Relationship between smoking and responsiveness to clopidogrel in non-cardiogenic ischemic stroke patients.

OBJECTIVE: Clopidogrel is used to prevent the recurrence of non-cardiogenic ischemic stroke, but individual responsiveness to the drug varies. Moreover, it is known that smoking, which is a risk factor for ischemic stroke, affects the drug's pharmacokinetics. The objective of the present study was to investigate a possible relationship between smoking and responsiveness to clopidogrel in non-cardiogenic ischemic stroke patients. METHODS: The study involved 209 non-cardiogenic ischemic stroke patients who were administered oral clopidogrel at a dosage of 75 mg/day for at least 1 week. Platelet aggregation in response to adenosine diphosphate (20 µM) was measured in each patient using the VerifyNow P2Y12 Assay. Platelet aggregation and the incidence of resistance to clopidogrel were compared between a smokers group (70 patients) and a non-smokers group (139 patients). Clopidogrel resistance was defined as a P2Y12 Reaction Units (PRU) value >230 and/or % inhibition <20%. RESULTS: The mean PRU was 128.3±85.5 in the smokers group and 167.7±86.6 in the non-smokers group (p=0.002). The incidence of PRU >230 was 12.9% (9 patients) in the smokers group and 25.9% (36 patients) in the non-smokers group (p=0.033). The mean % inhibition was 48.6±30.7% in the smokers group and 36.9±27.6% in the non-smokers group (p=0.009). The incidence of patients with % inhibition <20% was 24.3% (17 patients) in the smokers group and 34.5% (48 patients) in the non-smokers group (p=0.155). CONCLUSION: The incidence of clopidogrel resistance was lower in the non-cardiogenic ischemic stroke patients who were smokers, thus indicating that these patients' responsiveness to this drug may be enhanced.

Clinical characteristics of cardioembolic transient ischemic attack: comparison with noncardioembolic transient ischemic attack.

BACKGROUND: Previous studies show that 6%-31% of transient ischemic attacks (TIA) were caused by cardiogenic cerebral embolism (cardioembolic TIA). As prompt initiation of therapy is essential in TIA to prevent subsequent strokes, determining their cause is important. In this study, we aim to determine the features of cardioembolic TIA and to compare them with those of noncardioembolic etiology. METHODS: We retrospectively reviewed patients with a tissue-defined TIA who were admitted to our hospital from April 2007 to August 2013. The etiology was categorized according to Trial of Org 10172 in Acute Stroke Treatment, and TIA of cardioembolic origin and cervicocerebrovascular etiology (noncardioembolic TIA) were included in this study. Those with 2 or more possible causes or undetermined etiologies were excluded. Age, sex, comorbidities, ABCD2 score, and CHADS2 score were assessed and compared between the 2 groups. RESULTS: There were no significant differences in the neurologic symptoms and their duration, morbidities of hypertension, diabetes, and dyslipidemia between the 2 groups. Coronary and peripheral artery diseases were more common in the cardioembolic TIA group (18.4% vs. 6.9%). Incidences of prior stroke and cerebral infarction determined by MRI were similar between the 2 groups. The ABCD2 score showed a similar distribution, but the CHADS2 score was significantly different; the cardioembolic TIA group showed a higher score (P = .005). CONCLUSIONS: Clinical features are similar in tissue-defined TIA of cardioembolic and noncardioembolic etiologies. The CHADS2 score can be useful in assessing the probability of cardioembolic TIA.

Effects of rosuvastatin on serum lipids and arteriosclerosis in dyslipidemic patients with cerebral infarction.

