[in Japanese]

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The plasma dopamine (DA) level has scarcely been investigated in acute cerebrovascular diseases (CVD), although sympathetic hyperactivity has been well demonstrated. We measured the plasma DA and norepinephrine in acute CVD, and examined whether or not the plasma DA level had any significant relationship to sympathetic nervous function or clinical prognosis in acute CVD. The subjects comprised 12 patients (74 ± 11 yo, mean ± SD) with intracerebral hemorrhage (ICH) and 18 (63 ± 9 yo) with cerebral infarction (CI) within 3 days after onset. Healthy controls adjusted for age to each group were also included in the study (25 for ICH and 36 for CI). Based on observations for 3 months, the patients were divided into two groups : surviving and non-surviving groups. The numbers in the surviving and non-surving groups were, respectively, 7 and 5 cases in the ICH group, and 5 and 13 cases in the CI group.
(1) Plasma catecholamines : The DA level in acute ICH was significantly higher compared to that in the control (52 ± 18 pg/ml vs. 10 ± 1; mean ± SE, p <0.005). The DA level in acute CI was also higher than that in the control (22.0 ± 6.9 vs, 9.7 ± 0.9, p < 0.05). The NE level in acute ICH was higher compared to that in the control (1240 ± 252 vs. 337 ± 31, p <0.0005). The NE level in acute CI was higher than that in the control (570 ± 126 vs. 327 ± 24, p <0.05).
(2) DA vs. norepinephrine : The relationship between the DA and norepinephrine levels displayed significantly positive correlations in both ICH (r = 0.905, p =0.0001) and CI (r = 0.868, p =0.0001).
(3) DA vs. clinical prognosis : Among patients with ICH, the plasma DA level tended to be lower in the surviving group (28 ± 9) as compared to the non-surviving group (86 ± 38). Among patients with CI, the DA level was significantly lower in the surviving group (12 ± 3) than in the non-surviving group (49 ± 20) (p < 0.05).
In conclusion, the above data indicate that an increased plasma DA in acute CVD is a parameter of sympathetic nervous function and may be useful for predicting the clinical prognosis in acute CVD.

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Computed tomography performed in conjunction with 39% stable xenon inhalation was used to evaluate regional differences in the autoregulation of cerebral blood flow (CBF). Ten monkeys (Macaca fuscata) of both sexes, weighing 5.5-9.0 kg, were used in the study. The local CBF was measured for 17 regions of interest (ROI) in the steady state and during hypotension induced by exsanguination. The 17 ROIs were divided into four groups. The steady-state CBF values in these groups were 90.8 ± 41.2 in the cerebral basal ganglia, 96.8 ± 35.1 in the cerebral cortex, 56.6 ± 21.1 in the cerebral white matter, and 50.0 ± 19.3 in the cerebellar hemisphere (ml/100 g brain/min, mean ± SD). Arterial blood gases and the hematocrit were determined concomitantly.
Cerebral autoregulation during hypotension induced by exsanguination was evaluated in terms of the mean autoregulation index [CBF mean (MABP 90-130 mmHg) -CBF₅₀ (MABP₅₀ mmHg) /CBF mean]. It was found that there was no statistically significant difference in the autoregulation of CBF among the cerebral basal ganglia, the cerebral cortex, the cerebral white matter and the cerebellar hemisphere.

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The usefulness of somatosensory avoked potential (SEP) recording and thermography for evaluating the symptoms and signs caused by thalamic hemorrhage was investigated in 32 patients. Most patients complained of sensory numbness (21) and coldness (8) of the impaired extremities, and few complained of warmth (3) or pain (4). Clinical signs of superficial sensory disturbance were observed in 19 patients, deep sensory disturbance in 14, and hemiparesis in 25. Computed tomography demonstrated that the thalamic hemorrhages were of the type located in the lateral nucleus in 21 patients of that in the medial nucleus in 4 and of the mixed type in 7. SEP recording revealed that 16 of 21 patients with numbness, 6 of 8 with coldness, 9 of 11 with severe superficial sensory disturbance, and 6 of 7 with severe deep sensory disturbance had either absence or prolonged latency of the N20 wave. Thermography demonstrated an abnormally high or low skin temperature on the impaired extremities as compared with the uninvolved side in 14 of 21 patients with numbness, 9 of 11 with severe superficial sensory disturbance, 7 of 7 with severe deep sensory disturbance. 18 of 25 with hemiparesis, and 12 of 14 with large hematoma. Thirteen of 20 patients with SEP abnormality had abnormal skin temperatures on their thermograms. Severe superficial and deep sensory disturbance was correlated with an abnormal SEP and thermography findings in patients with lateral nucleus hemorrhage. SEP recording is considered useful for the evaluation of severe clinical sensory disturbance, and thermography for investigating severe subjective and clinical sensory disturbances.

