Evaluation of cerebral blood flow reserve in patients with cerebrovascular disease by SPECT using technetium-99m-L, L-ethyl cysteinate dimer

A technique for measuring the resting and acetazolamide (Acz)-activated cerebral blood flow without blood sampling by consecutive single-photon emission computed tomography (SPECT) using technetium-99m-L, L-ethyl cysteinate dimer (99mTc-ECD), called the 99mTc-ECD-RVR method, was recently developed by Matsuda et al . and Takeuchi et al . We evaluated the cerebral blood flow reserve in 77 patients with cerebrovascular diseases and 24 controls using this method. Baseline mean CBF (mCBF)was calculated from the application of Patlak plot graphical analysis with radionuclide angiography, and quantitative regional CBF (rCBF) images were obtained from qualitative axial SPECT images by the mCBF and Lassen’s linearization correction. The activated SPECT images were obtained by subtraction of the first image from the second image. The mean increment ratio (IR) by calculating the mean CBF for the pre- and post-Acz in the controls was 1.26±0.12 (mean±SD). In patients with cerebrovascular disease, the reduction of the mean IR and regional IR was parallel with the degree of stenosis. This noninvasive method was also considered to be useful in evaluating the change in the hemodynamic reserve in cerebrovascular disease

Reactivity of CA19-9 and CA125 in Histological Subtypes of Epithelial Ovarian Tumors and Ovarian Endometriosis

Previous reports have shown that some ovarian endometrioid adenocarcinomas and ovarian clear cell adenocarcinomas derive from ovarian endometriosis (OE), and that endocervical-like mucinous borderline ovarian tumors are associated with OE. We examined the relationship between the staging and histological subtypes of OE or epithelial ovarian tumors (EOT) and the serum levels of carbohydrate antigen 19-9 (CA19-9) and carbohydrate antigen 125 (CA125) to evaluate the potential of these markers for preoperative diagnosis. First, we analyzed the preoperative serum levels of CA19-9 and CA125 in 195 patients who were histopathologically diagnosed with OE or EOT. We then performed a case-control study in which 308 women were enrolled, the 195 women described above and 113 healthy women as control subjects. Serum CA19-9 and CA125 levels were found to be useful in differentiating between OE and serous adenocarcinoma, but not between OE and other EOT. Moreover, serum CA19-9 levels were useful for preoperative assessment between OE and stage I mucinous borderline ovarian tumors, with or without the interstitial infiltration. In addition, considering that the serum CA19-9 levels in stage I mucinous borderline ovarian tumors were elevated via the interstitial infiltration of leukocytes and that precancerous lesions are associated with a cancerous glycosylation disorder in the process of inflammatory carcinogenesis, the CA19-9 level may be considered a suitable biomarker for estimating drug susceptibility

Comparison between early and late carotid endarterectomy for symptomatic carotid stenosis in relation to oxidized low-density lipoprotein and plaque vulnerability

ObjectiveAlthough carotid endarterectomy (CEA), the gold standard in stroke prevention, has been performed in the late stage after the insult, its optimal timing remains unclear. Using biomarkers in plaque and plasma, we evaluated oxidative stress and plaque vulnerability between early and late CEA in symptomatic patients.MethodsWe compared symptomatic stroke patients who underwent early CEA within 4 weeks of the last insult (group A; n = 15) with those who received CEA in the late stage beyond 4 weeks from the last symptom (group B; n = 57). They were divided into vulnerable (group Av, n = 13; group Bv, n = 33) and stable (group As, n = 2; group Bs, n = 24) subgroups according to the pathologic findings on their plaques. We studied the relationships among their primary symptoms, clinical findings, oxidized low-density lipoprotein levels, and gelatinase A (matrix metalloproteinase [MMP]-9) activity in their plaques and plasma.ResultsGroup A had a variety of symptoms; there was no difference in the outcome of CEA between groups A and B. The plaque and plasma oxidized low-density lipoprotein levels were higher in group A than in group B (P < .05). The incidence of pathologically vulnerable plaque was higher in group A than in group B. Plaque oxidized low-density lipoprotein levels and MMP-9 activity were similar in group Av and group Bv and were higher in those groups than in group As and Bs.ConclusionsWe first demonstrated that vulnerable plaques in patients subjected to early CEA manifested a remarkable increase in oxidized low-density lipoprotein and MMP-9 activation. Our findings suggest that early CEA may be beneficial in the aspect of oxidative stress

