Cerebral blood flow (CBF) was studied to elucidate the pathogenesis and pathophysiological mechanism of cases of TIA measured by IMP-SPECT and Xe-133 inhalation method.
Sixteen patients, six men and ten women, the mean ages being 62.1 years old, were investigated. Twelve patients were carotid artery territory TIA, and four were vertebrobasilar artery territory TIA. On the SPECT images, nine patients demonstrated multiple hypoperfusion areas, three patients showed single hypoperfusion areas and three patients demonstrated hypoperfusion at periventricular area. Only one patient had no abnormal findings. IMP-SPECT scans were compared with the X-ray computed tomographic (CT) scans. The IMP-SPECT abnormalities corresponded to an area of low density on the X-ray CT in only four patients. The SPECT reflected the clinical symptoms more than the X-ray CT in eleven patients and less in only one patient. Regional cerebral blood flow measured by Xe-133 inhalation method corresponded with the IMP-SPECT better than the clinical symptoms and the X-ray CT findings.
From this evidence it was suggested that the pathogenesis of TIA was closely connected with the cerebral blood flow insufficiency.

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A hypertensive 51 year-old Catholic clergyman was admitted to our service because of a sudden onset of vertigo and numbness in his bilateral perioral area and the left hand. Neurological examination revealed that he was alert and his speech was normal. Pupils were isocoric and the reaction to the light was prompt. The right side horizontal nystagmus was noted in the primary position and the right side gaze. Light touch was abnormal in the bilateral perioral area and pain-temperature sensation was decreased on the left side perioral region. Tactile and pain-temperature sensation was decreased in his left palm distally. No motor weakness was noted. The deep tendon reflexes were hyperactive on the left side, and the left Babinski's sign was noted. Cerebellar functions were normal. Brain CT two hours after the onset revealed a small high absorption area in the right paramedian pontine tegmentum. MRI using a 0.5 Tesla unit demonstrated a high signal lesion mainly involving the right medial lemniscus from the mid to the upper pontine levels in T1 and T2 images. It is suggested that the hematoma impaired the uncrossed fiber of the dorsal trigeminothalamic tract and the medial portion of the medial leminiscus in the unilateral paramedian pontine tegmentum. Cheiro-oral syndrome with the bilateral perioral sensory deficits is an important neurological syndrome suggesting a lesion in the unilateral pontine tegmentum.

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One of the cause of cerebrovascular accident in young adult is a wall dissection of the cerebral artery. There are a few case reports of wall dissection of the cerebral artery, but no experimental studies using animal models have been reported in the literature. We devised a new experimental model in the rabbit, and 55 cases of arterial wall dissection of common carotid artery were prepared. Chronological observations were done for a maximum of 3 months as follows : the animals were sacrificed at intervals (1 hour, 1 week, 1 month and 3 months) to examine the local pathophysiological changes and follow the healing processes.
Wall dissection was confirmed histologically in 25 animals and divided into three groups : re-entry formation (REF), pocket formation (PF), and lumen occlusion (LO) groups. The pathophysiological conditions of the REF and PF groups were in the progressing stage for the first 1 month after the onset, followed by the healing process during the next 2 months (stable stage in histological condition). Full recovery was already confirmed at 3 months after the onset in several cases. Thrombus formation was found in the angled corner of pseudolumen of the dissecting wall within 1 week in the earliest, suggesting the possibility of a subsequent cerebral embolism. In almost all 5 cases which showed LO, the LO was confirmed within a few hours after the onset, which indicated that complete occlusion of the vessel may occur in the very acute stage. A ruptured dissecting aneurysm was found in only one case; which was confirmed histologically in the post-mortem examination.