BACKGROUND: We investigated the effect of rosuvastatin, 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitor, on serum lipids and arteriosclerosis in dyslipidemic patients with cerebral infarction. METHODS: The subjects were 24 patients with noncardiogenic cerebral infarction complicated by dyslipidemia (low-density lipoprotein cholesterol [LDL-C] ≥ 140 mg/dL). Serum lipids and highly sensitive C-reactive protein (hs-CRP) were measured at the start of the study and at 3 and 12 months after the initiation of oral rosuvastatin (5 mg/day). Cardio-ankle vascular index (CAVI), intima-media thickness (IMT), and plaque score (PS) were also determined at the start of the study and at 12 months. RESULTS: Of the 24 patients admitted, 17 were eligible for statistical analysis. Total cholesterol (TC), LDL-C, and non-high-density lipoprotein cholesterol (non-HDL-C) (mean [standard deviation {SD}], mg/dL) were significantly decreased at 3 months (TC, 149.4 [20.4]; LDL-C, 78.7 [18.6]; non-HDL-C, 94.6 [21.7]) and at 12 months (TC, 154.9 [27.2]; LDL-C, 82.5 [23.3]; non-HDL-C, 100.2 [28.8]) compared with the baseline data (TC, 232.8 [29.7]; LDL-C, 162.2 [21.2]; non-HDL-C, 183.0 [27.7]). The serum hs-CRP level (mean [SD], ng/mL) was 1053.1 [818.8] at baseline, 575.2 [481.8] at 3 months, and 488.1 [357.7] at 12 months. The decrease in this parameter at 12 months was statistically significant. There was a decrease, although not statistically significant, in CAVI (mean [SD]) at 12 months (right [Rt.] 8.7 [.9]; left [Lt.] 8.6 [1.0]), compared with baseline (Rt. 9.1 [1.1]; Lt. 9.0 [1.1]). The max-IMT (mean [SD], mm) was (Rt. 2.11 [.97]; Lt. 2.01 [.75]) at baseline and (Rt. 2.18 [.82]; Lt. 2.06 [.79]) at 12 months of study treatment. The PS (mean [SD], mm) was 8.93 [4.33] at baseline and 9.61 [4.79] at 12 months; neither parameter showed a significant change. CONCLUSIONS: Rosuvastatin at 5 mg/day significantly reduced serum levels of TC, LDL-C, non-HDL-C, and hs-CRP in dyslipidemic patients with cerebral infarction. No significant change in CAVI, max-IMT, or PS was noted after the study treatment.

Clinical review of 24 patients with acute cholecystitis after acute cerebral infarction.

OBJECTIVE: Acute cholecystitis (AC) after acute cerebral infarction is rare and has not been fully investigated. Because patients with acute cerebral infarction often cannot complain of abdominal pain due to loss of consciousness, hemiparesis and aphasia, delays in diagnosis may increase the severity of the condition. It is clearly important to identify symptoms, reach a diagnosis and provide treatment as soon as possible. The purpose of this study was to investigate the clinical features of AC after acute cerebral infarction. METHODS: Among the 1,682 patients with acute cerebral infarction admitted to our hospital between April 2007 and July 2012, AC after acute cerebral infarction was diagnosed in 24 (1.4%). Data regarding age, sex, past history, fasting period, period from admission to the onset of cholecystitis, clinical type, severity of cholecystitis, diffusion-weighted imaging Alberta Stroke Program Early Computed Tomography Score, National Institutes of Health Stroke Scale (NIHSS) score at onset and modified Rankin scale at 90 days were investigated. RESULTS: The mean age of the 24 patients (15 men, 9 women) was 74.2±11.9 years (range, 45-90 years). The clinical type was atherothrombosis in five patients, lacunar infarction in seven patients, cardiac embolism in 10 patients and dissection in two patients. The past history included atrial fibrillation in 10 (42%) patients, hypertension in 20 (83%) patients and diabetes in 11 (46%) patients. The mean duration of fasting was 10.7 days (range, 1-32 days). The mean interval between the onset of cholecystitis and admission was 8.3 days (range, 0-24 days). The median NIHSS score at onset of cerebral infarction was 10, and 23 (96%) patients were bedridden at the onset of cholecystitis. CONCLUSION: AC after acute cerebral infarction was frequently observed in the patients with severe hemiparesis and those who were fasted. It is important to identify symptoms, accurately diagnose the condition and provide treatment as soon as possible in order to achieve early ambulation and resumption of food intake using a feeding tube.