ノウコウソク ノ キュウセイキ チリョウ : Stroke Care Unit オ チュウシン トシテ

Stroke remains the second or third leading cause of the death and major cause of adultdisability in Japan. Cerebral infarction is major cause of stroke, therefore, it is very importantthat precious diagnosis and acute treatment of cerebral infarction should be done.Recently diffusion-weighted (DWI) and perfusion-weighted MRI (PWI) were clinically used andsensitivity of these stools is superior to T2-MRI in diagnosis of acute cerebral infarction.We performed acute intra-arterial thrombolysis and evaluated this efficacy by DWI andPWI. For the patients with embolic cerebral infarction, anticoagulant therapy should beperformed and tarns-esophageal heart echography in acute stage of infarction is useful fordetection of embolic source. Stroke Care Unit (SCU) was opened in our hospital since lastNovember and 8 patients per month were admitted to SCU. Over 75% of patients weretreated conservatively, and 6 patients were performed intra-arterial thrombolysis. Over80% of patients with cerebral infarction in SCU showed good clinical recovery. We needmore patients to show the superiority compared to the general medical wards

Pathophysiology and treatment of cerebral ischemia

This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. It is useful to think of an ischemic lesion as a densely ischemic core surrounded by better perfused “penumbra” tissue that is silent electrically but remains viable. Reperfusion plays an important role in the pathophysiology of cerebral ischemia. Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. Brief occlusion of the MCA produces a characteristic, cell-type specific injury in the striatum where medium-sized spinous projection neurons are selectively lost ; this injury is accompanied by gliosis. Transient forebrain ischemia leads to delayed death of the CA1 neurons in the hippocampus. Immunohistochemical and biochemical investigations of Ca2+/calmodulin-dependent protein kinase II(CaM kinase II) and protein phosphatase (calcineurin) after transient forebrain ischemia demonstrated that the activity of CaM kinase II was decreased in the CA1 region of the hippocampus early (6- 12 hours) after ischemia. However, calcineurin was preserved in the CA1 region until 1.5 days after the ischemic insult and then lost ; a subsequent increase in the morphological degeneration of neurons was observed. We hypothesized that an imbalance of Ca2+/calmodulin dependent protein phosphorylation-dephosphorylation may be involved in delayed neuronal death after ischemia. In the treatment of acute ischemic stroke, immediate recanalization of the occluded artery, using systemic or local thrombolysis, is optimal for restoring the blood flow and rescuing the ischemic brain from complete infarction. However, the window of therapeutic effectiveness is very narrow. The development of effective neuroprotection methods and the establishment of reliable imaging modalities for an early and accurate diagnosis of the extent and degree of the ischemia are imperative

Cardiogenic embolism caused hypoglycemia

The direct relationship between a hypoglycemic attack and cerebral infarction remains unknown. It has been reported that a hypoglycemic attack can result in takotsubo syndrome, leading to cerebral infarction. We report a case of a cardiogenic cerebral embolism caused by a hypoglycemic attack, with additional literature review. A 71-year-old woman was admitted to our hospital in a semi-comatose state due to a severe hypoglycemic attack ; she developed hemiplegia one day after admission. Magnetic resonance imaging revealed cerebral infarction in the area supplied by the left middle cerebral artery. Takotsubo syndrome was suspected based on echocardiography. We diagnosed cerebral embolism due to takotsubo syndrome, caused by the hypoglycemic attack

ノウソッチュウ シンダン ノ サイゼンセン

Stroke Care Unit （SCU） in Tokushima University Hospital has been opened since November １９９９. Patients with acute stroke in SCU were diagnosed by stroke MRI and biomarker immediately after their admission. Diffusion MRI could diagnose the ultra-acute ischemic and hemorrhagic lesion except brainstem ischemic lesion within ３ hrs after onset. Diffusion-Perfusion mismatch was useful to indicate intra-arterial thrombolytic therapy. ３T-MRI was introduced since March ２００４，and it can measured functional MR spectroscopy and tractography more quickly compared to １．５T-MRI. Plasma oxidized LDL in patients with acute cerebral infarction was significantly higher than that in healthy control and it became peak level during ３‐５ day after stroke onset. In conclusion, stroke MRI and plasma oxidized LDL are useful diagnostic tools for acute stroke