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We examined the clinical and pathophysiological features of “multiple simultaneous intracerebral hemorrhages” in 73 patients, comprising 8 of our patients and 65 previously reported patients. We defined “multiple simultaneous intracerebral hemorrhages” as more than two hemorrhages in the initial cranial CT scan taken within 24 hours after onset. In the 73 patients, we investigated the clinical courses and presented manifestations, as follows : 1) age, 2) sex, 3) consciousness on admission, 4) blood pressure on admission, 5) location of hematoma on CT, 6) size of hematoma on CT, 7) leukoaraiosis on CT (using the classification of Aharon-Peretz et al.) and MRI using the classification of Gerard et al., 8) risk factors for stroke, 9) treatment, 10) outcome, and 11) pathological findings.
For some features, the results of the present study were not consistent with previous research, as follows :
1) Leukoaraiosis on CT and MRI was revealed in 80%, and might be correlated with the pathophysiology of “multiple simultaneous intracerebral hemorrhages”.
2) Hypertension could be the most frequent cause, although amyloid angiopathy may, unexpectedly, be less frequent.
These results probably reflect the current trends in the clinical pictures of “multiple simultaneous intracerebral hemorrhages”.

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We examined the amnesic symptoms including confabulation in 49 patients with ruptured anterior communicating artery aneurysm after operation. We studied the clinical and radiological findings of these patients before and after the operation. Amnesic symptoms developed more frequently in cases with severe neurological deficit due to subarachnoid hemorrhage and upward projection of the aneurysm. The CT findings after the operation revealed that focal cerebral damage involving basal forebrain lesion produced amnesic symptoms, and confabulation arose from more broad brain damage. In 8 patients, detailed neuropsychological investigations were performed. As a result, all patients with confabulat : on were found to show some memory disturbance, although the degree of memory disturbance was not correlated with the appearance of confabulation.

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Bilateral symmetrical pontine hyperintensities (PHI) on MRI are occasionally observed in the elderly. Pullicino et al. reported that a Binswanger's disease-like pathology was presented in this lesion, and concluded that this was the cause of the PHI. They designated the lesion as pontine ischemic rarefaction (PIR). To clarify the clinical meaning of PIR, we investigated the risk factors of PHI and examined the correlation between PHI and supratentorial changes. We selected 86 subjects with PHI by 0.5-tesla MRI over the period from March 1995 to February 1996. Wallerian degeneration and PHI combined with pontine hemorrhage were excluded. Patients with hyponatremia and alcoholism were also excluded. We classified the PHI into 3 groups : bilateral symmetrical (BS) (N=42), unilateral (U) (N=20), and bilateral asymmetrical (BA) (N=24). We compared the supratentorial changes among them (Kruskal-Wallis test, and chi-square test). The supratenotorial changes consisted of cerebral hyperintense signal abnormalities, cortical atrophy and ventricular dilatation.
We examinated the contribution of arteriosclerotic risk factors (age, sex, diabetes mellitus, hypertension, and hyperlipidemia) to each group (multiple logistic test). The severity of periventricular hyperintensity (PVH) was different among the groups (Kruskal-Wallis test, p = 0.023), and it was higher in group BS than in group U (Scheffe's test, p < 0.05). In group BS, the age of the subjects was higher (mean ± SD, 79.6 ± 8.2) and the ratio of hypertensive patients was lower than in the others (p <0.05). There were no risk factors to discriminate group BA from the others. Through comparison among the pontine hyperintensities, group U can be said to represent infarction because of the laterality and correlation to arteriosclerotic risk factors. PIR (group BS) was noted in higher aged and less hypertensive subjects and had a correlation with PVH.