A case of anterior cerebral artery dissection caused by scuba diving.

A 51-year-old man was admitted with right hemiparesis during scuba diving, without headache. Brain magnetic resonance (MR) imaging depicted high-intensity areas in the left superior frontal and cingulate gyri on diffusion-weighted imaging. Dissection of the anterior cerebral artery (ACA) was detected using axial MR angiography and 3-dimensional MR cisternography. Dissection of the ACA during and after scuba diving has not been reported before. Dissection of the arteries should be included in the differential diagnosis when neurologic symptoms occur both during and after scuba diving, even if the patient does not experience headache. Furthermore, the combination of MR cisternography and MR angiography is useful to detect ACA dissection.

MRI abnormality of the pulvinar in patients with status epilepticus.

OBJECTIVE: Recently, magnetic resonance imaging (MRI) abnormalities of the pulvinar in patients with epilepsy have received greater attention, but their occurrence and features have not been fully elucidated. Therefore, we investigated the clinical and radiological features of patients with epilepsy who presented MRI abnormalities of the pulvinar. PATIENTS AND METHODS: We retrospectively investigated 225 consecutive patients who came to our institute because of seizures and underwent an MRI within 24h. The patients who exhibited pulvinar MRI abnormalities, their profile, seizure type, efficacy of medication, and chronological changes of MRI findings were examined. RESULTS: Out of the 225 patients who underwent MRI within 24h of seizure, 17 exhibited MRI abnormalities of the pulvinar. All of these 17 patients presented status epilepticus. Bilateral pulvinar diffusion-weighted imaging (DWI) hyperintensity was observed in 3 patients and unilateral pulvinar DWI hyperintensity in the other 14. Out of these 14 patients, 7 exhibited DWI hyperintensity in the ipsilateral cerebral cortex, and 10 patients presented an old lesion due to stroke or trauma. CONCLUSIONS: Our results demonstrated that the involvement of the pulvinar in status epilepticus is more frequent than expected and consisted of unilateral or bilateral DWI hyperintensities that may completely normalize. These pulvinar MRI abnormalities possibly reflect the epileptogenic hyperexcitation of different cortical areas through their connections with the pulvinar.

Response to clopidogrel and its association with chronic kidney disease in noncardiogenic ischemic stroke patients.

OBJECTIVE: Noncardiogenic ischemic stroke patients with chronic kidney disease (CKD) are known to have a greater rate of ischemic stroke recurrence than those without. Although clopidogrel is often used to prevent the recurrence of noncardiogenic ischemic stroke, the relationship between the response to clopidogrel and CKD is unclear. In the present study, the relationship between the response to clopidogrel and the presence of CKD was investigated in noncardiogenic ischemic stroke patients. METHODS: A total of 129 noncardiogenic ischemic stroke patients receiving 75 mg/day of clopidogrel for ≥1 week were evaluated. The VerifyNow P2Y12 Assay was used to measure the level of platelet aggregation induced by 20 µM of adenosine diphosphate, and the degree of platelet aggregation and frequency of clopidogrel resistance were compared between 34 patients with CKD and 95 patients without CKD. Clopidogrel resistance was defined as a P2Y12 Reaction Units (PRU) value of >230 and/or % inhibition <20%. RESULTS: The PRU value was 201.9±91.3 in the patients with CKD and 163.3±86.4 in the patients without CKD (p=0.035). The frequency of a PRU value of >230 was 44.1% (15 patients) among the patients with CKD and 17.9% (17 patients) among those without CKD (p=0.002). The percent inhibition was 29.9%±28.1% among the patients with CKD and 41.1%±28.0% among the patients without CKD (p=0.030). The frequency of % inhibition <20% was 47.1% (16 patients) among the patients with CKD and 26.3% (25 patients) among those without CKD (p=0.026). CONCLUSION: The present study showed that noncardiogenic ischemic stroke patients with CKD have a greater frequency of clopidogrel resistance, thus suggesting that the response to clopidogrel is diminished in these patients.

Prediction of ischemic stroke in patients with tissue-defined transient ischemic attack.

