Japanese Journal of Stroke
Online ISSN : 1883-1923
Print ISSN : 0912-0726
ISSN-L : 0912-0726
Volume 8, Issue 4
Displaying 1-13 of 13 articles from this issue
  • Shinsuke Tsuzuki, Toshikatsu Indo
    1986Volume 8Issue 4 Pages 249-254
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Mood disorders in stroke patients are studied by using Hamilton rating scale for depression. In a selected group of right-handed patients with single stroke lesion of either the right (n=18) or left (n=14) hemisphere, we found that the severity of depression was statistically increased in patients with right hemisphere lesions. In addition, the severity of depression correlated significantly with proximity of the lesion on CT to the central axial line, which defines the boundary between the two hemisperes.
    No noteworthy relationship was derived between the lesion volume and the severity of depression.
    Furthermore, there were no relationship between the depression scores and the distance of lesion from the frontal pole, expressed as a percentage of the total anteroposterior distance.
    These findings suggest that intrahemispheric lesion location is in some way related to mood disorders in stroke patients, and that disorderd integration of two hemispheres may be the cause of mood disorders.
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  • Shoji Asari, Katsuzo Kunishio, Norio Sunami, Yuji Yamamoto, Kazuhiko S ...
    1986Volume 8Issue 4 Pages 255-260
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Forty-two cases with a total of 50 untreated unruptured cerebral aneurysms, who were experienced during 6 years from April 1979 to March 1985, were studied in this report. There were 15 males and 27 females and their age range was 38 to 75 years with a mean age of 60.4 years. 16 aneurysms located on the internal carotid artery, 14 on the anterior cerebral artery, 9 on the middle cerebral artery, 3 on the posterior cerebral artery, and 8 on the vertebrobasilar artery. 42 aneurysms were less than 10 mm in diameter, 4 from 10 to 20 mm, and 4 larger than 20 mm. Hypertension was associated in 12 cases, cerebral infarction in 7, head injury in 4, moyamoya disease in 2, and so on. Reasons for not operating were as follows : severe disability due to initial subarachnoid hemorrhage or underlying diseases in 13, advanced age in 8, unwillingness in 13, not notify to patient or family in 4, and technical problems for operation in 3. 4 aneurysms enlarged, 2 disappeared, and 8 unchanged by the follows-up examinations. 4 cases had bleeding from unruptured cerebral aneurysm, and three of these bleeding were fatal. One of them was operated on and had an uneventful course.
    At present, unruptured cerebral aneurysms are becoming on increasing important neurological problems. It is very significant to clarify the natural history of this lesion.
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  • Tamotsu Shinohara
    1986Volume 8Issue 4 Pages 261-268
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    In 1980, Tomita et al. reported a paradoxical phenomenon called “low perfusion hyperemia (LPH)”. It was observed in the acute stage of focal cerebral ischemia and was characterized by an increase of cerebral blood volume (CBV) despite a decrease of cerebral blood flow (CBF).
    The purpose of the present study was to compare the effects of reperfusion on ischemic cerebral circulation at two different stages : during the stage of LPH and at the declining phase of cerebral ischemia after LPH.
    Twelve cats were anesthetized with α-chloralose and urethane. The middle cerebral artery (MCA) was occluded by clipping through the transorbital approach. Continuous recording of CBV and frequent measurements of mean transit time of blood (t) were made by the photoelectric method. Cerebral blood flow was calculated from the Stewart-Hamilton equation. The cats were divided into 2 groups.
    In 6 cats, the clip was removed during LPH phase. Cerebral blood volume just before unclipping was + 1.56 ± 0.58 vol% above the control level. The duration of occlusion was 270 ±153 minutes. In this group, unclipping produced an immediate increase of CBV to the level of + 3.35 ± 0.71 vol% above the control level (p<0.05). Cerebral blood flow also increased from 41.4 ± 10.1% to 173.9 ± 51.5% of the control value (p<0.05). Cerebral blood volume and CBF returned to the control level 10 to 30 minutes after the restoration of cerebral perfusion.
    In the remaining 6 cats, unclipping was performed after LPH phase. Cerebral blood volume just before the unclipping was -2.33 ± 0.71 vol% below the control level. In this group, unclipping improved neither CBV nor CBF. The duration of occlusion in this group was 266 ±44 minutes.
    In conclusion, cerebral circulation recovered when reperfusion was performed during LPH phase. If reperfusion was performed after LPH phase, CBV and CBF remained low and did not show any tendency to revover.
