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T Kohriyama

Publications and source records attributed to T Kohriyama.

At least 19 recordsLinked to original sources
PubMed2006

Plasma total homocysteine levels are associated with advanced leukoaraiosis but not with asymptomatic microbleeds on T2*-weighted MRI in patients with stroke.

Both leukoaraiosis and asymptomatic microbleeds are associated with small-artery diseases. Although an association between hyperhomocysteinemia and leukoaraiosis has been reported, no studies have evaluated the association between total homocysteine (tHcy) level and presence of microbleeds in stroke patients. We evaluated the association between tHcy level and leukoaraiosis or microbleeds in stroke patients. In 102 patients with stroke (69.5 +/- 10.3 years old, 54 men and 48 women), microbleeds on T2*-weighted MR images were counted, leukoaraiosis on T2-weighted images was graded and fasting plasma tHcy concentrations were measured. Plasma tHcy level was significantly higher in patients with advanced leukoaraiosis than in those without advanced leukoaraiosis (13.9 +/- 4.6 micromol/l vs. 10.2 +/- 3.4 micromol/l, P < 0.0001). Plasma tHcy level was not significantly different in patients with microbleeds and those without microbleeds (11.3 +/- 4.1 micromol/l vs. 11.4 +/- 4.3 micromol/l, P = 0.9441). Elevated tHcy level is significantly and independently associated with advanced leukoaraiosis [odds ratio (OR), 1.330; 95% CI, 1.130-1.565] but not with the presence of microbleeds. Elevated tHcy level appears to be associated with ischemic small-artery disease rather than with bleeding-prone small-artery disease.

Aged↗
PubMed2006

Combinations of the presence or absence of cerebral microbleeds and advanced white matter hyperintensity as predictors of subsequent stroke types.

BACKGROUND AND PURPOSE: Previous studies have shown microbleeds to be a risk factor for intracerebral hemorrhage and white matter hyperintensity (WMH) to be a risk factor for ischemic stroke. This study was performed to determine whether combinations of the presence or absence of microbleeds and advanced WMH are risk factors for subsequent recurrent stroke types. METHODS: In 266 patients with stroke, microbleeds on T2*-weighted MR images were counted, and WMH on T2-weighted images was graded. Patients were divided into 4 groups by the combinations of the presence or absence of microbleeds and advanced WMH and were followed up for stroke recurrence. RESULTS: During a mean follow-up period of 564.8 +/- 220.5 days, 26 patients developed recurrent strokes, including 10 intracerebral hemorrhages and 16 ischemic strokes. Patients with microbleeds without advanced WMH (n = 42) developed only intracerebral hemorrhages (n = 8), and the recurrence rate of intracerebral hemorrhage in those patients estimated by the Kaplan-Meier method was the highest in the 4 groups (14.3% in 1 year and 21.2% in 2 years). In contrast, patients with advanced WMH without microbleeds (n = 39) developed only ischemic strokes (n = 6), and the estimated recurrent rate of ischemic stroke in those patients was the highest in the 4 groups (10.5% in 1 year and 17.4% in 2 years). Cox proportional hazards regression analysis revealed that microbleeds were associated with intracerebral hemorrhage (hazard ratio [HR], 85.626; 95% confidence interval [CI], 6.344-1155.649) and that advanced WMH was negatively associated with intracerebral hemorrhage (HR, 0.016; 95% CI, 0.001-0.258). Advanced WMH was associated with ischemic stroke (HR, 10.659; 95% CI, 2.601-43.678). CONCLUSION: It appears that patients at high risk of subsequent intracerebral hemorrhage or ischemic stroke can be identified by combinations of the presence or absence of microbleeds and advanced WMH.

Aged↗
PubMed2005

Clinical diagnosis of MM2-type sporadic Creutzfeldt-Jakob disease.