BACKGROUND: The risk of future stroke after transient ischemic attack (TIA) has been widely studied, but most findings were obtained for classically defined TIA (time-defined TIA). A new definition of TIA, that is, tissue-defined TIA, which requires the absence of fresh brain infarction on magnetic resonance imaging, could change stroke risk assessments. We, therefore, aimed to evaluate the risk of future stroke in patients with tissue-defined TIA. METHODS: We retrospectively reviewed 74 patients with tissue-defined TIA, who could be followed for 2 years. Clinical, laboratory, and radiological data were collected and compared between groups that did and did not develop ischemic stroke within the 2-year period. RESULTS: Ischemic stroke occurred in 11 patients (14.9%). Increased age, hemiparesis, and/or dysarthria during the TIA, old cerebral infarction revealed by magnetic resonance imaging, and large-artery stenosis detected by magnetic resonance angiography and/or ultrasonography tended to increase the risk of future stroke, but no individual factor showed statistically significant effect. TIA etiology did not significantly affect the risk. ABCD2 score, an established score for predicting stroke after time-defined TIA, showed only a weak association with future stroke. In contrast, new scores that we created reliably predicted future stroke; these included the APO (age, paresis, and old cerebral infarction) and APOL (age, paresis, old cerebral infarction, and large-artery stenosis) scores. The areas under the receiver operating characteristic curves were .662, .737, and .807 for ABCD2, APO, and APOL, respectively. CONCLUSIONS: Compared with the established measures, our newly created scores could predict future stroke for tissue-defined TIA more reliably.

CHADS2 score/CHA2 DS2 -VASc score and major artery occlusion in cardioembolic stroke patients with nonvalvular atrial fibrillation.

OBJECTIVE: The associations between the CHADS2 score/CHA2 DS2 -VASc score, and the presence of cerebral vessel occlusion on admission were examined in cardioembolic stroke patients with nonvalvular atrial fibrillation. METHODS: The subjects were 546 consecutive patients hospitalized between April 2007 and December 2012 with onset of cardioembolic stroke associated with nonvalvular atrial fibrillation within 24 h. The associations between the CHADS2 score/CHA2 DS2 -VASc score and the presence of occluded cerebral vessels on magnetic resonance angiography were evaluated retrospectively. Occluded cerebral vessels were classified into the internal carotid artery, middle cerebral artery (M1, M2), basilar artery, and other (anterior cerebral artery [A1], posterior cerebral artery [P1], vertebral artery). RESULTS: Major artery occlusion was seen in 52% of patients with CHADS2 score 0, 52% of patients with score 1, 57% with score 2, 75% with score 3, and 75% with score ≥4. As for the CHA2 DS2 -VASc score, major artery occlusion was seen in 62% of patients with score 0, 49% with score 1, 53% with score 2, 53% with score 3, 65% with score 4, 71% with score 5, and 82% with score ≥6. The incidence of concurrent major arterial occlusion increased as both scores rose. When classified by occluded blood vessel, the incidence of concurrent internal carotid artery occlusion increased as both the CHADS2 and CHA2 DS2 -VASc scores increased. CONCLUSION: As the CHADS2 and CHA2 DS2 -VASs scores increased, the incidence of concurrent major arterial occlusion, particularly internal carotid artery occlusion, increased in patients with cardioembolic stroke associated with nonvalvular atrial fibrillation.

A case of nonconvulsive status epilepticus with a reversible contralateral cerebellar lesion: temporal changes in magnetic resonance imaging and single-photon emission computed tomography finding.

A 67-year-old woman was brought to our institution because of unconsciousness. Clinical and electrophysiological findings lead us to diagnose her with nonconvulsive status epilepticus. Initial magnetic resonance imaging revealed hyperintensity in the left cerebral cortex and the right cerebellum on diffusion-weighted image and fluid-attenuated inversion recovery (FLAIR). Single-photon emission computed tomography showed increased blood flow in the left frontal cerebrum but not in the right cerebellum. The hyperintensity in the left cerebrum on the follow-up FLAIR was still present. The contralateral cerebellum remained undamaged even though the blood flow was not increased in this region because the excitotoxicity there was far lesser than that in the cerebrum.

