72). Overall Fleiss’ Kappa for all 4 raters was 0.373 (95% CI 0.306 to 0.439). Classification of infarct patterns by degree of carotid disease on CTA is shown in the table below. As is seen in the table above, infarct patterns in patients with 100% carotid occlusion were classified as borderzone by both Neuroradiologist and Vascular Neurologist pairs in less than 30% of patients. The Neuroradiologist pair commonly classified infarct patterns in 75% of patients with 70-99% stenosis as borderzone. The Vascular Neurologists too classified 80% of these patients with 70-99% stenosis as having a borderzone infarct. Amongst patients with <50% carotid stenosis, both pairs of raters classified >90% of infarct patterns as embolic. Conclusions: Carotid occlusion and near-occlusion were unexpectedly associated with a smaller proportion of borderzone infarction than 70-99% stenosis. Discrepancies between Neuroradiologists and Vascular Neurologists towards diagnosis of watershed infarcts suggest the need to develop common definitions/guidelines. MR DWI imaging may not be a sole/sufficient criterion to classify watershed versus embolic infarction.

Abstract 3180: Hypotensive Events at Stroke Onset in the absence of Severe Carotid Disease

Hypotensive strokes frequently occur in the context of severe carotid disease. Aside from this cohort, evidence is lacking for the role of hypotension in stroke. The aim of this study was to investigate the presence of hypotensive behavior at stroke onset in those who do not have severe carotid disease. Prospective screening was conducted on all acute stroke patients for hypotensive symptoms at stroke onset. Suitable patients were referred to a syncope unit for assessment. There they underwent head-up tilt and rhythm assessment at least 8 weeks post stroke. All underwent 1.5T MRI in the acute stroke period. Where borderzone infarction was suspected repeat 3T MRI took place with perfusion imaging software to confirm this diagnosis. In total, 318 acute stroke patients presented to St. James Hospital, Dublin during a 14 month period. Of these, 20 patients exhibited hypotensive symptoms at stroke onset and did not have severe carotid disease (6.3%). In 12 patients TILT assessment induced symptom reproduction, thus confirming hypotensive behavior,in 2 this occurred during active stand, in 4 expert opinion established a diagnosis of vasovagal syncope while in 1 patient bradyarrythmia and in 1 autonomic failure was attributed. Median carotid stenosis was 20-30% bilaterally (range 10-70%). Ten of 20 patients underwent MRA. No intracranial stenosis was detected. Mean age was 74 years and 70% were female (n=14). Using phasic blood pressure (BP) assessment during active stand the mean BP drop in these patients was 47/26mmhg. Nadir BP drop occurred within 15 seconds in 17 patients (85%) and thus may have gone undetected by a sphygmomanometer. 19 patients reported a prior history of presyncope(95%). The mean duration of symptoms was 4.9 years (0.1-30 years), mean frequency 6 episodes per month. In 13 patients the neurological deficit resolved within 24 hours. An acute infarct was detected in 3 of 13, all borderzone infarction. In 7 patients the deficit persisted beyond 24 hours. An acute infarct was detected in 4 of 7, all borderzone infarction. Both cortical and internal borderone infarcts were detected. Mean 24 hour blood pressure was 143/77. Neither mean BP, nor BP variability statistically differed from 40 age and gender matched stroke controls. Hypotensive symptoms do occur at the time of stroke onset. Patients are often female, describe a prior history of hypotensive symptoms, have hypotensive disorders and exhibit a strong tendency for borderzone infarction. Caution is advised regarding the use of aggressive anti-hypertensive therapy in these patients.

Abstract 122: Stroke Patterns And Causative Mechanisms Of Ischemia In Patients With Symptomatic Intracranial Atherosclerotic Stenosis

