The two patients with ruptured vertebral-posterior inferior cerebellar artery junction aneurysm (VA-PICA AN) with paraparesis are reported.
One was a female patient of 58-year-old, whose onset was headache, nausea, vomiting and conciouslessness. And she presented paraparesis and abducens paresis. A CT scan revealed severe subarachnoid hemorrhage (SAH), and a four-vessel study showed Rt. VA-PICA AN. Six days after aneurysm rupture, neck ligation & clipping were performed. After the operation, paraparesis was improved by degrees.
Another case was 61-year-old, whose onset was conciouslessness. And she presented tetraparesis (leg>arm), and had severe SAH and Rt. VA-PICA AN. Three days after the operation, tetraparesis was improved by degrees.
Paraparesis was not recognized as a specific symptom of VA-PICA AN. There is only one report that presents paraparesis with VA-PICA AN, however, two cases of symmetric paraparesis were picked up, which might occur on condition that an aneurysm was located at the center of medulla oblongata and that the direction of an aneurysm was upward and backward.

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A 32-year-old male with tuberculous meningitis with right tuberothalamic artery territory infarction was reported. The patient had a family history of pulmonary tuberculosis.
On 5th December 1988 he had fever, and headache on 10th. On 5th January 1989 he developed disorientation, confusional state and hypersomnia. When he was admitted to a local hospital on 4th February, he showed disorientation, fever and Kernig's sign. He was diagnosed of tuberculous meningitis because of 598/3 white blood cells, 170 mg/dl protein, 15 mg/dl glucose, 11.9 IU/1 adenosin deaminase, and positive culture of mycobacterium tuberculosis in cerebrospinal fluid. He was admitted to our hospital because of persistence of fever despite of therapy with INH and SM. On 7th February brain CT showed a low density area in the right tuberothalamic artery territory. And on 3rd March CT showed isodensities (increased attenuation) in the basal cisterns and Sylvian fissures, and marked enhancement in the same region. In MRI performed on 15th March, the arteries in basal cisterns were demonstrated as low intensity areas in Ti-& T2-weighted images due to flow void phenomenon. The Basal cisterns showed isointensities in Ti-weighted image, slight high intensities in T2-weighted image, and marked enhancement in Gd-enhancement. These lesions were considered as granulomas due to granulomatous basal arachnoiditis, and specific in tuberculous meningitis.
This patient had a right tuberothalamic artery territory infarction caused by tuberculous meningitis. This lesion was considered to cause disorientation, cofused state and hypersomnia. Cerebral angiography disclosed absence of the right P1 segment and that the thalamoperforating artery supplied only the left thalamus. It is necessary to consider a possibility of cerebral infarction when a patient with tuberculous meningitis has developed consciousness disturbance or mental disorder.

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Lp (a) is a LDL-like lipoprotein, whose high concentration in serum is associated with angina, myocardial infarction, and cerebral infarction. Apo (a) exhibits 7 phenotypes according to their mobility on SDS-PAGE, called F, B, S_1-4, and 0 (null; not detectable). Attempts were made to investigate the relation of Lp (a) concentration with these phenotypes in Japanese controls (n=198) and patients with cerebral infarction (Cortical artery type : n=51, Perforating artery type : n=47). The median Lp (a) concentration in patients with cerebral infarction of cortical artery type is 16.8 mg/dl, which is significantly higher than serum Lp (a) concentrations in healthy controls (13.0 mg/dl), and also those in patients with cerebral infarction of perforating artery type (12.6 mg/dl) (p<0.05). The mean Lp (a) concentration is relatively low in S₃, S₄, and 0 type (12.9, 10.2, 7.9 mg/dl), and high in S₁, S₂ type (20.8, 19.5 mg/dl). When mean Lp (a) concentration of each phenotype were compared among these 3 groups-healthy controls and patient with cerebral infarctions of cortical artery type and perforating artery type-, no significant difference were observed. On the other hand, phenotype frequencies are quite differen between healthy controls and cerebral infarction of cortical artery type. S₃, S₄, and 0 type occupies 59.0% in healthy controls but 47.0% in cerebral infarction of cortical artery type S₁, S₂ type occupies 10.8% in former but 31.4% in the latter. No significant difference were observed between healthy controls and patients with cerebral infarction of perforating artery type. Apo (a) phenotype, probably inherited as an autosomal dominant trait, is considered useful for risk assessment of cerebral infarction.