Dual antiplatelet therapy clopidogrel with low-dose cilostazol intensifies platelet inhibition in patients with ischemic stroke.

OBJECTIVE: We previously reported that the antiplatelet action is intensified with combined use of clopidogrel and cilostazol in ischemic stroke patients using the VerifyNow P2Y12 Assay. In this study, the relationship between the cilostazol dose and the platelet function achieved with combination therapy was investigated. METHODS: The subjects included 231 patients with noncardiogenic ischemic stroke treated at our hospital (18 patients treated with a combination of clopidogrel (75 mg) and cilostazol (100 mg), 52 patients treated with a combination of clopidogrel (75 mg) and cilostazol (200 mg), 126 patients treated with clopidogrel (75 mg) alone and 35 patients treated with cilostazol (200 mg) alone). The platelet function achieved with 20 µM of adenosine diphosphate was measured using the VerifyNow P2Y12 Assay. Clopidogrel resistance was defined as P2Y12 Reaction Units (PRU) >230 and/or % inhibition <20%. Results The PRU was >230 in 32 patients (25.4%) receiving clopidogrel alone, one patient (5.6%) receiving combination therapy with cilostazol (100 mg) and one patient (1.9%) receiving combination therapy with cilostazol (200 mg). The rate of PRU >230 was significantly lower in both of the cilostazol combination groups than in the clopidogrel alone group. The percent inhibition was <20% in 41 patients (32.5%) receiving clopidogrel alone, one patient (5.6%) receiving a combination with cilostazol (100 mg) and one patient (1.9%) receiving a combination with cilostazol (200 mg). The rate of % inhibition <20% was significantly lower in both of the cilostazol combination groups than in the clopidogrel alone group. CONCLUSION: Clopidogrel resistance was clearly decreased with combination clopidogrel (75 mg) and low-dose (100 mg) cilostazol therapy. The use of combination therapy with clopidogrel and low-dose cilostazol may be one means of overcoming clopidogrel resistance.

[Secondary degeneration of the substantia nigra after cerebral infarctions including the striatum].

Secondary degeneration of the substantia nigra (SN) after damage to the ipsilateral striatum has been widely reported in animal stroke models. Secondary degeneration of the SN frequently occurs in stroke patients with damage to the striatum. Decreased γ-aminobutyric acid in the striatonigral pathway causes disinhibition of the SN pars reticulata, which consequently causes neuronal degeneration there. The SN pars compacta, in constant, degenerates in a retrograde manner. Diffusion-weighted imaging reveals this secondary degeneration as a high-intensity lesion, which may be misdiagnosed as a new infarction.

The CHA(2)DS(2)-VASc score reflects clinical outcomes in nonvalvular atrial fibrillation patients with an initial cardioembolic stroke.

BACKGROUND: Whether the CHA(2)DS(2)-VASc score reflects severity or clinical outcomes in patients with an initial cardioembolic stroke associated with nonvalvular atrial fibrillation (NAVF) was investigated. METHODS: This study included 327 patients hospitalized between April 2007 and March 2012 for an initial cardioembolic stroke associated with NVAF with no history of stroke. The National Institutes of Health Stroke Scale (NIHSS) score on admission and clinical outcome (modified Rankin Scale [mRS] score after 90 days) were retrospectively evaluated according to the CHA(2)DS(2)-VASc score. RESULTS: CHA(2)DS(2)-VASc scores were 0, 3.1%; 1, 9.1%; 2, 24.5%; 3, 26%; 4, 20.8%; 5, 14.4%; and 6, 2.1%. The median NIHSS scores for CHA(2)DS(2)-VASc scores of 0-6 were 4.5, 8, 8, 10, 11, 17, and 23, respectively. Severity differed according to the CHA(2)DS(2)-VASc score. The clinical outcomes according to the CHA(2)DS(2)-VASc scores were as follows: score 0, mRS scores of 0-2 (80%) and 3-6 (20%); score 1, mRS scores of 0-2 (80%) and 3-6 (20%); score 2, mRS scores of 0-2 (64%) and 3-6 (36%); score 3, mRS scores of 0-2 (48%) and 3-6 (52%); score 4, mRS scores of 0-2 (28%) and 3-6 (72%); score 5, mRS scores of 0-2 (26%) and 3-6 (74%); and score 6, mRS scores of 0-2 (29%) and 3-6 (71%). The clinical outcome worsened as the CHA(2)DS(2)-VASc score increased. On logistic regression analysis, age, NIHSS score on admission, and thrombolytic therapy were related to a clinical outcome. CONCLUSIONS: The severity of NVAF-induced initial cardioembolic stroke increased with higher CHA(2)DS(2)-VASc scores, and the outcomes were poor. The present study suggests that the CHA(2)DS(2)-VASc score may be useful not only for the evaluation of stroke risk but also for the prediction of clinical outcomes after stroke.