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We carried out endovascular surgery for the treatment of 50 cavernous dural arteriovenous fistulas (CdAVF). Transarterial embolization with alcohol, glucose and/or polyvinyl alcohol (PVA) particles was successfully performed in 8 of 10 cases with mild arteriovenous shunt flow. Transvenous embolization with copper wires, a segmented guide wire and/or platinum microcoils was successfully performed in 36 of 39 cases. Generally, transvenous approaches via an anterior route (angular vein to SOV), medial route (intercavernous sinus) and posterior route (jugular vein to IPS) made the embolization of the CdAVF successful. Although only fistulas should be occluded, a part or all of the cavernous sinus including fistulas is usually packed with coils. In the case of stenotic or occlusive IPS, multi-stage embolization should be avoided because a relatively increased venous flow after incomplete embolization of the fistulas and occlusion of abnormal draining routes such as the SOV and sphenoparietal sinus may cause venous infarction or hemorrhagic infarction in the posterior fossa. Thus, embolization for CdAVF can be performed safely and perfectly, if an appropriate strategy of occlusion is selected for each patient.

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The roles of remaining blood in the convexity following subarachnoid hemorrhage (SAH) in the mechanism of delayed cerebral vasospasm (VS) and normal pressure hydrocephalus (NPH) were analyzed in 83 patients with aneurysmal SAH. Examinations by X-ray computed tomography (X-CT) were performed 5 times (on admission, postoperatively, and at 1, 2, and 4 weeks after the onset), and the severity of the remaining SAH in the convexity was classified into 4 groups according to the X-CT findings. The remaining SAH decreased significantly with the time course. However, in elderly patients, exclusion of SAH was delayed and the grade was significantly worse than in the younger patients. Delayed exclusion of SAH was also observed in patients with VS and with NPH. This suggests that remaining SAH in the convexity may be involved in the mechanism of VS and NPH. Furthermore, exclusion of the SAH might be influenced by the age of the patient.

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The present study examined the clinical features of 41 stroke patients (mean age, 68.0 ± 9.1 years) with pulmonary embolism (PE). Lung scintigraphy or autopsy was performed in order to diagnose PE. The primary diagnosis was cerebral infarction in 28 patients, cerebral hemorrhage in 10, and subarachnoid hemorrhage in 3. The most frequent symptoms in the 41 patients were dyspnea, hypotension, tachypnea, tachycardia, and chest pain. Clinical examinations revealed that hypoxemia was accompanied by a low partial pressure of carbon dioside in the arterial blood (PaCO₂) and that the serum lactic dehydrogenase activity (LDH) tended to increase gradually before PE, reaching a peak within 2 weeks after PE. The strongest risk factors associated with PE were a bedridden state due to disturbance of consciousness and motor paresis, and heart disease. Atrial fibrillation was observed in 17 of 29 patients with heart disease. The mortality rate was 39% among the PE patients. Twenty-one patients received thrombolytic therapy with urokinase and/or anticoagulant therapy with heparin and/or warfarin.
Fourteen of the 21 patients survived, and the efficacy of the above therapies was thus 67%. Early detection of PE requires close scrutiny of the clinical symptoms and an analysis of the arterial blood gases in addition to the use of lung scintigraphy or other methods. In order to prevent PE, stasis in the leg veins must be decreased by early rehabilitation after the stroke as well as leg elevation and the use of elastic stockings during the acute stage because a bedridden state may easily cause stasis in the leg veins, and thrombi may be formed soon after the stroke, Management of heart function is also important for stroke patients with heart disease in order to prevent PE. The LDH changes seen in most PE patients suggest that LDH activity could provide an indicator for the risk of PE.

