Japanese Journal of Stroke
Online ISSN : 1883-1923
Print ISSN : 0912-0726
ISSN-L : 0912-0726
Volume 15, Issue 5
Displaying 1-10 of 10 articles from this issue
  • Fumihiko Kashiwagi, Hironaka Igarashi, Yasuo Katayama, Akiro Terashi
    1993 Volume 15 Issue 5 Pages 333-339
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    SM-6586 (SM) is a new derivative of dihydronyridine with a potent calcium blocking activity and an inhibitory activity of Na+/H+ and Na+/Ca++ exchange transport. The effects of SM on survival rate, brain edema and metabolites were evaluated using a global ischemic model in spontaneously hypertensive rats (SHR). Further, the effects of SM on the brain water content and T1 relaxation time using NMR were examined in focal cerebral ischemia. Global ischemia was induced by bilateral common carotid artery ligation (BLCL), and focal ischemia was induced by middle cerebral artery occlusion. The survival rate after BLCL was higher in the SM-treated group. The brain water content was lower, the ATP levels were higher and the lactate levels were lower in the SM-treated group as compared to the control group. In the focal ischemia model, the SM-treated group showed a reduction in T1 relaxation time. Also, the brain water content was significantly decreased in the SM-treated group. These results indicate that SM was effective in ameliorating the ischemic insult in both the global and focal cerebral ischemia models.
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  • Megumi Shimada, Satoru Komatsumoto, Masaharu Nara, Fumio Gotoh
    1993 Volume 15 Issue 5 Pages 340-345
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    The plasma concentrations of atrial natriuretic peptide (ANP) were measured in 14 patients with intracranial hemorrhage, including 7 patients with brain edema and 7 without any evidence of brain edema. The plasma ANP concentrations in the patients with brain edema were elevated to 123.8 ± 28.1 pg/ml on day 1, followed by a gradual decrease to 111.4 ± 23.0 on day 3, 101.0 ± 21.6 on day 5, and 106.3 ± 25.7 on day 7, respectively. The ANP concentrations on day 14 showed a significantly lower level of 77.2 ± 17.6 (p<0.05). On the other hand, the patients without brain edema displayed no significant change in their plasma ANP concentrations, as follows : 46.3 ± 5.5 pg/ml on day 1, 44.4 ± 7.4 on day 3, 38.8 ± 4.8 on day 5, 40.8 ± 4.6 on day 7, and 36.9 ± 6.4 on day 14, respectively. The present findings indicate that the concentrations of ANP are elevated in intracranial hemorrhage with brain edema, suggesting that ANP may play an important role in the regulation of the intracranial pressure dynamics.
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  • Correlation with radiological findings
    Masaki Watanabe, Nobuko Ujihira, Yoshio Hashizume, Yoji Yoshida
    1993 Volume 15 Issue 5 Pages 346-352
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    We evaluated the arteriolar adventitial proliferative rate (AP) in the white matter of 118 autopsied brains (58 control cases, C group; 43 hypertensive cases. HT group; and 17 Binswanger type vascular dementia cases. VD group), together with the sclerotic rate (AS) of the middle cerebral artery. In the C group, AP increased with age, advancing rapidly in subjects over 80 years old. In contrast, AS increased slowly in subjects over 80 years old. There was no difference between AS in the VD and HT groups, while the VD group showed a greater AP than did the HT group. The results of CT scans performed in 45 cases revealed that while AP demonstrated a significant correlation with leukoaraiosis (LA), AS showed no such correlation. Our results suggest that arteriolar adventitial proliferation plays a more important role in the onset of Binswanger type vascular dementia and the progress of LA. We also observed a strong relationship between ischemic changes in the cerebral white matter and arteriolar adventitial proliferation.
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  • Yasumasa Yamamoto, Ichiro Akiguchi, Kaiyo Oiwa, Satoshi Satoi, Jun Kim ...
    1993 Volume 15 Issue 5 Pages 353-359
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Leukoaraiosis is commonly observed on magnetic resonance imaging (MRI) in elderly patients. Although a heterogeneous pathogenesis is suggested, the postulation of ischemic leukoencephalopathy resulting from arteriolar lesions that preferentially involve the long medullary arteries, is broadly supported. Lacunar infarct is a penetrating artery obstruction with hypertensive arteriosclerosis. The mechanisms of those two kinds of small artery disease were analyzed by 24-hour blood pressure recording.