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We reported a 50-year-old male with paramedian thalamic and midbrain infarcts presented Korsakoff syndrome after the attack of acute myocardial infarction. He lost his consciousness after the heart attack. After recovery of consciousness disturbance, he developed anterograde and retrograde amnesia, disorientation, confabulation, and lack of insight into his own disability. This condition was considered Korsakoff syndrome. He had mild disturbance of language. Vertical gaze palsy (downward gaze dominantly at early period, but upward gaze dominantly at late period) and bilateral mild palsy of abducens nerve (peudosixth nerve palsy) were found. There were no disturbances of sensory and motor system, and gait. There was significant difference between verbal and performance IQ (verbal IQ 73 and performance IQ 92, and total IQ 81) on Day 56. Serum CK was increased, and electrocardiogram and ultrasonography of his heart were showed antero-inferior wall infarction. Brain CT scan disclosed low density areas in bilateral thalamus and left midbrain on Day 7. And we found the same lesions in MRI. Cerebral angiography showed no significant findings in vertebro-basilar system and both internal carotid arteries. There was no significant perfusion defect in SPECT. This case was considered top of the basilar syndrome due to cerebral embolism. Because Korsakoff syndrome was persisted, his social life was restricted. Therefore this condition was considered thalamic dementia.
In this case, main lesions were in the areas of bilateral paramedian thalamic artery, and the areas of bilateral tuberothalamic artery were partially included too. Therefore it was considered that damage of bilateral mammillothalamic tracts were responsible for Korsakoff syndrome.

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A case of recurrent minor stroke with pulmonary infarction is described. A 45-year-ord right-handed man presented with left hemiparesis. A CT scan showed a low-density lesion in the socalled “watershed” area of the right middle cerebral and anterior cerebral artery. Cerebral angiography was completely normal. At admission, the patient was normotensive. There was no history of hypertension. With the exception of elevated platelet factor 4 and β-thromboglobulin, other laboratory values were almost normal. Several weeks later, the patient developled lateral surface pain of left lower extremity. Myelography and MR imaging revealed left L4/5 intervertebral disc hernia that was surgically treated. During the postoperative period, the patient complained of right chest pain. Chest X-ray and other radiological investigation revealed pulmonary infarction of the right lung field. Several days later, when he stood up, impaired consciousness and left hemiparesis occurred. Orthostatic hypotension was noticed at the time. Several months later, the patient suddenly experienced right hemiparesis after heavy alcohol consumption and a water bath. A CT scan showed a low-density lesion in the region supplied by the terminal branch of the left anterior cerebral artery. After a second ischemic attack, the patient had recurrent right chest pain. Digital subtraction angiography of the pulmonary artery revealed an avascular area of right B⁶. In this case, a concomitant factor in the development of cerebral and pulmonary infarction was platelet hypercoagulopathy with elevated platelet factor 4 and β-thromboglobulin. Besides platelet hypercoagulopathy, hemodynamic factors such as orthostatic hypotension and hemoconcentration after heavy drinking played a significant role in the occurrence of cerebral infarction. Platelet hypercoagulopahty and bed rest after lumbar discectomy contributed to the pulmonary infarrtion

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The expansion of the hematoma during the very acute stage of putaminal hemorrhage was detected by repeated CT measurements in 7 patients. We examined whether the changes in blood pressure during the initial 24 hours after admission have any effect on the expansion of the hematoma. Clinical and CT studies were made during the very acute stage in 46 patients with hypertensive putaminal hemorrhage which were graded as IVb or better according to the Criteria of the Japanese Conference on Surgery for Cerebral Stroke. Blood pressure on admission was not significantly different between the progressive group (in which the hematoma became expanded) and the nonprogressive group. In the nonprogressive group, blood pressure gradually decreased with time following admission whether the initial size of hematoma was large or small. In the progressive group, the increase in blood pressure occurred both during the 3rd hour and the 24th hour after admission. The initial elevation of blood pressure was considered to be responsible for the expansion of the hematoma, while the later elevation of blood pressure seemed to be the consequence of the increase in the intracranial pressure.
Our data suggested that blood pressure should be controlled in patients with hypertensive putaminal hemorrhage if blood pressure continued to increase after admission.

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We present the first case of medial medually syndrome demonstrated by magnetic resonance imaging (MRI) in this country, and report details of the clinical signs. A 73-year-old male was diagnosed as having medial medullary syndrome on the the basis of left hemiplegia, tongue deviation to the right and left deep sensory impairment. We detected a high signal intensity area in the right side of his medulla oblongata by MRI (T2-weighted image; TR 3000 msec, TE 90 msec). Since Spiller's first clinical description in 1908, confirmation of the lesion has only been made by pathological examination, except for some reports on CT findings and one by Fox et al. on MRI findings.
A review of the literature pertaining to this disease has disclosed that the combination of clinical signs described as typical in some textbooks is in fact rather unusual.