BACKGROUND: No method for the clinical diagnosis of MM2-type sporadic Creutzfeldt-Jakob disease (sCJD) has been established except for pathologic examination. OBJECTIVE: To identify a reliable marker for the clinical diagnosis of MM2-type sCJD. METHODS: CSF, EEG, and neuroimaging studies were performed in eight patients with MM2-type sCJD confirmed by neuropathologic, genetic, and western blot analyses. RESULTS: The eight cases were pathologically classified into the cortical (n = 2), thalamic (n = 5), and combined (corticothalamic) (n = 1) forms. The cortical form was characterized by late-onset, slowly progressive dementia, cortical hyperintensity signals on diffusion-weighted imaging (DWI) of brain, and elevated levels of CSF 14-3-3 protein. The thalamic form showed various neurologic manifestations including dementia, ataxia, and pyramidal and extrapyramidal signs with onset at various ages and relatively long disease duration. Characteristic EEG and MRI abnormalities were almost absent. However, all four patients examined with cerebral blood flow (CBF) study using SPECT showed reduction of the CBF in the thalamus as well as the cerebral cortex. The combined form had features of both the cortical and the thalamic forms, showing cortical hyperintensity signals on DWI and hypometabolism of the thalamus on [18F]2-fluoro-2-deoxy-d-glucose PET. CONCLUSION: For the clinical diagnosis of MM2-type sporadic Creutzfeldt-Jakob disease, cortical hyperintensity signals on diffusion-weighted MRI are useful for the cortical form and thalamic hypoperfusion or hypometabolism on cerebral blood flow SPECT or [18F]2-fluoro-2-deoxy-d-glucose PET for the thalamic form.

14-3-3 Proteins↗
PubMed2004

Significance of serum soluble thrombomodulin level in acute cerebral infarction.

The purpose of the present study was to investigate sequential changes in serum soluble thrombomodulin (sTM) concentrations in patients with acute cerebral infarction (ACI), and to correlate sTM concentrations with the severity of ACI evaluated by Japan Stroke Scale. Eighty-three consecutive patients with ACI were enrolled, and blood examinations were carried out soon after admission and 1 month after. sTM concentrations at admission in patients with cardioembolic infarction (3.2 +/- 1.2 ng/ml) were significantly lower than those of lacunar infarction (3.9 +/- 1.2) (P < 0.05). Serial examinations revealed that sTM concentrations increased significantly 1 month after admission (3.8 +/- 1.2), compared with those at admission (3.6 +/- 1.2) (P = 0.02). Of three ACI subtypes, sTM concentrations during 1 month significantly increased in atherothrombotic infarction (P = 0.002) or, not significantly, in cardioembolic infarction (P = 0.09). The sTM concentrations at admission showed a significant inverse correlation with the severity of ACI (P = 0.04). Although sTM concentrations serve as a useful marker for endothelial cell damage, they are decreased in patients with severe ACI, especially in atherothrombotic and cardioembolic infarctions. Lower sTM concentrations may play some important role in disease progression or in the recurrence following ACI, although the exact mechanism of this unique result should be clarified.

Acute Disease↗
PubMed2001

Folic acid-responsive neurological diseases in Japan.

Folic acid (folate) levels were measured in the serum of patients with various neurological diseases in Japan. Thirty-six patients showed decreased serum folate levels among 343 consecutive neurological patients (10.5%). Folate administration (15 mg/d) to folate-deficient patients improved neurological symptoms in 24 of 36 cases (67%). Serum folate levels were significantly lower in female than in male folate-deficient patients. Folate-deficient patients showed predominantly axonal neuropathy, which responded to folate supplementation more markedly. Male patients more frequently exhibited neuropathy, especially demyelinating and motor-dominant neuropathy, than females. Anemia was correlated with male sex and low serum folate levels. Male patients were more responsive than females to folate treatment. More male patients had taken excess alcohol or received gastrectomies than females. Neurological symptoms were more frequently improved by folate supplementation in patients with neuropathy than exclusive encephalopathy. Serum folate levels were lower in patients with encephalopathy, especially those with dementia, while folate therapy was more effective in neurological patients without dementia. Dysgeusia and anemia improved in all patients after folate administration. Neurological patients with malabsorption or treated with continuous drip infusion were resistant to folate therapy. Since folate-responsive neuroencepahlopathies are not rare among patients with neurological diseases in Japan, the serum folate level would serve as a valuable indicator for folate supplement therapy.

