Effects of a parasympathetic blocker on the heart rate of loggerhead sea turtles during voluntary diving.

Diving bradycardia is a reduction in the heart rate mediated by the parasympathetic system during diving. Although diving bradycardia is pronounced in aquatic mammals and birds, the existence of this response in aquatic reptiles, including sea turtles, remains under debate. Using the parasympathetic blocker atropine, we evaluated the involvement of the parasympathetic nervous system in heart rate reduction of loggerhead sea turtles (Caretta caretta) during voluntary diving in tanks. The heart rate of the control group dropped by 40-60% from the pre-dive value at the onset of diving; however, administration of atropine significantly inhibited heart rate reduction (P<0.001). Our results indicate that, similar to mammals and birds, the heart rate reduction in sea turtles while diving is primarily mediated by the parasympathetic nervous system. In conclusion, we suggest that diving bradycardia exists not only in aquatic mammals and birds but also in aquatic reptiles.

Analysis of why sea turtles swim slowly: a metabolic and mechanical approach.

Animals with high resting metabolic rates and low drag coefficients typically have fast optimal swim speeds in order to minimise energy costs per unit travel distance. The cruising swim speeds of sea turtles (0.5-0.6 m s-1) are slower than those of seabirds and marine mammals (1-2 m s-1). This study measured the resting metabolic rates and drag coefficients of sea turtles to answer two questions: (1) do turtles swim at the optimal swim speed?; and (2) what factors control the optimal swim speed of turtles? The resting metabolic rates of 13 loggerhead and 12 green turtles were measured; then, the cruising swim speeds of 15 loggerhead and 9 green turtles were measured and their drag coefficients were estimated under natural conditions. The measured cruising swim speeds (0.27-0.50 m s-1) agreed with predicted optimal swim speeds (0.19-0.32 m s-1). The resting metabolic rates of turtles were approximately one-twentieth those of penguins, and the products of the drag coefficient and frontal area of turtles were 8.6 times higher than those of penguins. Therefore, our results suggest that both low resting metabolic rate and high drag coefficient of turtles determine their slow cruising speed.

High resting metabolic rates with low thermal dependence induce active dives in overwintering Pacific juvenile loggerhead turtles.

The metabolic rate and activity of sea turtles generally decreases with decreasing seasonal ambient temperature. Juvenile loggerhead turtles in the Mediterranean Sea made prolonged inactive dives (>400 min), indicating a state of dormancy during the cold winter period. However, seasonal differences in dive duration were not detected in juvenile loggerheads in the western North Pacific, even though the ambient water temperature changed by more than 10°C. Thus, metabolic states might differ among populations, explaining differences in the diving behaviour of juveniles during winter. Here, we tested the hypothesis that the active overwintering behaviour of juvenile loggerheads in the western North Pacific is driven by a high resting metabolic rate (RMR) with low thermal dependence. The RMR of juveniles in the western North Pacific (N=13) was 1.4-5.7 times higher (Q10=1.8) than that of juveniles in the Mediterranean Sea (Q10=5.4). To validate the high RMR values in the western North Pacific, the difference between core body temperature and ambient water temperature (ΔTb) was estimated from measured RMR and was compared with measured ΔTb The measured and estimated ΔTb matched each other. In addition, most of the dives conducted by the turtles in the western North Pacific were within the calculated aerobic dive limit (cADL) expected from the measured metabolic rate. Our results indicate that high RMR with low thermal dependence induces active diving during the overwintering periods of juvenile loggerheads in the western North Pacific, supporting the suggestion that metabolic states differ among populations.

Isolated Hypoglossal Paralysis Caused by Ischemic Infarction in the Centrum Semiovale.

In the present report, we discuss the case of a 66-year-old woman with isolated unilateral hypoglossal paralysis due to cerebral infarction in the centrum semiovale. To date, it has hardly been discussed where the corticolingual tract passes through in the centrum semiovale. Brain magnetic resonance imaging revealed a small ischemic infarction in the contralateral centrum semiovale. We could demonstrate a route of the corticolingual tract.

Platelet-endothelial cell interaction in brain microvessels of angiotensin II type-2 receptor knockout mice following transient bilateral common carotid artery occlusion.

