Sheehan症候群を伴った無酸素脳症の1例

A CASE OF ANOXIC ENCEPHALOPATHY ASSOCIATED WITH SHEEHAN'S SYNDROME

I．はじめに

　酸化炭素やバルビツール酸誘導体による脳無酸素症が，そのselective vulnerabilityに特徴性をもつがゆえによく知られているのに対して，循環系の虚脱・ショックによるものは，Brierley^3）の総説的見解がありはするものの，そこでも意識障害の時期を免れて生存したものについての剖検例は少なく，定見的表現は避けられている。

　ここに報告する例は，分娩時の大量出血によつてショック状態となり，重篤な意識障害をきたし，その恢復後，1年余にわたつて生存し，この間に，いわゆるSheehan症候群を星したもので，循環障害性病変による脳酸素症の結果としての精神神経症状と内分泌障害による症状がみられ，脳病変の選択的侵襲部位の問題を考えるにあたり，重要な中枢神経系病理所見を示したものである。

The authors reported 32-year-old woman whosuffered from anoxic encephalopathy with endo-crinological disorders. The patient was attackedby gradually massive bleeding of the after-birth inher second birth. After three minutes cardiacarrest, she fell in the condition of severe un-consiousness. Several months later, she obtainedthe awake-sleep rythm pattern again but could notspeak and sometimes displayed negativistic attitudeand psychomotoric excitement. Meanwhile, shebegan to demonstrate dry skin, mamillar atrophy,amenorrhea, poliosis and baldness of axillar andpubic hairs. Laboratory findings revealed the dys-function of thyroid gland. With these symptomesand results, the authors guesses post-partumpituitary necrosis (Sheehan) and then administratedsteroid, decicated thyroid and neuroleptica. Butwith few change of clinical symptomes, she expired15 months after the onset of the complaints.

At necropsy, macroscopically, there were diffusecerebral atrophy, particularly great damage werebilateral middle-and inferior frontal gyri, superior-and middle temporal gyri, precuneus and lateraltemporooccipital gyri. The vertico-frontal sectionsshowed the moderate dilatation of ventricule andslight atrophy of caudate and putamen but globuspallidus was respected. There were no pathologicalfinding in thalamus, brainstem and cerebellum.Histopathologically, in cerebral cortex, diffuselaminar necrosis with spongy state and proliferationof small vessels and gemistocytic astroglias wereobserved. In Ammon's horn, there was slightly is-chemic change of nerve cell but in Sommer's sector,moderate loss of neuron and astrocytic proliferation.The caudate and putamen were only minor change.In globus pallidus, there were neither hemorragic nornecrotic foci. Thalamus, hypothalamus, brain stemwere intact. Cerebellum did not show remarkablechange. In white matter, variable diffuse pallorof myelin staining were seen. In hypophysis, macro-scopically, severe atrophy was ascertained andhistologically, it had diffuse fibrosis with partiallysmall hemorragic patch in the anterior lobe celland interstitial proliferation, but posterior lobe waswell concerved.

About the finding above mentioned, the authorsdiscussed the following points: Though there are many reports concerning toanoxic encephalopathy caused by anoxic poison,neuropathological observation of anoxic encephalo-pathy by hemodynamic disturbance were few justlike this which showed selective vulnerability ofacute circulatory shock that were observed inseveral cases by Brierley. But it is of interestthat there was no pathological change in globuspallidus in this case.

As for post-partum pituitary necrosis (Sheehan),the clinical course was confirmed by the necropsy.Although psychic disorder observed in the case ofSheehan's syndrome were, in general, almost mild,some symptomes of this case let be fluctuated bydosage of medicaments. It would be possible thatthe neuropsychiatric disorder of this case are ex-plained under the spect of influence of anoxicencephalopathy and endocrinological dysfunction.