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.

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.

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.

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.

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.

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.

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.

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.

Bilateral caudate nucleus infarction associated with a missing A1 segment.

We describe a case of bilateral caudate nucleus infarction caused by cardioembolic stroke associated with a variant circle of Willis. The patient was an 81-year-old man with atrial fibrillation who presented with a sudden disturbance of consciousness. When he became more alert a few days later, he was abulic with no spontaneous speech or activity. A magnetic resonance imaging scan of the brain revealed cerebral infarction of bilateral caudate nucleus heads and the left frontal lobe. The left A1 segment was absent on 3-dimensional computed tomography angiography. One year later, abulia had completely resolved. Bilateral caudate nucleus infarction with variant circle of Willis is rare.

Relationship of obesity to recanalization after hyperacute recombinant tissue-plasminogen activator infusion therapy in patients with middle cerebral artery occlusion.

BACKGROUND: This was a retrospective analysis of factors related to recanalization after hyperacute recombinant tissue-plasminogen activator (rt-PA) infusion therapy in patients with middle cerebral artery occlusion. METHODS: Of the 50 patients (39 males and 11 females; mean age 70 ± 11 years) with cerebral infarction who were able to undergo diffusion-weighted magnetic resonance imaging (MRI)/magnetic resonance angiography (MRA) of the head within 24 hours of starting rt-PA infusion therapy while hospitalized at our center between April 2007 and October 2010, 23 patients (18 males and 5 females; mean age 71 ± 9.4 years) with hyperacute cerebral infarction with findings of obstruction in the proximal segment of the middle cerebral artery (MCA-M1) served as subjects. RESULTS: Of the 23 patients with MCA occlusion, 13 (57%) were recanalized. Analysis of factors related to recanalization revealed a significant difference (P = .019) for obesity (body mass index >25 kg/m(2)), with significantly more obese patients in the nonrecanalized group than in the recanalized group. The study revealed no significant differences in other factors between the 2 groups. CONCLUSIONS: The results suggest that obesity may be involved in recanalization after hyperacute rt-PA infusion therapy in patients with MCA occlusion.

Spontaneous cervicocephalic arterial dissection with headache and neck pain as the only symptom.

BACKGROUND AND OBJECTIVE: Cervicocephalic arterial dissection can cause both ischemic stroke and hemorrhagic stroke. However, spontaneous cervicocephalic arterial dissection presenting only with headache and neck pain has rarely been reported. The clinical features of patients with spontaneous cervicocephalic arterial dissection presenting only with headache and neck pain were investigated. METHODS: The subjects were seven patients with spontaneous cervicocephalic arterial dissection with headache and neck pain alone who were admitted to our hospital during the past 3 years. The clinical features of these patients were investigated. The diagnosis of arterial dissection was based on the criteria of the Strategies Against Stroke Study for Young Adults in Japan. RESULTS: The age of the patients (3 males, 4 females) ranged from 35 to 79 (mean, 51.0 ± 16.2) years. Six patients had vertebral artery dissection, one had internal carotid artery dissection, and one had an association of vertebral and internal carotid artery dissection. With the exception of one patient, the headache and neck pain were unilateral. All patients with vertebral artery dissection complained of posterior cervical or occipital pain. In the cases of internal carotid artery dissection, one patient complained of temporal pain, and one patient with co-existing vertebral artery dissection complained of posterior cervical pain. The mode of onset was acute in five patients, thunderclap in one, and gradual and progressive in one. The pain was severe in all cases. Five patients complained of continuous pain, while two had intermittent pain. The quality of the pain was described as throbbing by five patients and constrictive by two. The headache and neck pain persisted for 1 week or longer in six of the seven patients. CONCLUSION: Cervicocephalic arterial dissection should be suspected when patients complain of intense unilateral posterior cervical and occipital pain or temporal pain.

[A case of occipital epilepsy with anti-GluRepsilon2 antibody in cerebrospinal fluid, presenting as repeated visual disturbance and headache].

A 78-year-old man was admitted to our hospital with repeated attacks of headache and visual hallucinations, which had begun 10 days before. He also displayed left hemispatial neglect and left homonymous hemianopsia during attacks. Brain magnetic resonance imaging (MRI) showed an abnormal high-intense area in the right occipital lobe on diffusion weighted imaging (DWI) and fluid attenuated inversion recovery (FLAIR) weighted imaging; this lesion was demonstrated as an area of hyperperfusion on ECD-single photon emission computed tomography (SPECT) and hypoperfusion on 123I-BZ-SPECT. Electroencephalography during an attack demonstrated epileptogenic discharges in the right occipital region. Acute urinary retention due to meningoencephalitis appeared 2 weeks after onset of the first attack. Autoantibodies against glutamate receptor epsilon2 were detected in cerebrospinal fluid. We diagnosed the patient with occipital epilepsy due to anti-NMDA receptor antibody encephalitis. Epileptic attacks diminished and MRI and SPECT findings improved following two administrations of intravenous bolus steroid therapy.

[A case of neuro-neutrophilic disease presenting with 5 months' with cognitive decline, meningoencephalitis, and marked systemic inflammatory findings, and diagnosed with brain biopsy].

A 63-year-old man was admitted to our hospital with cognitive decline. On admission, he had a fever and mild cognitive dysfunction, suggesting chronic meningoencephalitis. Apart from a mild increase in serum C-reactive protein level and marked neutrophilia, laboratory findings were unremarkable. Brain magnetic resonance (MR) imaging showed multiple small T2-hyperintense lesions in the white matter. Systemic evaluations for infectious organisms, autoantibodies, and malignancy were all negative. For 5 months we conducted therapeutic trials of various antibacterial, antifungal, and antituberculous drugs, but these were completely ineffective, and both meningoencephalitis and inflammatory signs persisted. Repeated brain MRI during the clinical course showed growth of the white matter lesions and progressive cerebral atrophy. C11-methionine positron emission tomography demonstrated a bright focus in the right frontal lobe, and this was biopsied. Key neuropathological findings were neutrophilic infiltration in the subarachnoid space and the frontal lobe without necrotic angiitis. These findings confirmed the diagnosis of neuro-neutrophilic disease, although skin tissue findings characteristic of Sweet disease and a B51, B54, or Cw1 HLA-profile were absent. After intravenous bolus administration of steroid and prolonged oral steroid therapy, fever and inflammatory signs diminished and cognitive symptoms improved.

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.

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.