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The clinical features of intracranial hemorrhage were studied retrospectively in 645 cases of chronic renal failure with or without dialysis therapy admitted during the period, 1988 to 1994.
(1) Incidence : Cerebral hemorrhage occurred in 16 of 457 cases undergoing chronic intermittent dialysis (3.50%) and in 5 of 188 cases receiving conservative therapy (2.66%). (2) Risk factors and site of hemorrhage : All 21 cases of cerebral hemorrhage were statistically significant hypertensive (p <0.01) as compared to 574 cases of age-matched non-bleeders with chronic renal failure. The most common site of hemorrhage was the putamen, internal capsule and thalamus (13 cases) followed by the brain stem and cerebellum (6 cases) and occipital regions (2 cases). Among the cases of supratentorial cerebral hemorrhage, 4 manifested intraventricular hemorrhage and 3 died (75%). (3) Mode of dialysis : Among the 21 cases of cerebral hemorrhage, 13 were under chronic intermittent hemodialysis and 3 were under peritoneal dialysis (CAPD). Five cases were on conservative therapy. (4) Mortality : The overall mortality in cerebral hemorrhage was 9/12 (43%), comprising 8 on hemodialysis and 1 on CAPD. It is worthy of note that the mortality for brain stem and cerebellar hemorrhage was 4 out of 6 (66.7%). (5) Other details : Subarachnoid hemorrhage was found in 1 case and was successfully treated surgically. Subdural hematoma was noted in 5 cases, and 1 died. Conclusion : Intracebral hemorrhage was found in 21 of 645 cases with chronic renal failure. These 21 with intracerebral hemorrhage showed the highest mortality (43%) as a direct cause of death. In comparison with our previously reported series of autopsy-proven cases in 1976 and 1985, a tendency towards a decrease in mortality was noted, while there was a definite increase in brain stem hemorrhage. Of the risk factors hypertension and coagulation abnormalities involving the prothrombin time and thrombo test (p < 0.05) were factors of significance.

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The clinical characteristics of ischemic cerebrovascular disease as a complication of chronic renal failure (CRF) were investigated. The materials consisted of 645 cases of CRF admitted to our service, among which 49 cases of cerebral infarct (CI) were found (7.6%).
These cases were subdivided into three groups : (1) 15 out of 293 hemodialysis patients (5.1%) [HD], (2) 7 out of 148 patients on peritoneal dialysis (4.7%) [PD], and (3) 27 out of 204 patients on conservative therapy (13.2%) [non-D]. As regards the underlying diseases, diabetic nephropathy ranked second after chronic glomerulonephritis. In the HD group, the incidence of hemiparesis was significantly lower as an initial symptom. On cranial CT and MRI examination, a higher incidence of lacunar infarct was noted. Concerning complications, the incidences of ischemic heart disease and diabetes mellitus were significantly high. An analysis of the respective parameters revealed that the hematocrit value was significantly lower in the HD group. CI as a complication of CRF was observed at a higher incidence in the non-D group, and especially in those with risk factors of diabetes mellitus, ischemic heart diseases, advanced age (i.e. elderly) and hypertension. It is worthy of note that main truncal artery occlusion as a cause of direct death was rather rare in CI of CRF. The fact that there was a higher incidence of lacunar infarct, especially in the HD group, suggests a possible relation to a lower hematocrit value and complication with diabetes. Further studies are needed to clarify the relationship between use of erythropoetin and hematocrit value in the etiology of ischemic cerebrovascular diseases.

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A 30-year-old woman, on hMG-hCG therapy for sterility, was referred to our hospital because of sudden onset of confusion and left hemiplegia. Her family members reported that abdominal distension and oliguria had appeared several days before. She was mute and restless, with concurrent enlarged ovaries and ascites. MRI revealed an extensive infarction in the territory of the right middle cerebral artery (MCA) and an infarction in the left temporal cortex. MR angiography (MRA) performed at 57 days after the onset demonstrated a patent MR portion and an occluded M2 portion in the right MCA. On admission, thrombin-antithrombin III complexes and D-dimer were increased. The sudden onset of symptoms and MRA findings suggested embolic infarction, probably caused by hypercoagulability due to ovarian hyperstimulation syndrome.

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