    Eighty-three patients with leukoaraiosis or/and lacunar infarct located in the area of the basal ganglion as diagnosed by MRI (1.5) were investigated. In each patient, the degrees of leukoaraiosis, lacunar infarct and dementia were classified into 4 grades (03). Blood pressure recording was performed every 30 min for 24 hours using a portable blood pressure recorder (ABPM-630, Colin, Japan). All blood pressure values for 24 hours were averaged (A-BP) and the short-term blood pressure variability (ST-V) was expressed as the mean difference in two successive blood pressure values.
    Age, A-BP, ST-V and the severity of dementia increased in relation to the degree of leukoaraiosis. However, age and ST-V were unrelated to the severity of lacunar infarct. A-BP was correlated with the degree of lacunar infarction from grade 0 to grade 2, but decreased rather in grade 3 as compared to grade 2, so that the severity of dementia was remarkable in grade 3. It was inferred that A-BP decreased in the severe multiple lacunar state, and could consequently have prompted the process of vascular dementia.
    High short-term blood pressure variability may be a risk factor for leukoaraisosis, but is irrelevant to lacunar infarction.
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  • Tsutomu Takahashi, Yoshiyasu Tsuda, Yoshinari Izumi, Motoomi Ohkawa, H ...
    1993 Volume 15 Issue 5 Pages 360-369
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    We investigated the hemorheological changes and correlations among aging, cerebral atrophy, and silent infarct lesions in patients with silent cerebral infarctions (n=46) and in patients with symptomatic cerebral infarctions. We measured the whole blood viscosity, corrected blood viscosity at a standard hematocrit level of 45%, plasma viscosity, plasma fibrinogen concentration, fibrinogen/albumin ratio, and yield shear stress index as hemorheological parameters. For the evaluation of cerebral atrophy, the parenchyma/skull-volume ratio and parenchyma/ (ventricles + subarachnoid space) -volume ratio were estimated using a planimeter or digitizer.
    The patients with silent cerebral infarctions (n=36) revealed significantly lower values for the corrected blood viscosity, plasma fibrinogen concentration, fibrinogen/albumin ratio, and yield shear stress index than those in patients with chronic cerebral infarction (n=25) (4.36 vs. 4.63 mPa·s, p<0.05 ; 280.0 vs. 379.0 mg/dl, p<0.05; 71.2 vs. 105.0 p<0.05; and 0.056 vs. 0.080, p<0.01, respectively). Among the patients with silent cerebral infarct lesions, those with more progressive lesions showed significantly higher plasma fibrinogen concentrations and fibrinogen/albumin ratios than those with less progressive lesions (P<0.010.05).
    The increase in numbers of silent white matter lesions (WML) was significantly correlated with aging and severity of cerebral atrophy (p<0.050.01). In patients with silent infarctions, the severity of periventricular hyperintensity (PVH) was significantly correlated only with the increase in numbers of WML (p<0.010.05). In patients with silent infarctions together with patients with symptomatic cerebral infarctions of perforating arteries (n=16), the severity of PVH became significantly correlated with the increase in numbers of WML, aging, and severity of cerebral atrophy (p<0.010.05).
    It is suggested that increases in plasma fibrinogen concentration might play a role in the progression of silent cerebral infarct lesions, and extensions of the silent cerebral infarct lesions may be significantly correlated with aging and cerebral atrophy.
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  • Hidenao Fukuyama, Hidehiko Nabatame, Kazuo Nakamura, Jun Kimura
    1993 Volume 15 Issue 5 Pages 370-373
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Employing MRI, we evaluated the frequency of hemorrhagic infarction after treatment with ozagrel sodium in cerebral thrombosis at the acute state. We found that high intensities in T1 weighted images and low intensities in T2 weighted images showed no remarkable changes in their frequencies irrespective of the treatment. We conclude therefore that the frequency of hemorrhagic infarction still remained unchanged after ozagrel sodium treatment.