Central nervous system lymphoma initially diagnosed as tumefactive multiple sclerosis after brain biopsy.

A 72-year-old man was admitted with left homonymous hemianopsia and hemiparesis. Magnetic resonance imaging revealed a heterogeneously enhanced lesion in the right parietal lobe. A brain biopsy showed acute demyelination without malignancy, which led to a diagnosis of tumefactive multiple sclerosis (MS). The patient received corticosteroid therapy and experienced clinical and radiological improvement. Six months later, new lesions appeared, and a second biopsy revealed proliferation of dysplastic lymphocytes. This led to a revised diagnosis of primary central nervous system lymphoma (PCNSL). Because PCNSL mimics MS both clinically and radiologically, PCNSL is difficult to diagnose. Performing repeated brain biopsies may therefore be required when PCNSL is strongly suspected.

Rate of antithrombotic drug use and clinical outcomes according to CHADS2 scores in patients with an initial cardioembolic stroke who had nonvalvular atrial fibrillation.

BACKGROUND: This study investigated the relationship between CHADS2 scores and the rate of antithrombotic drug use and clinical outcomes in patients with an initial cardioembolic stroke who had nonvalvular atrial fibrillation (NVAF). METHODS: In 234 patients (135 men and 99 women; mean age [± SD] 76 ± 11 years) with initial cardiogenic cerebral embolism with NVAF who were admitted to our hospital between April 2007 and March 2011, the CHADS2 score, use of warfarin, and clinical outcomes were retrospectively investigated. RESULTS: CHADS2 scores were as follows: 0 points, n = 21 (9%); 1 point, n = 72 (31%); 2 points, n = 92 (39%); 3 points, n = 47 (20%); and 4 points, n = 2 (1%). The overall warfarin use rate was low (14.1%; n = 33), and it was significantly (P = .023) lower for paroxysmal atrial fibrillation (8%) than for chronic atrial fibrillation (18.5%). The clinical outcomes evaluated by the modified Rankin Scale (mRS) score after 3 months were: CHADS2 score 0 points, mRS 0 to 2 (81%) and 3 to 6 (19%); 1 point, mRS 0 to 2 (46%) and 3 to 6 (54%); 2 points, mRS 0 to 2 (46%) and 3 to 6 (54%); and ≥ 3 points, mRS 0 to 2 (29%) and 3 to 6 (71%). The clinical outcome worsened as the CHADS2 score increased (P = .002). Logistic regression analysis revealed that being ≥ 75 years of age and having a high National Institutes of Health Stroke Scale (NIHSS) score on admission were related to a poor outcome (P < .001). CONCLUSIONS: The overall warfarin use rate was low in initial cardioembolic stroke patients with NVAF. Clinical outcomes deteriorated with increases in the CHADS2 score, age ≥ 75 years, and NIHSS score on admission were related to a poor clinical outcome.

Treatment outcomes of tissue plasminogen activator infusion for branch atheromatous disease.