The purpose of this study was to investigate the behavior of platelets (rolling and adhesion) in cerebral microvessels of angiotensin II type-2 receptor-knockout (AT2RKO) mice after transient bilateral carotid artery occlusion using intravital fluorescence microscopy. Twenty AT2RKO mice, consisting of 11 mice in the sham group and 9 mice in the ischemia reperfusion group (reperfusion after 15 min of bilateral, total carotid artery occlusion) were used in this study. The hole traversed the bone and dura mater, but arachnoid, pia mater, and cerebral parenchyma were preserved. Platelets were harvested from donor mice and stained using carboxyfluorescein diacetate succinimidyl ester. The number of platelets showing rolling and adhesion to pial vessels in AT2 deficient mice at 3 and 6 h after cerebral ischemia reperfusion was significantly higher than that in the sham group (P < 0.05). In addition, AT2 receptor has an inhibitory role in platelet rolling and adhesion after cerebral ischemia reperfusion.

Ischemic stroke with essential thrombocythemia: a case series.

BACKGROUND: Essential thrombocythemia (ET) is considered a rare cause of stroke partly because it is not detected if the platelet count is not elevated. However, early detection of ET is important because thrombosis can recur frequently, unless adequately treated. METHODS: We retrospectively collected data from 10 stroke cases with ET. Clinical characteristics, location of stroke, laboratory data (platelet and leukocyte count, hemoglobin, and JAK2 V617F mutation), and treatment were reviewed. RESULTS: The population consisted of 7 women and 3 men aged 18-83 years. Most patients had atherosclerotic risk factors. Half of the patients had a history of ischemic stroke. In 8 patients, ischemic stroke was the first manifestation of ET. Of 13 acute cerebrovascular events, 4 were transient ischemic attacks and 9 were cerebral infarctions. Three patients presented with watershed-type infarcts without large artery stenosis. Two patients had atherosclerotic stenosis of the large artery and experienced atherothrombotic infarction. The mean platelet count was 966 ± 383 × 10(9)/L. JAK2 V617F mutation was found in 5 of 7 patients. Despite treatment with combined antiplatelet and cytoreductive therapy in all patients, 3 experienced recurrent ischemic stroke. CONCLUSIONS: These findings suggest that ET is an adjunctive risk factor for stroke and the patients with ET are subject to watershed-type infarcts even in the absence of large artery stenosis. Early diagnosis of ET and strict management of vascular risk factors may help prevent additional cerebrovascular events.

Cilostazol inhibits platelet-endothelial cell interaction in murine microvessels after transient bilateral common carotid artery occlusion.

BACKGROUND: The purpose of this study was to investigate the effects of cilostazol on platelet behavior (rolling and adhesion) in murine cerebral microvessels after transient bilateral carotid artery occlusion using intravital fluorescence microscopy. METHODS: We used 41 C57BL/6J mice for the experiment. Fourteen mice were used as sham group (no ischemia and reperfusion, no medication); an ischemia (induced by 15-minute occlusion of bilateral common carotid arteries) and reperfusion (I/R) group (n = 17); and an I/R + cilostazol (I/R + CZ) group (receiving 30 mg/kg of cilostazol orally at 30 minutes before ischemia) (n = 10). A cranial window was prepared in the right parietal region. Platelets obtained from donor mice were labeled with a fluorescent dye (carboxyfluorescein iodoacetate succinimidyl ester) in vitro. Labeled platelets were intravenously administered at 3 or 6 hours after reperfusion, and then platelet behavior (rolling and adhesion) in the brain microvessels was observed. The numbers of rolling and adhering platelets in the arteriole and venule were calculated. RESULTS: Numbers of rolling and adherent platelets at 3 and 6 hours after reperfusion were significantly higher in the I/R group than in the sham or I/R + CZ groups in both venule (P < .05) and arteriole (P < .05). CONCLUSIONS: Cilostazol inhibits platelet-endothelial interactions following cerebral ischemia and reperfusion.

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.

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.

Research article: clinical characteristics of isolated anterior cerebral artery territory infarction due to arterial dissection.