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544 patients who had ruptured aneurysms were analyzed by Kaplan-Meier's method and follow-up study was done by questionaries for the individual patients. Activity of daily life at discharge was well correlated to survival rate. The patients aged under 65 have a good survival rate up to maximal 8 years follow up study, however, the patients aged over 65 have a poorer survival rate especially in the group of ADL 3 through 6. At the end of follow up study, two third of the patients have relation to the hospital as for either in-patient or out-patient.
Not only the operative and postoperative management, but also improvement of activity of the daily life as better as possible is important for the patients with ruptured cerebral aneurysms.

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The clinical, radiological, and surgical features of 20 cases of cavernous angioma verified histologically, were analyzed. The age ranged 6 to 75 years with a mean age of 34 years, including 5 young cases less than 15 years. There were 7 cases in male and 13 cases in female. Of 23 lesions including multiple lesion in 3 cases, 17 were located in supratentorial region, and 5 in brainstem. There was one familial occurrence. All case had various initial symptoms, which were divided into 8 cases with neurological deficits and 8 cases with convulsive attacks. Three cases developed more severe clinical manifestations due to rebleeding at various intervals ranging from 1 to 26 months. In most cases, plain CT demonstrated the lesion as high density area, and MR imaging revealed it more clearly as multiseparated, high signal intensity. We have surgically treated, and the postoperative courses in all cases were uneventful. No additional neurological deficits were seen. In conclusion, we emphasize that radical extirpation of cavernous angioma, especially exhibiting symptoms, prevents not only rebleeding, but also prevents mass effects on the surrounding tissues, even if the lesion was located in brainstem.

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In spite of acute operation with postoperative intensive care, the prognosis for severe cases of ruptured intracranial aneurysm is poor. We performed acute operation for 77 cases of poor grade (Botterell grade III & IV) ruptured aneurysms and only 45.5% of them showed good outcome. We analyzed the factors affected prognosis in severe cases from retrospective follow up of 12 months.
The factors concerned with severity of disease were aged, intracerebral hemorrhage and acute hydrocephalus. In acute stage after operation (within one month), the rate of good outcome was 84.7% in mild cases (Botterell I & II) and 27.3% in severe cases (Botterell III & IV). Within one month from operation, vasospasm highly affected mortality rate, but after one month, systemic complication was the most important prognostic factor. Severe cases showed no improvement after 6 months from operation. The patients with reversible vasospasm showed marked improvement after 6 months from operation. The mean age of good outcome patients was younger than poor outcome patients. Hydrocephalus after operation was seen 59.7% of severe cases, but almost all patients were improved by shunt operations. Patients with intracerebral hematoma showed no improvement.
The prognostic factors in severe cases were age, systemic complications and intracerebral hematoma. So postoperative intensive care was important to prevent vasospasm and systemic complications in severe cases of ruptured intracranial aneurysm.

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Among 120 patients with thalamic hemorrhage admitted to our hospital during the year of 1979-1989, 117 patients presented with hemiparesis. In 12 of these patients weakness was dominant in the lower extremity compared to the upper extremity. CT scan of these 12 patients showed that hematoma was extending to the posterior half of corona radiata. In only 2 of these patients hematoma was also extending to the posterior part of the posterior limb of internal capsule.
Since the damage to the posterior half of corona radiata was responsible for the hemiparesis dominant in the lower extremity, it was suggested that corticospinal fibers to the lower extremity is passing in the posterior half of corona radiata.

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A 66-year-old male who had isolated trigeminal sensory disturbance (face, oral cavity and tongue) due to hemorrhage in the left paramedian pontine tegmentum and base junction with no other neurological symptoms is reported. Pontine hemorrhage with symptoms limited to the trigeminal region is rare, and only one case has been reported in the literature. Pontine hemorrhage must also be suspected in patients with sudden facial sensory disorders.

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