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  • Yoshihiro Sato, Katsuhiro Mizoguchi, Yousuke Sato, Kazuhito Shojima, T ...
    1986Volume 8Issue 4 Pages 269-274
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    In the present study, concentration of myoglobin in serum was measured from 170 patients with acute stroke including 40 subarachnoid hemorrhage, 74 cerebral hemorrhage and 56 cerebral infarction and was compared with creatine phosphokinase (CPK) and aldolase activities in serum.
    The results were listed as follows :
    1) Myoglobin concentration, CPK and aldolase activity were elevated in these patients and no difference in the results was observed from each type of stroke.
    2) The amount of myoglobin was correlated well with the CPK activity, but not with aldolase.
    3) Relationship between myoglobin and level of consciousness was not observed.
    4) No difference in myoglobin concentration was observed between the died within a month and the survived. However, patients of either subarachnoid hemorrhage or thalamic hemorrhage who had higher myoglobin concentrations died at higher percentage in acute stage than those of normal value.
    These results indicated that measurement of serum myoglobin in acute stroke would not be useful for determining the type, severity and prognosis of the diseases.
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  • Shuhei Yamaguchi, Shotai Kobayashi, Mitsuhiro Kitani, Tokugoro Tsunema ...
    1986Volume 8Issue 4 Pages 275-280
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    The effect of a calcium antagonist nicardipine on hemodynamics in collateral circulation through the the circle of Willis after the occlusion of common carotid arteries (CCAs) was studied.
    Materials and methods : The experiments were performed on 10 adult cats anesthetized with alpha-chloralose and urethane. After partial craniotomy, pial arterial blood pressure (PAP) was continuously recorded by a micropressure recording device (Model 900), and cerebral blood flow (CBF) was measured by hydrogen clearance method. In 6 cats systemic arterial blood pressure (SAP), PAP, and CBF were measured in steady state, and after unilateral CCA and bilateral CCAs occlusion. After recirculation of CCAs, the same procedures were done with continuous intravenous infusion of nicardipine (2 μg/kg/min). In 4 cats the reproducibilities of SAP, PAP, and CBF in repeated occlusions of CCAs were studied.
    Results : Repeated occlusions resulted no significant change in SAP, PAP and CBF. Despite significant reduction of SAP and PAP after nicardipine administration, a significant increase of CBF was observed in the steady state. The reduction of PAP was greater than that of SAP. Even after the occlusions of unilateral or bilateral CCAs, CBF was increased with a reduction of PAP during infusion of nicardipine. The reduction of small arterial resistance (PAP/CBF) was significantly greater than that of large arterial resistance ((SAP-PAP) /CBF) during infusion of nicardipine. Moreover, nicardipine decreased the resistance of the anterior part of the circle of Willis more markedly than that of the posterior part, although both reductions were significant as compared with control group.
    Conclusion : These results indicate that the cerebral artery has a regional difference in reactivity to this calcium antagonist. This drug may be clinically effective even in conditions of low cerebral perfusion pressure induced by carotid occlusion in man.
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  • Yoshinori Inada
    1986Volume 8Issue 4 Pages 281-293
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    For the purpose of investigaing how the hypertensive intracerebral hematoma increases in size, the author retrospectively reviewed angiograms and CT scans in 31 patients who showed extravasation on angiograms.
    Of these patients, 28 patients (90.3%) had angiography and CT scannign within six hours after onset. Twenty seven patients (87.1%) showed extravasation on arterial phase of angiogram, 21 patients (67.7%) had multiple leakage of contrast medium, and 14 patients (45.2%) demonstrated two or more ruptured striate arteries.
    Changeing the level and width of the CT window, the author found that a large hematoma consisted of several smaller hematomas, some of which had possible bleeding points in their corners.
    The rationals for surgical treatment of hypertensive intracerebral hemorrhage was based on the assumption that the hemorrhage had a single bleeding point on a single striate artery and that the earliest possible hemostasis was mandatory.
    The author's investigation, however, showed multiple extravasation and a close relationship between expanding form of hematoma and distribution of multiple extravasation of contrast medium. This proved that the hypertensive intracerebral hematoma increased in size with increase in number of ruptured striate arteries.
    From these results, in order to prevent hematoma from rapidly increasing in size and to make Ruminant hemorrhage manageable, the author emphasizes the importance of intensive hypotension therapy that control bleeding from multiple ruptured arteries in the acute stage of hypertensive intracerebral hemorrhage.
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  • An angiographic study
    Shin Ueda, Seiji Kannuki, Masaaki Obayashi, Keizo Matsumoto, [in Japan ...