BACKGROUND: Isolated brain infarction in the anterior cerebral artery (ACA) territory is rare, and its etiology has not yet been fully elucidated. Thus, we aimed to determine the etiologic and clinical characteristics of patients with isolated ACA territory infarction due to arterial dissection. METHODS: Of 2315 patients with acute cerebral infarction admitted to our hospital between April 2007 and September 2013, 34 patients (1.5%; 28 men, 6 women; mean age, 65 ± 15 years) suffered isolated ACA territory infarction. We performed cranial magnetic resonance (MR) imaging and MR angiography for all the patients. Whenever possible, we also performed 3-dimensional computed tomography angiography, digital subtraction angiography, and MR cisternography to diagnose the stroke subtype. RESULTS: The stroke subtypes of the 34 patients with isolated ACA territory infarction were atherothrombotic infarction, cardioembolic infarction, arterial dissection, and unclassified in 11 patients (32%), 11 patients (32%), 11 patients (32%), and 1 patient (3%), respectively. The mean ages at onset were 48 ± 9 and 72 ± 11 years in the dissection and nondissection groups, respectively (P < .001). Headaches were present at onset in 4 patients (36%) and 1 patient (4%) with and without dissection, respectively (P = .026). Blood pressure at onset was significantly higher among patients with dissection (systolic, 179 ± 34 mm Hg; diastolic, 102 ± 17 mm Hg) than among patients without dissection (systolic, 155 ± 30 mm Hg; diastolic, 86 ± 21 mm Hg; P < .05), and d-dimer values were significantly lower among patients with dissection (P = .034). Favorable clinical outcome (modified Rankin Scale score, 0-2) at discharge was achieved in 9 patients (82%) and 10 patients (43%) with and without dissection, respectively (P = .035). CONCLUSIONS: Patients with isolated ACA territory infarction demonstrated a relatively high frequency of dissection (32%). Patients with dissection were younger, had a higher frequency of headaches, and demonstrated more favorable prognoses than patients without dissection.

Clinical outcomes of persistent and paroxysmal atrial fibrillation in patients with stroke.

BACKGROUND: We compared the clinical outcomes of persistent atrial fibrillation (PeAF) and paroxysmal atrial fibrillation (PAF) in patients with cardioembolic stroke caused by nonvalvular atrial fibrillation (NVAF) because the nature of the fibrillation can cause persistent cerebral infarction. METHODS: We classified 619 of 964 patients hospitalized with cardioembolic stroke between April 2007 and December 2013 within 24 hours of onset as having PeAF (n = 447) and PAF (n = 172) according to a retrospective analysis of their clinical records, including National Institutes of Health Stroke Scale (NIHSS) scores on admission, clinical outcomes (modified Rankin Scale [mRS] scores) at 90 days after admission, and major cerebral artery occlusion. RESULTS: The PeAF group was significantly older (P < .001) and had a higher prevalence of hypertension (P = .007), diabetes (P = .039), heart failure (P = .004), previous coronary artery disease (P = .002) and cerebral infarction (P < .001), medication with anticoagulants (P < .001), and elevated blood glucose on admission (P = .002). Neurologic severity assessed by NIHSS scores on admission was significantly worse in the PeAF than in the PAF group (P < .001). Significantly more patients in the PAF group had favorable outcomes (mRS, 0-2) after 90 days (P < .001). The incidence of major cerebral artery occlusion was significantly higher in the PeAF group (P < .001). CONCLUSIONS: Patients with PeAF and cardioembolic stroke due to NVAF had more severe neurologic deficits on admission, more frequent major arterial occlusion, and poorer outcomes than those with PAF.

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.

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.

Detection of benzotriazole-type ultraviolet stabilizers in sea turtles breeding in the Northwest Pacific Ocean.

Benzotriazole-type ultraviolet stabilizers (BUVSs) are emerging contaminants whose exposure to wildlife is of concern. In this study, we investigated the contamination status of BUVSs in green turtles (Chelonia mydas) breeding at Ogasawara Islands, Japan, through chemical analysis of 10 BUVSs and 26 congeners of polychlorinated biphenyls (PCBs) in adipose tissue (n = 21) and blood plasma (n = 9). BUVSs were detected significant levels in adipose tissue (19 of 21 turtles), and UV-327 (not detected - 14.8 ng/g-lipid, detection frequency: 76 %), UV-326 (not detected - 24.1 ng/g-lipid, 29 %), and UV-328 (not detected - 5.8 ng/g-lipid, 24 %) were frequently detected. Turtles exhibiting sporadically high concentrations of BUVSs (>10 ng/g-lipid) did not necessarily correspond to individuals with high total PCB concentrations (1.03-70.2 ng/g-lipid). The sporadic occurrence pattern of BUVSs suggested that these contaminants in sea turtles cannot be explained solely by diet but are likely derived from plastic debris.

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.

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.

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.

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 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.