Anemia↗
PubMed2000

Gallyas-positive argyrophilic and ubiquitinated filamentous inclusions in rapidly progressive motor neuron disease: immunohistochemical and electron microscopic studies.

In an autopsy case of sporadic rapidly progressive lower motor neuron disease (MND), Gallyas-positive argyrophilic and ubiquitinated filamentous intracytoplasmic inclusions were found in the neurons. Clinically, 7 months prior to death, a 68-year-old woman experienced a history of rapidly progressive muscle weakness of all four extremities and bulbar sign, without sensory and autonomic disturbance. Two months later, she became unable to stand or walk. Four months after onset, she needed respiratory support, and subsequently died due to cardiorespiratory arrest. Neuropathological examinations revealed neuronal loss and associated gliosis in the lower motor neurons, except for ocular motor nuclei, Clark's column, and accessory cuneate nucleus, and tract degeneration was observed in the middle root zone of the posterior column and spinocerebellar tract. No Bunina bodies or Lewy body-like hyaline inclusions were found in the anterior horns. Gallyaspositive argyrophilic filamentous inclusions were found in the lower motor neurons and in nerve cells of the Clark's column, intermediate zone, posterior horn and accessory cuneate nucleus. These were positive with anti-ubiquitin antibody but negative with anti-tau (tau-2 and AT8) and neurofilament antibodies. Electron microscopic examinations disclosed randomly arranged tubular-like filamentous profiles, with a diameter of 12-14 nm, sometimes with amorphous granules in the perikaryon. This is the first report on the Gallyas-positive argyrophilic and ubiquitinated filamentous inclusions in neurons in MND.

Aged↗
PubMed2000

Elevation of serum soluble E-selectin and antisulfoglucuronyl paragloboside antibodies in amyotrophic lateral sclerosis.

Immunological abnormality is often found in amyotrophic lateral sclerosis (ALS). Antibodies to sulfoglucuronyl paragloboside (SGPG) were reported in ALS, although the pathogenetic significance of the antibodies is still unknown. We have already demonstrated that SGPG, a unique glycolipid, is present in both peripheral nerve and vascular endothelial cells. To investigate whether serum anti-SGPG antibodies would participate in activation and/or injury of endothelial cells in ALS, we examined serum anti-SGPG antibodies in association with serum soluble E- and P-selectins, which are markers of activated endothelial cells, in 25 patients with ALS and 14 age-matched patients with other neurological diseases (ONDs) using the microtiter-ELISA method. Seven out of 25 ALS patients had anti-SGPG antibodies. Levels of sE-selectin were significantly higher in patients with ALS (48.5 +/- 23.4 ng/ml) compared with ONDs (24.0 +/- 11.8 ng/ml) (P < 0.005). Four out of seven ALS patients with anti-SGPG antibodies had concomitantly high sE-selectin levels. The mean sE-selectin levels were higher in patients with anti-SGPG antibodies (61.9 +/- 25.2 ng/ml) than in those without anti-SGPG antibodies (43.3 +/- 21.1 ng/ml). Anti-SGPG antibodies may take part in the activation and/or injury of endothelial cells. The increased expression of E-selectin may be related to an immunological process in some ALS patients.

Aged↗
PubMed2000

[An autopsy case of catastrophic antiphospholipid syndrome presenting with recurrent multiple cerebral infarction associated with lung cancer].

We reported an autopsy case of cerebral infarction with primary lung cancer. The patient was a 50-year-old man. Despite having been treated with warfarin potassium and ticlopidine hydrochloride, he relapsed cerebral infarction. His laboratory data on admission showed that lupus anticoagulant was positive, together with a high value of beta-thromboglobulin, thrombin-antithrombin III complex, markers of platelet and coagulation activation, CEA and CA 19-9. The autopsy finding revealed a primary papillary adenocarcinoma in the right lower lung, multiple cerebral infarction, renal infarction, pulmonary infarction and splenic infarction. The atherosclerotic changes were mild in the whole tissues and findings of vasculitis were not observed. Recurrence of cerebral infarction was effectively suppressed with the addition of steroid therapy to antithrombotic therapy. This case was considered as catastrophic antiphospholipid syndrome. It is necessary to differentiate antiphospholipid syndrome in case of the abnormal coagulation and fibrinolytic factors with recurrent cerebral infarction. Moreover, systemic examinations are important, because malignant tumor may exist on the background of the case.