BACKGROUND: The objective of this study was to evaluate treatment outcomes of tissue plasminogen activator (t-PA) infusion for hyperacute branch atheromatous disease (BAD) within 3 hours after onset. METHODS: A total of 152 BAD patients with lenticulostriate artery (LSA) or paramedian pontine artery (PPA) territory infarcts (LSA 114; PPA 38) were hospitalized between April 2007 and June 2012. Of these, 21 BAD patients (LSA 19; PPA 2) arrived at the hospital within 3 hours after onset, and, among these, 8 patients who received t-PA infusion (.6 mg/kg) were included in this study. All BAD patients who received t-PA infusion had LSA territory infarcts. RESULTS: Six of 8 patients (75%) had improvement of neurologic findings within 60 minutes after t-PA infusion, but neurologic findings deteriorated within 24 hours in 4 of these patients (67%). In all patients with deterioration, diffusion-weighted imaging after 24 hours revealed infarct expansion. One patient (13%) had symptomatic intracranial hemorrhage. After 3 months, the modified Rankin Scale (mRS) score was 0 to 2 in 6 patients (75%) and 3 to 6 in 2 patients (25%). CONCLUSIONS: With t-PA infusion for BAD, symptoms transiently improved, but the rate of symptom deterioration was high. The outcome after 3 months was relatively good.

Additional endovascular therapy in patients with acute ischemic stroke who are nonresponsive to intravenous tissue plasminogen activator: usefulness of magnetic resonance angiography-diffusion mismatch.

BACKGROUND: In patients who are not responsive to intravenous tissue plasminogen activator (IV t-PA), the present study aimed to report recanalization rates, the incidence of hemorrhagic transformation (HT), and clinical outcomes of additional endovascular therapy (AET), and to investigate the usefulness of magnetic resonance angiography-diffusion mismatch (MDM) in a selection of patients eligible for AET. METHODS: Fifty-eight patients who received IV t-PA therapy because of intracranial major artery occlusion between April 2007 and November 2010 were divided into 2 groups: 18 patients in the AET group and 21 patients in the IV t-PA nonresponders group. The remaining 19 patients were responders to IV t-PA and therefore not eligible for this study. Recanalization rates, HT incidence, and 3-month outcomes were assessed, and the relationship between MDM and clinical outcome was examined. RESULTS: A 3-month modified Rankin Scale (mRS) score of 0 to 3 was seen more frequently in the AET group (72% in the AET group v 29% in the nonresponder group; P = .01). Serious outcomes (3-month mRS of 5-6) were seen significantly less often in the AET group (17%) than in the nonresponder group (57%; P = .019). There were no differences in the incidence of HT. In the AET group, reappraisal considering MDM revealed a significantly higher rate of a 3-month mRS of 0 to 3 in the MDM-positive group compared to the MDM-negative group (86% v 25%, respectively; P = .044). Serious outcomes were observed significantly less frequently in the MDM-positive group compared to the MDM-negative group (0% v 75%, respectively; P = .005). CONCLUSIONS: AET for nonresponders to IV t-PA was safe, improved recanalization rates, and led to better prognoses. MDM was a very good predictor of improved prognosis in a selection of eligible patients for AET after IV t-PA.

Clinical review of 28 patients with basilar artery occlusion.

BACKGROUND: We retrospectively analyzed factors related to the outcomes of patients with basilar artery occlusion. METHODS: Twenty-eight patients with basilar artery occlusion admitted to our hospital within 24 hours after onset between April 2007 and December 2010 were included. We investigated parameters related to outcome, such as coexisting disease, clinical type, clinical severity at admission, the site of occlusion and the infarction lesion, the collateral flow from posterior communicating artery, therapy, and time to therapy after onset. RESULTS: Of 28 patients with basilar artery occlusion, good outcomes occurred in 6 patients (21%) and poor outcomes occurred in 22 patients (79%). Clinical severity on admission was significantly different between the 2 groups. Three of 5 patients with percutaneous transluminal angioplasty achieved recanalization. Two of 3 cases with recanalization resulted in poor outcomes. CONCLUSIONS: Clinical severity on admission was the determinant factor of functional prognosis in patients with basilar artery occlusion.