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Recent development of the ¹³³Xe inhalation technique has made it possible to measure cerebral blood flow (CBF) noninvasively. Recording of the head curves from the frontal and temporal areas during inhalation of ¹³³Xe, however, is contaminated by the artifact from the air passages. A method based on Fourier transforms was reported to be able to eliminate air passage artifact (APA) effectively. However, it was pointed out that such an algorithm does not give a complete correction if the artifact seen by the head detectors differs in shape from that recorded from the airways at the mouth, which may happen when there is a slow isotope convection in the nasal and sinus cavities. The purpose of this study was to compare the CBF values calculated by the Fourier method with those by the conventional method of Obrist (VM method). Mean hemispheric gray matter flow (F₁) calculated by the VM method in 11 subjects, including normal volunteers and patients with various neurological diseases, was 69.2 ± 13.2 mg/100 g brain/min, whereas F₁ calculated by the Fourier method in the same subjects was 64.4 ± 13.5, indicating that APA can be effectively eliminated by the Fourier method.
The F₁ values calculated by the Fourier method from the frontal and temporal regions were relatively high, and closer to the F₁ values calculated by the VM method. The size of the APA was large in these regions. It was concluded that the deformed APA contaminated the results in these regions, and could not be eliminated effectively by the Fourier method. It is suggested that the shape of the head curve and the size of APA should be carefully examined to ensure that CBF data are reliable.

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The prognosis of thalamic hemorrhage was studied on the basis of neurological gradings on admission, mode of extension and hematoma size on brain CT. The subjects were 126 patients with thalamic hemorrhage who were admitted to Ashikaga Red Cross Hospital during the past ten years. Among the subjects, 120 patients (ages 64 ± 10 yr; mean ± SD) were treated with conservative therapy, and 6 patients (ages 59 ± 10 yr) with surgical therapy (ventricular drainage). Brain CT scans were done within 48 h. after onset in all patients. Neurological gradings, brain CT classification and prognosis were investigated according to the criteria of the Japanese Conference on Surgery for Cerebral Stroke.
The results of conservative therapy were as follows :
1) Neurological gradings on admission vs. prognosis : In the grade I group, 29 of the 39 patients (74%) recovered to full work or an independent life, and none of them died. In the grade IV and V groups, mortality rate was 86%.
2) CT classification vs. prognosis : The prognosis was more unfavorable in type III than in types I and II. Twenty-six of the 36 patients (73%) with type I-a recovered to full work or an independent life. Twenty-five of the 34 patients (74%) with the type III-bdied.
3) Hematoma volume vs. prognosis : Only 4 of the 75 patients (5%) with less than 10 ml of hematoma volume died. In contrast, all 14 patients with more than 25 ml of hematoma volume died.
4) Ventricular rupture vs. prognosis : The mortality rate among patients with ventricular rupture (47%) was significantly higher than that among patients without ventricular rupture (2%) (p<0.001).
5) Hydrocephalus vs. prognosis : The mortality rate of patients with acute hydrocephalus (83%) was significantly higher than that of patients without acute hydrocephalus (20%) (p<0.001).
From the above results, it is suggested that neurological grading, brain CT classification, hematoma volume, ventricular rupture and acute hydrocephalus are important prognostic factors for thalamic hemorrhage.

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The validity and indication of thromboendarterectomy for total carotid artery occlusion associated with neurologic deficits are still controversial. In this report, the two successful cases of thromboendarterectomy for total internal carotid artery occlusion performed in subacute stage after the onset were presented.
Case 1 was 67-year-old man who had the progressing symptoms of right hemiparesis and motor aphasia. He admitted on the eighth day after the onset and the left neck internal carotid artery occlusion with good intracranial collateral was revealed on angiogram. The surgical management was performed immediately, and the restration of blood flow was acquired after the thromboendarterectomy of severely advanced atheroma. Case 2 was 68-year-old man who had the right neck internal carotid artery occlusion causing progressing symptoms of left hemiparesis and dysarthria. The surgical management was performed after non-surgical treatment on the fifth day of the onset. The fresh intraluminal clots associated with the advanced atheroma obstructed the internal carotid artery. The blood flow was restored by the thromboendarterectomy of atheroma and embolectomy, and STA-MCA anastomosis was added. In both cases, no intra-and postoperative complications were observed and the clinical symptoms improved apparently after the surgery. The sufficient patencies were comfirmed on the following angiograms.

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A 69-year-old woman with mitral stenosis showing chronic atrial fibrillation abruptly began to present left hemiplegia and disturbances of consciousness. Computed tomography showed an extensive hypodense area in the territory of right middle cerebral artery. The patient was diagnosed as having experienced cerebral embolism of cardiac origin. Anticoagulation was started one month after the onset. However, on the sixteenth day of anticoagulation a large peduncular thrombus at the left atrial wall was found by two-dimensional echocardiography. Moreover, on the twenty-second day of the treatment a floating large ball thrombus measuring 20 mm in diameter and showing undulating motion with heart beats was found by echocardiography in the left atrium. An emergent thrombectomy was done on the same day. A ball thrombus of 24 mm in diameter and several fragments of wall thrombi at appendage were found in the left atrium at surgery. The result indicates that anticoagulation to patients with mitral stenosis showing chronic atrial fibrillation should be started carefully while examining the left atrial thrombi by means of two-dimensional echocardiography.