Adenocarcinoma, Papillary↗
PubMed2000

[An analysis of characters and changes of the blood pressure in 29 cases on recurrence of cerebral infarction].

We investigated changes of the blood pressure in 29 stroke patients before stroke recurrence and after recurrence. Additional antihypertensive drugs were not administered to all patients after stroke recurrence. Twenty-five lacunar infarct patients and 4 atherothrombotic infarct patients were included in this study. A significant difference was observed between the systolic blood pressure(SBP) within 4 weeks before recurrence and that just after recurrence(132.8 +/- 17.2 mmHg vs. 157.4 +/- 21.3 mmHg, Wilcoxon rank sum test, p < 0.001), or between the SBP just after and 2 weeks after stroke recurrence(157.4 +/- 21.3 mmHg vs. 138.0 +/- 18.3 mmHg, Wilcoxon rank sum test, p < 0.001). The similar difference was found in the diastolic blood pressure(DBP) or in the mean arterial blood pressure(MABP). There was no significant difference in the SBP, the DBP or the MABP between the patients before and 2 weeks after the stroke recurrence. These results suggested that the elevation of the blood pressure at recurrence decreased spontaneously to the pre-recurrence level of the blood pressure in about 2 weeks.

Aged↗
PubMed1999

[A patient of myasthenia gravis complicated by lichen planus 9 years after thymectomy].

We report a 39-year-old woman with myasthenia gravis (MG) complicated by lichen planus, elevated liver enzymes of unknown cause and mucosal lesions of the colon and anus. Although the etiology of lichen planus is uncertain, an autoimmune abnormality is considered to be a possible cause. Lichen planus is sometimes associated with thymoma. This patient had hyperplasia of the thymus which was surgically removed nine years prior to lichen planus development. Myasthenic symptoms worsened when the lichen planus appeared and the liver enzymes were elevated. Steroid therapy was effective for the above symptoms. The clinical course suggests that MG, lichen planus and elevated liver enzymes in this patient results from common underlying autoimmune abnormality.

Adult↗
PubMed1998

Characteristic magnetic resonance imaging findings in spinocerebellar ataxia 6.

OBJECTIVE: To clarify the characteristic magnetic resonance imaging (MRI) findings in patients with spinocerebellar ataxia 6 (SCA6) diagnosed by genetic analysis. PATIENTS AND METHODS: Using MRI, we examined 10 patients genetically diagnosed as having SCA6 and 40 control subjects. RESULTS: The mean (+/-SD) CAG repeat length in 10 patients with SCA6 was 22.9 +/- 1.3. There was a significant inverse correlation between the CAG repeat size and age at onset in the SCA6 group (r = -0.86, P = .003). In patients with SCA6, the areas of the cerebellar vermis and hemispheres in sagittal MRI were significantly smaller than those in the control subjects. In transaxial MRI, the anteroposterior diameter of the pons and the diameter of the middle cerebellar peduncle were mildly decreased and the red nucleus was slightly atrophied in patients with SCA6. There was no significant difference in the diameter of the midbrain, medulla oblongata, fourth ventricle, superior cerebellar peduncles, dentate nucleus, or globus pallidus between the SCA6 and control groups. A high-signal intensity in the transverse pontine fibers was not observed in any of the patients with SCA6 on T2-weighted and/or proton-weighted axial MRI. CONCLUSIONS: The cerebellum and its afferent and efferent systems were affected in patients with SCA6. These results seem to distinguish the MRI findings of SCA6 from those of other forms of spinocerebellar ataxia.

Adult↗
PubMed1998

QTc interval, and autonomic and somatic nerve function in diabetic neuropathy.