Magnetic resonance angiography-diffusion mismatch reflects diffusion-perfusion mismatch in patients with hyperacute cerebral infarction.

BACKGROUND: We evaluated whether clinical-diffusion mismatch (CDM) or magnetic resonance angiography (MRA)-diffusion mismatch (MDM) is useful in detecting diffusion-perfusion mismatch (DPM) in hyperacute cerebral infarction within 3 hours after stroke onset. METHODS: Among patients with cerebral infarction who arrived within 3 hours after stroke onset at our hospital between May 2007 and December 2010, we included 21 patients (16 men and 5 women; mean age 70 ± 7.8 years) with cerebral infarction of the anterior circulation, and in whom magnetic resonance imaging (diffusion-weighted imaging)/MRA and computed tomograpic perfusion of the head were performed at the time of arrival. DPM-positive status was defined as a difference between DWI abnormal signal area and mean transit time prolongation area (≥ 20% on visual assessment). CDM-positive status was defined as a National Institute of Health Stroke Scale score ≥ 8 and DWI-Alberta Stroke Program Early CT Score (ASPECTS) ≥ 8. MDM-positive status was defined as a major artery lesion and DWI-ASPECTS ≥ 6. RESULTS: Ten of 21 patients had DPM. In all DPM-positive patients, MRA revealed a major artery lesion. Of the 10 DPM-positive patients, 6 were CDM-positive. CDM detected DPM with a sensitivity of 60% and a specificity of 64%. The positive likelihood ratio was 1.65. Of the 10 DPM-positive patients, all were MDM-positive. MDM detected DPM with a sensitivity of 100% and a specificity of 82%. The positive likelihood ratio was 5.5. CONCLUSIONS: In hyperacute cerebral infarction within 3 hours after onset, MDM, as compared with CDM, was able to detect DPM with higher sensitivity and specificity. This suggests that MDM is more reflective of DPM.

Magnetic resonance imaging investigation of secondary degeneration of the mesencephalic substantia nigra after cerebral infarction.

Secondary degeneration of the mesencephalic substantia nigra after cerebral infarction is widely known to occur in animal experiments, but has yet to be sufficiently investigated in human cerebral infarction. This study investigated the background and features of patients exhibiting secondary degeneration of the mesencephalic substantia nigra. The subjects comprised 43 patients admitted to our hospital for cerebral infarction between April 2007 and October 2010 showing secondary degeneration of the mesencephalic substantia nigra on cranial magnetic resonance imaging (MRI). We investigated clinical disease type, location of vascular occlusion, lesion site, and time from onset of symptoms to lesion identification by MRI. The clinical disease type was cardiogenic embolism in 29 patients (67%), atheromatous embolism (artery to artery) in 8 patients (19%), embolism (origin unknown) in 2 patients (5%), infarction after coil embolization for internal carotid aneurysm in 1 patient (2%), arterial dissection in 2 patients (5%), and vasculitis due to Takayasu disease in 1 patient (2%). Magnetic resonance angiography (MRA) identified the occluded vessel as the internal carotid artery in 19 patients (44%), the middle cerebral artery (M1) in 20 patients (47%), and the middle cerebral artery (M2) in 3 patients (7%); MRA was not performed in 1 patient (2%). The cerebral infarctions were striatal in 7 patients (16%) and striatal and cortical in 36 patients (84%). Hyperintense regions in the mesencephalic substantia nigra were observed in all patients after 7-28 days (mean, 13.3 days) on diffusion-weighted imaging or fluid-attenuated inversion recovery and T2-weighted MRI. Most patients with secondary degeneration of the substantia nigra demonstrated clinical disease comprising vascular occlusion of the internal carotid artery or the neighborhood of the middle cerebral artery, which was envisaged to cause a sudden drop in brain circulation across a wide area. Striatal infarctions were observed in all patients. Secondary degeneration of the substantia nigra appeared at 1-4 weeks after onset and disappeared after several months.