    1986Volume 8Issue 4 Pages 294-300
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    We examined the incidence and location of occlusive lesions in cerebral vessels in 100 consecutive CVD cases of which 4 vessel angiographical study were done. Stenotic or occlusive changes of more than 10% were found in 80 cases and 236 lesions. The ratio of extra-to intracranial lesions was 150 : 86. Stenotic lesions in the cervical internal carotid artery (ICA) was the most common. There were 72 lesions causing moderate or severe stenosis (more than 50%) or complete occlusion. The ratio of extra-to intracranial lesions was 32 : 40. The incidences of affected cervical ICA and middle cerebral artery (MCA) were equal. However, stenotic or occlusive lesions in the M1 portion of MCA were primarily responsible for clinical symptoms.
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  • Report of a case with generalized migratory thrombophlebitis
    Susumu Kusunoki, Makoto Iwata, Yasuo Shimada, Yasuo Toyokura, Tohru Ma ...
    1986Volume 8Issue 4 Pages 301-305
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Superior sagittal sinus thrombosis is usually a severe, acute neurological disease with intracranial hypertension, loss of consciousness and often with fatal outcome. But there are some rare cases of milder neurological manifestations without increased intracranial pressure. The present authors report a case of such benign superior sagittal sinus thrombosis with focal motor seizures and right hemiparesis without intracranial hypertension.
    A 60-year-old totally blind man with history of bilateral uveitis in his early forties developed clonic convulsion of the left lower extremity at age 39. At age 45, he was operated due to the recurrent attacks of gastrointestinal symptoms, but no pathological findings were noted at the time of operation. At age 57, the patient developed several attacks of loss of consciousness associated with right hemiconvulsion resulting in right hemiparesis as sequale, he was admitted to the Department of Neurology at the University of Tokyo Hospital in November 13, 1980.
    On admission, consciousness was clear and general physical examination revealed no particular abnormality. Bilateral blindness (right eye enucleated and left ophthalmophthisis), slight dysarthria and right hemiparesis with hyperreflexia and Babinski sign were noted on neurological examination. Laboratory tests showed increased ESR, strongly positive CRP and high fibrinogen level in blood. CSF pressure was normal but total protein and immunoglobulins were markedly elevated. During his hospital days, left facial edema and migrating thrombophlebitis of right upper extremity appeared. Right hemiconvulsion associated with transient consciousness disturbance were also observed. Carotid angiography and CT scan revealed occlusion of the superior sagittal sinus.
    After the discharge, right focal seizures and facial edema recurred intermittently. On November 4, 1981, he became drowsy and was readmitted ot our department. Phenytoin overdosis was found and the consciousness recovered to normal after the withdrawal of phenytoin. The precipitation of cryofibrinogen was noted during the second admission. Due to the subsequent episode of aphasia of conduction type several months later, he was put on prednisolon. After that, CRP and fibrinogen gradually returned to normal and the recurrent focal seizures subsided completely.
    As a causative disease of superior sagittal sinus thrombosis in the present patient, Behget disease was suspected with generalized thrombophlebitic manifestations. But the definite diagnosis could not be obtained due to the lack of ophthalmological confirmation of Behçet disease.
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  • Nobuhide Masawa, Yoji Yoshida, Tatsuru Mihara, Takashi Joshita, Genju ...
    1986Volume 8Issue 4 Pages 306-315
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Cardiac thrombosis associated with atrial fibrillation (AF) has been regarded as an important cause of cerebral embolism. However, at autopsy of patients with cerebral embolism accompanied by AF, macroscopic thrombi are often absent, and thus the origin of the thrombi can not be confirmed. Therefore, we studied the morphological changes in the heart suggestive of the presence of cardiac thrombi when they are macroscopically undetectable, to clarify the mechanism of cardiac thrombus formation in AF.
    After detailed macroscopic observation for the origin of emboli in the heart of 30 autopsy patients with cerebral embolism, serial strip sections of the endocardium of the left atrium were made and examined by a light microscopy. The. endocardial surface of the patients with AF but without macroscipic cardiac thrombi was studied by a scanning electron microscopy.
    Macroscopic observation of the endocardium of the left atrium showed edematous thickening, fine or rough folds, a fine granular or rough surface, deposition of fibrin and occasional hemorrhagic foci in 15 of 20 patients with AF. We called these findings rough endocardium (RE). In 13 of these cases, histological evaluation of the RE areas showed fresh or organized microthrombi, as well as varying degrees of endocardial edema, infiltration of neutrophils and small round cells, hemorrhagic foci, deposition of hemosiderin and serum infiltration. Scanning electron microscopic observation on the endocardium of the RE sections revealed that many microvilli sprouting from the cell surface, partial exfoliation, thrombus formation on the exposed subendothelial connective tissue and attachment of monocytes and neutrophils to the less damaged surface. The frequency and extent of these findings were significantly greater in the patients with AF than those in the controls without AF.