Background/objectives: Putative mechanisms of stroke in intracranial atherosclerotic stenosis (ICAS) include hypoperfusion, artery-to-artery embolism or perforator occlusion, each of which may be characterized by different stroke patterns on neuroimaging. Our aims are to determine: 1) the different stroke patterns in patients with ICAS; 2) the correlation of angiographic factors (collaterals, degree and location of stenosis) with stroke patterns; and 3) if the patterns of recurrent stroke in the same territory are similar to qualifying strokes. Methods: From the WASID dataset, we selected patients with a stroke at baseline who had conventional angiographic information on collaterals (n=136), and patients with a recurrent stroke in the territory during follow-up (n= 47). We categorized stroke patterns as follows: for anterior circulation-subcortical (SC), cortical (C), territorial (T), borderzone (BZ) and multiple (M); for posterior circulation,-subcortical (SC), cortical (C), cerebellar (CB) and multiple (M). We defined an embolic mechanism if C, T, CB or multiple were present. The association between stroke patterns and collateral grade assessment (ASITN/SIR), location and degree of stenosis, and treatment assignment (warfarin vs aspirin) was analyzed using Chi-Square and McNemar’s tests. Results: Anterior circulation patterns (n=72) at baseline were: 14(19%) SC, 5(7%) T, 2(29%) C, 12(17%) BZ and 20(28%) M. All isolated BZ stroke patterns were located in internal borderzone region. BZ pattern was equally distributed among patients with no collaterals (5/40=12%) vs. patients with collaterals (7/32=22%) (p= 0.29) and among patients with moderate (8/43=19%) vs. severe stenosis (4/29=14%) (p=0.59). Posterior circulation patterns (n= 64) at baseline were: 25(39%) SC, 5(8%) C, 10(16%) CB and 24(38%)M. Embolic stroke pattern at baseline was the most frequent (85/136=62.5%). Among patients with a recurrent stroke in the territory (n=47), embolic pattern was also the most frequent (32/47, 68%). The probability of having a recurrent embolic stroke pattern was related to stenosis degree (81% in severe vs 50% in moderate stenosis, p= 0.03), collateral grade (83% with collaterals vs 53% no collaterals, p= 0.09), and previous embolic stroke pattern (74 % who had baseline embolic stroke vs 25% who had baseline non-embolic stroke,p= 0.01). Having a recurrent embolic stroke pattern was not influenced by treatment assignment (67% treated with warfarin vs 69% treated with aspirin, p=0.85). Conclusions: Artery-to-artery embolism seems to be the most frequent mechanism of stroke in ICAS patients and was not modified by antithrombotic treatment. Isolated BZ infarcts were less frequent, and were not related to poor collaterals or more severe stenosis.

Foreign Body Removal by Snare Loop: During Intracranial Stent Procedure

We present a case of successful retrieval of an intracranial stent using a snare wire. A 52-year-old woman presented with left border zone infarction. On cerebral angiography, the C6 segment of the left internal carotid artery (ICA) showed significant stenosis. We attempted stenting of the lesion, although stent dislodgement occurred in the ICA C4 segment. We successfully removed it using a snare loop, and there were no complications during the procedure.

Ataxic hemiparesis in a patient with posterior cortical borderzone infarction

Dear Sir, A 76-year-old woman was admitted to our institution with weakness and lack of coordination along the left side of her body. Review of her medical history revealed that she had hypertension and diabetes mellitus, had undergone stent-assisted coil embolization for a saccular aneurysm on the right distal internal carotid artery, and had taken aspirin, antihypertensive drugs, and glucose-lowering medication. Physical examination revealed a blood pressure of 150/90 mmHg, but no other specific findings were noted. Neurological examination indicated a slight impairment of motor power in the patient’s left arm (Medical Research Council grade 4?) and leg (grade 4?). With regard to cerebellar function, finger-to-nose and heel-to-shin tests showed observable dysmetria of the arm and leg, respectively. All aspects of the sensory system including proprioception were normal. Tandem gait was affected; the patient tended to tilt slightly towards the left. These findings suggested ataxic hemiparesis (AH), and hence, lacunar stroke was strongly suspected. However, the results of magnetic resonance imaging performed on admission and on the fourth day after admission showed distinct right posterior cortical borderzone infarction between the middle and posterior cerebral arterial territories (Fig. 1a). A wedge-shaped lesion was seen on the right posterior parietal area (Fig. 1b) alongside a lesion resembling a ‘string of beads’ on the right posterior centrum semiovale. The previously undertaken stent-assisted coil embolization was evident from the initial computerized tomographic angiography results (Fig. 2a); thereafter, irregular stenosis in the stent was observed on magnetic resonance angiography performed on the fourth day after admission (Fig. 2b). We carried out cardiac evaluation procedures, including electrocardiography and transthoracic echocardiography, but there was no indication of cardioembolism. Finally, we concluded that the posterior cortical borderzone infarction was caused by thromboembolism from the stenotic lesion in the stent. The patient fully recovered and was discharged on the seventh day after admission. Dual antiplatelets with aspirin and clopidogrel were prescribed for secondary prevention. This is the first reported case of AH caused by cortical borderzone infarction; a thorough review of literature indicated no reports of borderzone infarction causing AH [1]. In this study, we deduced that hemiparesis is associated with the lesion on the centrum semiovale, which involves the pyramidal tract. Ataxia was assumed to be associated with a wedge-shaped posterior parietal lesion. This is a common site for the occurrence of cortical borderzone infarctions [2]. Previously, kinetic ataxia has been reported in a patient with an acute posterior parietal infarction [3]. This association is very rare, but the interruption of cerebellar projections on the cortex was postulated as a possible mechanism [3]. Prior to this study, an autopsy report showed parietal ataxia related to the right postcentral gyrus in the arm [4]. In this article, however, proprioceptive impairment rather than dysmetria was regarded as the neurological basis of ataxia [4]. The neurologic deficits in our patient suggest pyramidal involvement near the centrum semiovale and kinetic ataxia due to a posterior parietal lesion, both of which represent AH. This association of AH with posterior cortical borderzone infarction is novel; AH is traditionally D. H. Shin S. W. Lee Y. H. Hong J. M. Hong J. S. Lee (&) Department of Neurology, Ajou University Medical Center, Ajou University School of Medicine, San 5, Wonchondong, Suwon, Youngtonggu 443-721, South Korea e-mail: jinsoo22@gmail.com