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  • Surgical indications
    Tomoichiro Kimura, Takashi Ueda, Shinichiro Wakisaka
    1993 Volume 15 Issue 5 Pages 374-379
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    During the last 6 months, we encountered 3 male patients with cerebellar infarction who recovered well following neurosurgical decompressive therapy. In the cases of patients No. 1 (59-year-old) and No. 3 (79-year-old), at 5 days after the onset, their consciousness level decreased to J.C.S. IIIrd grade and brain herniation was found to be progressing. In these cases, external ventricular drainage was effective. In the case of patient NO. 2 (61-year-old), the neurological findings were worsening, and a CT scan demonstrated a tight posterior fossa. We performed decompresion the patient was surgery by extended suboccipital craniectomy, and the patient was discharged quite soon after with full recovery. It is usually difficult to make an accurate diagnosis in patients with cerebellar infarction because they do not display typical symptoms, signs and severity. Nevertheless, neurosurgical decompressive therapy gives them a chance of following a good clinical course.
    It is very important therefore to observe the changes in neurological findings carefully, including the consciousness level, while serial examinations by CT scan can provide us with useful information.
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  • Mie Kitagawa, Hiroshi Sugihara, Kimihiro Yoneyama, Tooru Shimizu, Isao ...
    1993 Volume 15 Issue 5 Pages 380-385
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    A 62-year-old man suddenly suffered from cerebral infarction during coronarography. Subsequent examinations revealed right hemiplegia accompanied by lateral deviation of the right eye, vertical oculomotor disorder, and retraction nystagmus in the dounward gaze. An electro-oculogram showed that downward gaze was more prominent than upward gaze, Doll's eye phenomenon, however, was preserved and remained unchanged. A caloric test elicited upward nystagmus in the supine position and pendular nystagmus in the prone position. Bell's phenomenon was positive. Brain MRI demonstrated a discrete infarction in the paramedian midbrain including the rostral interstitial nucleus of MLF (riMLF). It is suggested therefore that the vertical oculomotor disorder was caused by the lesion of the riMLF. Based on MRI, predominantly downward gaze palsy might be ascribable more to a lesion of the mediocaudal part than one of the dorsolateral part of the riMLF.
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  • Kazuhiko Tsuruya, Hiroaki Ooboshi, Setsuro Ibayashi, Seizo Sadoshima, ...
    1993 Volume 15 Issue 5 Pages 386-391
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    A 56-year-old hypertensive man suddenly developed dysesthesia and paresthesia of the left hand and bilateral perioral region. He also had a past history of bilateral perioral dysesthesia which lasted for a week, 10 years previously. A brain CT scan taken 3 days after the present attack demonstrated a focal high density area in the paramedian region of the right pontine tegmentum. MRI at 18 days after the onset disclosed a small high intensity area in the same region on the T1 weighted image, as well as a small high intensity spot with a low intensity rim on the T2 weighted image. The sensory disturbance of the left hand and bilateral perioral region was thought to be caused by the small pontine hemorrhage. The mechanism of this bilateral cheiro-oral syndrome was hypothesized to be as follows. A hematoma impaired the fibers which crossed the pontine tegmentum from the ipsilateral main sensory nucleus of the trigeminus to the contralateral ventral trigeminothalamic tract, in addition to disturbance of the ipsilateral medial lemniscus and the ventral trigeminothalamic tract. Furthermore, the T2 weighted image of MRI was considered to have revealed another small lesion derived from an old hemorrhage close to the new hematoma which appeared to be responsible for the bilateral perioral dysesthesia.
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  • Haruhiko Hoshino, Shingo Yamagata, Makoto Takagi, Tetsuya Inafuku, Yas ...
    1993 Volume 15 Issue 5 Pages 392-398
    Published: October 25, 1993
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    We report a 46-year-old male with cerebral infarction caused by artery-to-artery embolism from right internal carotid artery stenosis. He was admitted because of progressive left hemiparesis. At admission, CT demonstrated a watershed infarction between the middle cerebral artery and posterior cerebral artery. The mechanism underlying this infarction appears to have been hemodynamic insufficiency. At the 3rd hospital day, the patient's hemiparesis suddenly worsened. CT revealed new right striatocapsular infarction. At the 7th hospital day, cerebral angiograms demonstrated 90% stenosis of the right internal carotid artery at the origin, and occlusion of the right middle cerebral artery at the trifurcation. One month later, repeated angiograms showed recanalization of the middle cerebral artery. Artery-to-artery embolism from the right internal carotid stenosis was diagnosed. Three months later, carotid endarterectomy was performed without any complications. This case suggests that artery-to-artery embolism is one of the important preventable mechanisms of cerebral infarction in patients with internal carotid artery stenosis.
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