脳のMR画像上の微小病変の臨床的意義は不明である.私たちは径15mm以下の梗塞巣以外の局在病変を含まない390例を検討した.部位別に,径3mm以下の均質で境界鮮明な周囲に変化のない微小病変と,血管疾患の危険因子との関連を分析した.さらに微小病変と脳梗塞の発症との関連を調査した.微小病変は前有孔質,基底核,皮質下白質に多かった.基底核の微小病変は年齢と高血圧,皮質下白質の微小病変,特にT1WI低信号,T2WI高信号の病変は高血圧,空腹時血糖値と関連があったが,前有孔質では関連がなかった.脳梗塞は29例に発症した.基底核上部のT1WI低信号,T2WI高信号,proton/FLAIR低信号の多発例からの脳梗塞発症が多かった.[結論]前有孔質の微小病変の臨床的意義は小さいが,基底核上部の微小病変は血管性危険因子と関連し,その多発は脳梗塞再発の予知因子となる.

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analysis in 96 multi-infarct patients without dementia and 40 multi-infarct patients with dementia (MID). Only subjects with small infarcts in the territory of the perforator artery or deep white matter were studied. The diagnosis of MID was diagnosed according to DMS-III criteria and Hachinski's ischemia score. Location and area of patchy high-intensity areas including small infarcts, the degree of periventricular high intensity (PVH), and the degree of brain atrophy were examined with MR images. Independent variables were: history of hypertension, diabetes mellitus, other complications; systolic and diastolic blood pressure, atherosclerotic index, hematocrit, history of smoking, level of education, and activities of daily life (ADL). Hayashi's quantification method II was used to analyze the data.
The most significant correlation was found between history of hypertension and dementia (partial correlation coefficient: 0.39). Significant correlations were also found between ADL and dementia (0.32), between thalamic infarction and dementia (0.31), and between PVH and dementia (0.27). Age, brain atrophy index, and history of diabetes mellitus contributed little to dementia. The contribution to dementia did not differ significantly between right and left patchy high-intensity areas on MR images.
Location of infarcts, except for bilateral thalamic infarcts and large PVH, contributed little to dementia. Thus it would be difficult to base a prediction of the prevalence of vascular dementia on MRI findings. However, both hypertention and ADL contribute to vascular dementia and both are treatable, which may be significant for the prevention of dementia.

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無症候性脳梗塞患者の非特異的自覚症状に注目, 脳循環所見を軸とした検討を行った.対象はMRIにて穿通枝領域に病巣を認めた, 無症候性脳梗塞例73例および症候性脳梗塞例80例, 非回転性めまい/四肢しびれ感/頭痛・頭重感等の非特異的自覚症状を主訴とする不定愁訴患者22例とした.脳血流量の測定は¹²³IMP SPECT-ARG法を用いた.無症候性脳梗塞例の52%が, 非特異的自覚症状を有していた.無症候性脳梗塞自覚症状群の脳血流量は, 不定愁訴例と比較して有意な低値を示したが, 症候性脳梗塞例とは有意差を示さなかった.高血圧を有する無症候性脳梗塞自覚症状群の前頭葉, 側頭葉領域の脳血流量は, 高血圧を有さない無症候性脳梗塞非自覚症状群と比較して有意な低値を示した.以上は, 無症候性脳梗塞患者に対して, 自覚症状の有無と高血圧の存在を考慮に入れた臨床的対応をする必要性を示す結果である.

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多発性脳梗塞例 (著明なPVHを有するPVH (+) 群17例, PVHのないPVH (-) 群16例) を対象とし, ¹⁵O, ¹¹CO吸入法を用いたPETにより, PVHの存在と, 虚血および痴呆との関係について脳循環代謝面から検討した.
PVH (+) 群におけるCBFの低下とOEFの上昇は非痴呆例におけるPVH領域, 前頭葉帯状回領域ですでに認められ, 痴呆例ではPVH領域, 皮質各領域におけるCBFの低下と, PVH領域および前頭葉を中心としたCMRO₂の低下, OEFの上昇を認めた.その変化はPVH領域に最も著しかった.またPVH (+) 群, 特にPVH領域のCBVおよびCBF/CBVは低値を示した.
以上は多発性脳梗塞例におけるPVHの存在が, 同部位および皮質領域を含めた広範な脳動脈硬化性変化に由来する, 脳組織低灌流状態の存在を反映することを意味している.さらに持続する低灌流状態は脳組織に虚血性変化をもたらし, 結果として脳神経機能を低下, 痴呆発現を助長するという機序を示唆する結果であると考えられる.

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In this study, vascular dementia (VD, 31 cases), senile dementia of Alzheimer type (DAT, 36 cases) and mixed type dementia (14 cases) were studied by means of magnetic resonance imaging (MRI). Diagnosis of dementia was made according to DSM-III and Hachinski's ischemic score. The areas of periventricular high intensity lesions (PVH) and those of brain parenphyma were measured by digitizer which was connected to a computer.
The PVH score was obtained by dividing the areas of PVH by those of brain parenchyma at the level of the body of the lateral ventricule. A multiple variable analysis was applied to the PVH scores and risk factors for dementia using Hayashi's quantification method I.
The multiple correlation coefficient between the PVH and the risk factors was 0.685. The most significant correlation was found between Hachinski's ischemic score and the PVH score (partial correlation coefficient: 0.58). Significant correlations were also found between ADL and the PVH score (0.25), as well as between the Hasegawa dementia score and the PVH score (0.24). Using the student T test, it was shown that the large PVH group was significantly correlated to poor ADL, whereas the small PVH group was not. The large PVH group in VD showed lower Hasegawa score than the small PVH group. On the other hand, there was no such correlation in DAT.
PVH with prolongation of T2 could exist in various pathological states irrespective of their causes. Diffuse PVH tended to be frequently observed in VD together with poor ADL. It was therefore thought that brain ischemia was the main cause of PVH.

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