Quality of Life in Adult Survivors of Pediatric Kidney Transplantation

There are few studies assessing long-term adult outcome and health-related quality of life (HRQOL) in former pediatric high-risk kidney transplant (TX) recipients. Twenty-one patients were assessed at mean age of 21.1 years. Mean age at first TX was 2.4 years. Brain arterial border zone infarcts had been documented in 54% of the children. HRQOL was assessed with the general 15-dimensional (15D) instrument generating an index on a 0 and 1 scale (1 for best). The results were compared with the corresponding childhood 17-dimensional instrument and an adult control group from the general population. Psychosocial adjustment was assessed with the ASEBA Adult Self Report (ASR) and compared with the childhood Child Behavior Checklist assessments. Half of the patients (52%) had a secondary level general or vocational education. The educational outcome was evenly distributed (compulsory vs. secondary) regardless of previous childhood brain ischemia. The ASR Total Problems score was in the normal range for all patients. Four patients had scores in the pathological range for Externalizing or Internalizing Problems. There was a correlation between the childhood Child Behavior Checklist problem scores and the adult ASR scores for Internalizing and Total Problems but not for Externalizing Problems. Their mean 15D HRQOL index was 0.94 and lower than for the control group (0.97, P=0.04). There was a strong correlation between the childhood 17-dimensional and the adult 15D HRQOL index (r=0.63, P=0.003). The long-term outcome is fair in former high-risk pediatric TX patients with neurological comorbidity. Childhood psychosocial adjustment and HRQOL may predict the outcome in adults.

Clinical Outcomes of Cerebral Infarctions in Neonates

Cerebral infarctions are uncommon in neonates. However, they should be considered among causes of neonatal seizures. We describe seven neonates with cerebral infarctions. Clinical presentations, perinatal history, perinatal risk factors, cranial magnetic resonance imaging and electroencephalography findings, thrombophilic factors, and clinical outcomes were reviewed. Six patients manifested seizures, whereas one exhibited cyanosis. Six neonates manifested left middle cerebral artery infarctions, and one exhibited a borderzone infarction between the anterior cerebral and middle cerebral arteries. Electroencephalograms indicated epileptiform discharges on the left hemisphere in three neonates with left middle cerebral artery territory infarctions, and epileptiform discharges on both hemispheres in one patient. At most recent follow-up visit, five patients had achieved normal development, whereas one exhibited right hemiparesis and aphasia, and another manifested toe-in gait. These findings may help predict neurodevelopmental outcomes in neonates with cerebral infarctions.

Borderzone Strokes and Transcortical Aphasia

Borderzone infarcts (BZIs) are anatomically defined as ischemic lesions occurring at the junction between two arterial territories, accounting for 2% to 10% of strokes. Three types of hemispheric BZIs are described according to topography (ie, superficial anterior, posterior, and deep). Although published series on related aphasia are rare in the setting of BZI, aphasia is of transcortical (TCA) type, characterized by the preservation of repetition. TCA can be of motor, sensory, or mixed type depending on whether expression, understanding, or both are impaired. Recent studies have reported specific aphasic patterns. BZI patients initially presented with mixed TCA. Aphasia specifically evolved according to the stroke location, toward motor or sensory TCA in patients with respectively anterior or posterior BZI. TCA was associated with good long-term prognosis. This specific aphasic pattern is interesting in clinical practice because it prompts the suspicion of a BZI before the MRI is done, and it helps in the planning of rehabilitation and in providing adapted information to the patient and family concerning the likelihood of language recovery.

Border Zone Infarcts: Pathophysiologic and Imaging Characteristics

Border zone or watershed infarcts are ischemic lesions that occur in characteristic locations at the junction between two main arterial territories. These lesions constitute approximately 10% of all brain infarcts and are well described in the literature. Their pathophysiology has not yet been fully elucidated, but a commonly accepted hypothesis holds that decreased perfusion in the distal regions of the vascular territories leaves them vulnerable to infarction. Two types of border zone infarcts are recognized: external (cortical) and internal (subcortical). To select the most appropriate methods for managing these infarcts, it is important to understand the underlying causal mechanisms. Internal border zone infarcts are caused mainly by hemodynamic compromise, whereas external border zone infarcts are believed to result from embolism but not always with associated hypoperfusion. Various imaging modalities have been used to determine the presence and extent of hemodynamic compromise or misery perfusion in association with border zone infarcts, and some findings (eg, multiple small internal infarcts) have proved to be independent predictors of subsequent ischemic stroke. A combination of several advanced techniques (eg, diffusion and perfusion magnetic resonance imaging and computed tomography, positron emission tomography, transcranial Doppler ultrasonography) can be useful for identifying the pathophysiologic process, making an early clinical diagnosis, guiding management, and predicting the outcome.