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We describe a 62-year-old male with four episodes of intracerebral hemorrhage. No other members of the family or close relatives had a similar bleeding tendency. Computed tomography and cerebral angiography were carried out but they were negative. Biopsy of the brain around the hematoma was carried out which revealed no brain tumor, arteriovenous malformation and no cerebral amyloid angiopathy. Coagulation tests such as bleeding time and prothrombin time were also negative, but quantitative analysis of coagulation factors revealed incomplete deficiency of factor XI and factor XIII. The value of factor XI and factor XIII were 50.4% and 40-70% respectively.Therefore repeated intracerebral hemorrhage may be caused by these factor deficiencies.
Computed tomography or cerebral angiography in patients with repeated non-traumatic intracerebral hemorrhage may uncover an underlying cause of disorder. But quantitative analysis of coagulation factors is also recommended in all patients with unexplained non-traumatic intracerebral hemorrhage.

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We report two elderly patients with putaminal hemorrhage possibly related to multiple angiographically occult intracranial vascular malformations (AOIVM) which were verified only with high-field magnetic resonance imaging (MRI).
Case 1. A 77-year-old woman was admitted to the hospital because of sudden onset of left hemiparesis on Day 2. Computed tomography (CT) exhibited a hyperdense area in the right putamen compatible with hypertensive putaminal hemorrhage, although she did not have a clear history or evidence of hypertension. Cerebral angiography demonstrated no abnormality.High-field MRI operating at 1.5 Tesla, however, revealed multiple small low intensity areas, combined with high-or isointensity signals, scattered in putamens, thalami, white matters, cerebellum of both sides and pons. Four months later she developed another intracerebral hematoma adjacent to the previous hematoma, although her blood pressure remained normal.
Case 2. A 66-year-old normotensive woman developed a massive hemorrhage in the right putamen. She did not have any possible cause of cerebral hemorrhage such as hypertension, hemorrhagic diathesis, etc. Cerebral angiogram showed a mass sign but no vascular abnormalities. MRI demonstrated multiple small low intensities with or without high-intensity spots in addition to a hematoma.
MRI findings of these patients were compatible with those of AOIVM reported in the literature. Although AOIVM has been diagnosed clinically with high-field MRI since 1986, it is not documented that multiple AOIVMs may cause ganglionic hematoma in the elderly patients. The present cases indicate that we should be aware of the presence of AOIVM as a cause of deep-seated cerebral hemorrhage even in the elderly. Clinical implications of AOIVM may be changed if patients with cerebral hemorrhage are more carefully investigated with high-field MRI.

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A 64-year-old female was admitted to our hospital due to progressive visual deterioration on the right eye. Computed tomography (CT) scan showed a slightly high dense mass in the suprasellar region with a homogeneous enhancement. Angiography revealed a giant aneurysm (4.5 × 3.8 × 3.5 cm) in the C1 portion of the right internal carotid artery. The ligation of the right common carotid artery was performed and the postoperative course was uneventful.
About five years later, she was readmitted because of memory disturbance. CT scan showed a marked enlargement of the previously demonstrated giant aneurysm with the evidence of partial thrombosis. Right retrograde brachial angiograms confirmed a collateral circulation between vertebral artery and carotid artery, in which there was the flow from the muscular branches of vertebral artery to the right occipital artery and then to the external and internal carotid artery. She was discharged without operation because her family refused any further attempts at treatment.
This case suggested that the giant aneurysm may enlarge even after the ligation of common carotid artery. Therefore, follow-up study is necessary for a long term, and if the aneurysm failed to be thrombosed the ligation or trapping of the internal carotid artery should be considered.

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We reported a case of 45-year-old man who presented a peculiar ocular sign “non-paralytic pontine exotropia” associated with MLF syndrome. He had a history of hypertension, and developed acute onset diplopia. On admission, severe left hemiparesis, dysarthria, right internuclear opthalmoplegia and left exotropia were noted. MRI taken 4 days after the onset showed right paramedian infarction located from ventral to dorsal portion of middle pons. Vertebral angiography demonstrated severe arteriosclerotic changes of the basilar artery.
Non-paralytic pontine exotropia is a rare ocular sign. We suggest that the posible lesion of non-paralytic pontine exotropia may be in a part of paramedian pontine reticular formation (PPRF) with ipsilateral medial longitudinal fasciculus (MLF) at the pontine tegmentum, and the lesion of non-paralytic pontine exotropia seems to be located in the area which causes the MLF syndrome and doesn't cause the one-and-a-half syndrome. And furthermore, we think that hemiparesis with non-paralytic pontine exotropia is the sign that ventral pons is affected, and the more severe hemiparesis is, the more caudal portion of pons, will be injured.

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We have recently encountered a case of pseudogout with high fever, which may be induced by cerebrovascular stroke. In the acute stage of cerebrovascular stroke associating with disturbance of consciousness and frequent fever, signs of the pseudogout are apt to be overlooked. Therefore, physicians should bear the following points in mind in order to obtain quickly accurate diagnosis of the pseudogout in the acute post-stroke period.
1) Attack of Pseudogout can be often induced by cerebrovascular stroke.
2) Pseudogout is frequently accompanied by fever.
3) Attack of the pseudogout usually subsides in a short period, but it sometimes persists for a long time.
4) In the acute stage of cerebrovascular stroke, symptoms such as arthralgia, etc., are frequently overlooked by disturbance of consciousness and dementia.

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