    Though thrombi in the left atrium were macroscopically identified only in 40% of the patients with AF, histoligical evaluation made on the RE area increased the detection rate to 70%. These results show that, in patients with cerebral embolism accompanied by AF, the RE in the left atrium probably caused by AF can be a finding suggestive of cardiac thrombi when it is macroscopically undetectable. Endothelial injury seems to play an important role in the formation of cardiac thrombi by AF.
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  • Evaluation of serial angiographic findings
    Akihiko Takechi, Hisanori Yoshimoto, Keiji Ohta, Takashi Mikami, Tohru ...
    1986Volume 8Issue 4 Pages 316-321
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    A case of a left middle cerebral artery stenosis with moyamoya phenomenon was experienced. A healthy 13-year-old girl complained a headache, nausea and vomiting after taking a bath and she was admitted to a near hospital on June 22, 1984. One day later she was referred to Matsue Red Cross Hospital under diagnosis of subarachnoid hemorrhage by the lumbar puncture that yielded bloody spinal fluid. On admission, CT scan showed the left frontal subcortical hemorrhage. The left internal carotid angiography revealed the stenosis of the left middle cerebral artery at the M2 portion with moyamoya phenomenon and the right accessory middle cerebral artery originated from the anterior communicating artery.
    The right internal carotid and bilateral vertebral angiographies revealed neither occlusion, stenosis, nor moyamoya phenomenon.
    Fourteen months later the follow up left internal carotid angiography revealed the improvement of the stenosis of the left middle cerebral artery and the reduction of moyamoya phenomenon.
    The authors have reviewed the literatures and emphasise that a long term follow up is necessary in order to make an exact and a differential diagnosis from moyamoya disease.
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  • Hidetada Hino, Shinpei Aoki, Fumihiko Sakai, Tadashi Kanda, Yoshiaki T ...
    1986Volume 8Issue 4 Pages 322-327
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Bilateral medial medullary infarction occurs rarely with symptoms of respiratory paralysis, vertical nystagmus, and quardriplegia. The following is a case of bilateral medial medullary infarction which was verified by CT.
    A 68-year-old woman with a longstanding history of hypertention and diabetes mellitus complained of sudden onset of nausea, vomiting and weakness of bilateral extremities. Several hours later she was admitted to the hospital because of progression of the weakness and shortness of breath. She was alert and cooperative. Her eyes were markedly conjugated downward and coarse upbeating vertical nystagmus was noted in upward gaze. Her bilateral upper and lower limbs were flaccid and completely paralyzed and movement of the head was also absent. Soon after admission ventilatory assistance was uregently required because of respiratory arrest. Within a month following the onset spontaneous respiration was restored and conjugated eyes returned to the normal position with disappearance of vertical nystagmus. However, there was no sign of functional recovery in any of the limbs. A CT scan performed 38 days after the onset revealed a low density area in the bilateral medial region of the medulla, which was indicative of infarction.
    A review of literature pertaining to the disease disclosed 8 cases of bilateral medial medullary infarction. To the best of our knowledge this is the first case of medial medullary infarction demonsrated by CT.
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  • Toshihiko Iwamoto, Tatsuru Mihara, Nobuhide Masawa, Hisashi Joshita
    1986Volume 8Issue 4 Pages 328-337
    Published: August 25, 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
    Seven patients with megadolicho anomaly were studied for the complication of cerebral infarction. Cerebral infarction was diagnosed in 6 of them, mainly lacunar infarction, by CT or autopsy. They tended to be hypertensive, younger in age of onset than patients without megadolicho anomaly and have a stepwise deterioration of neurological deficits. As to the cause of the high frequency of lacunar infarction in patients with megadolicho anomaly, the decrease of “Windkessel function” due to the absence of elasticity of the seemed to accelerate the arteriosclerotic changes at the perforating arteries associated with lacunar infarctions. Therefore, it was suggested that non-stenotic arteriosclerotic changes of the main trunk induced lacunar infarction because of the reduction of “Windkessel function”.
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  • 1986Volume 8Issue 4 Pages 345
    Published: 1986
    Released on J-STAGE: September 03, 2009
    JOURNAL FREE ACCESS
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