QTc intervals were measured using an electrocardiogram and other autonomic function tests, in 66 neuropathy patients with non-insulin-dependent diabetes mellitus (59.0 +/- 12.5 years; mean +/- SD). The change in R-R interval did not influence the QTc interval, as calculated by the equation: QTc = QT + (1000 - R-R)/7 (ms), compared with the conventional Bazett's equation which appeared to overcompensate in the case of a small R-R interval. The QTc interval in the diabetic patients was significantly longer than that in age-matched controls. The QTc interval showed an inverse correlation with the coefficient of variation of the R-R interval and skin blood flow at rest. However, no correlation was found between QTc interval and blood pressure change, change in heart rate on standing, or results of the sympathetic skin response. The QTc interval did not correlate significantly with motor or sensory nerve conduction parameters. We conclude that the QTc interval can be a simple and useful autonomic indicator for diabetic neuropathy relatively independent of other abnormalities of autonomic and somatic nervous system function.

Aged↗
PubMed1998

Association between carotid atherosclerosis and hemostatic markers in patients with cerebral small artery disease.

The purposes of this study were to investigate the association between carotid atherosclerosis and hemostatic markers, and to elucidate the difference in hemostatic markers between intima-media thickening and plaque formation in patients with cerebral small artery disease. We investigated carotid atherosclerosis by assessing diffuse intima-media thickness measurements and localized plaque using B-mode ultrasonography, and we measured the concentrations of plasma fibrinogen, beta-thromboglobulin and platelet factor 4 as markers for platelet activation, and the activity of plasma von Willebrand factor as a marker for endothelial damage. The intima-media thickness was significantly associated with age, male sex, the concentrations of plasma beta-thromboglobulin and platelet factor 4, and the activity of plasma von Willebrand factor. The plaque score showed a significant association with male sex, the concentration of fibrinogen, and the activity of plasma von Willebrand factor. These results may indicate that underlying mechanisms are not the same between the intima-media thickness and plaque formation. We suggest that hemostatic markers could reflect the severity of carotid atherosclerosis in patients with cerebral small artery disease, and that preventive antiplatelet therapies against brain infarction might be necessary for patients with severe carotid atherosclerosis.

Adult↗
PubMed1997

CAG repeat length and disease duration in Machado-Joseph disease: a new clinical classification.

To evaluate the clinical characteristics of Machado-Joseph disease (MJD) with reference to CAG repeat length and disease duration, we analyzed neurologic findings in 108 patients from 84 families. The majority of MJD patients presented with an ataxic gait as the initial symptom. Dysarthria and nystagmus were observed from an early stage. Bulging eyes, muscle atrophy and bradykinesia developed later. Patients with a shorter CAG repeat length or later onset had more frequent involvement of proprioceptive sensory deficit. Incidence of abnormal reflexes, tones, and proprioceptive sensation was not associated with disease duration, but with CAG repeat length. Based on these results, we propose a new clinical classification: type A (juvenile type), with hyperreflexia and dystonia, but without a proprioceptive sensory deficit; type C (adult type), with hyporeflexia and a proprioceptive sensory deficit, but without dystonia; and type B (intermediate type), the remaining patients with a mixed presentation.

Adult↗
PubMed1997

[Endothelial cell activation and/or injury in multiple sclerosis: analysis with von Willebrand factor and thrombomodulin].

Breakdown of the blood-brain barrier, which consists of endothelial cells, is implicated essential in the pathogenesis of multiple sclerosis (MS). To examine the endothelial cell damage, we determined the von Willebrand factor and thrombomodulin, markers for endothelial cell activation and/or injury, in the peripheral blood of patients with MS. The subjects were 26 patients with relapsing-remitting MS and 35 control subjects (mean age +/- standard deviation, 44.8 +/- 9.6 years). Patients with systemic vasculitis were excluded. The plasma activity of von Willebrand factor was significantly higher in patients with MS in the active phase (n = 23; 44.6 +/- 9.6 years) than in the age-matched controls. This suggests that von Willebrand factor could be a useful marker for evaluating the breakdown of blood-brain barrier resulting from endothelial damage in MS. In contrast, the serum level of thrombomodulin was not significantly different between patients with active MS and the controls. In MS patients (n = 15; 44.2 +/- 2.2 years), the plasma activity of von Willebrand factor was significantly lowered after immunosuppressive treatment. This suggests that von Willebrand factor could be used as a parameter for assessing the effect of treatment in MS.

Adult↗