The purpose of the present study is to investigate the time course of the noradrenergic nervous function in patients with cerebrovascular disease (CVD) from the view point of circulating dopamine-β-hydroxylase (DβH).
Serum DβH activities were measured in 50 patients. Twenty seven patients had occlusive CVD which consited of 16 hemispheric and 11 brainstem infarctions. Hemorrhagic CVD consited of 18 intracerebral, 3 brainstem and 2 subarachnoid hemorrhages. Serum DβH activities were measured using the method by Nagatsu and Udenfriend.
The DβH activities in the patient with occlusive CVD slightly increased in the early stage and rapidly returned to the normal or subnormal value. On the other hand, in the patients with hemorrhagic CVD, DβH activities elavated higher immediately after the attack and decreased gradually with some fluctuations. The values of DβH activities in the patients with hemorrhagic CVD were higher than those in the patients with occlusive CVD in their entire course.
In occlusive CVD, the patients with a good recovery showed a mean value of 22.8±2.1 (mean±SE) unit. The patient who recovered enough to be able to sit by themselves showed a mean activity of 12.2±2.3 unit. The patients who remained bedridden showed a low activity of 7.4±2.9 unit. The mean value for the patients with good recovery was significatnly higher than that for the patients with poor prognosis (p<0.01). In hemorrhagic CVD, the patients with good recovery showed higher DβH activities (24.6±2.5 unit). In contrast, the patients who either expired or remained bed-ridden, revealed significantly lower DβH activities (10.2±2.2 unit) than those of the former (p<0.005).
The above data suggest that the noradrenergic nervous function was impaired in acute or subacute stage of cerebrovascular disease, and that the prognosis of the patients was grossly predictable from the value of DβH activities in acutestage.

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Two cases of an unilateral occlusion or stenosis of the ophthalmic artery with asymmetric diabetic retinopathy are reported.
Case 1, a 31-year-old female, has been diabetic for seven years and was admitted for her diminished visual acuity on the right. Diabetic retinopathy was severer on the right and the oculo-plethysmography (OPG) suggested an occlusion of the right internal carotid artery. Carotid angiograms did not show any occlusion of the internal carotid artery, but revealed severe stenosis of the right ophthalmic artery. She has no neurological symptoms and signs except for her diminished vision.
Case 2 was a male of fifty years old who was admitted for his right hemiparesis with nonfluent aphasia. He has been diabetic for twenty years and his left visual acuity has been diminished for these four years. His diabetic retinopathy was severer on the left and OPG suggested an occlusion of the left internal carotid artery. The carotid angiograms revealed the occlusion of both left middle cerebral and left ophthalmic artery, and not that of the internal carotid artery.
In both cases the diabetic retinopathy was severer on the same side as the ophthalmic arterial lesion, and it is suggested that circulatory disturbance of the ophthalmic artery may have an aggravating effect on the diabetic retinopathy.
The pathophysiology and the pathogenesis of the asymmetric diabetic retinopathy with unilateral ophthalmic artery occlusion are discussed.

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Three cases of primary thrombocythemia with cerebral thrombosis are reported.
Case 1 : A white-collar worker aged 53 was admitted to Shinshu University Hospital on October 4, 1978, because of cerebral thrombosis. He had a hitory of good health until 1975, when he began to have attacks of epigastralgia. He was not seen at hospital until May, 1976, when he was found to have hepatosplenomegaly. A blood test proved almost normal. A diagnosis of portal hypertension was considered most likely, and a splenectomy was carried out in July, 1976. Subsequently, successive blood tests always revealed thrombocythemia (range 1, 588, 000 to 2, 960, 000/mm³.), and he experienced recurrent transient ischemic attacks with dysarthria and numbness of the right hand. Two years later he developed cerebral thrombosis.
Case 2 : A farmer aged 55 was admitted to Shinshu University Hospital on July 10, 1976, because of cerebral thrombosis. He was in good health until 1975, when he began to have transient ischemic attacks with dysarthria and gait disturbance. Several months later he developed cerebral thrombosis with dysarthria, ataxia, right hemiparesis, and periodic disturbance of consciousness.
Case 3 : A seventy-six-year-old woman was admitted to Shinshu University Hospital on July 18, 1979, because of right hemiballismus. Prior to admission she experienced transient ischemic attacks of unconsciousness and vertigo on January 17, 1979. A month later she developed cerebral thrombosis and two months later right hemiballismus appeared.
Each patient had a prolonged history characterized by transient ischemic attacks and developed cerebral thrombosis thereafter. All three cases were found to have thrombocythemia (more than one million/mm³), and an increase of megakaryocytes in the bone marrow. There was no leukemic infiltration in bone marrow and the Philadelphia chromosome was absent in all patients. Each patient sufficed the diagnostic criteria of primary thrombocythemia. Their platlets showed decreased aggregation by ADP, epinephrine, and collagen, when they were diluted to 300, 000/mm³. Clinical symptoms, platelet function, and therapy of primary thrombocythemia are discussed in each case.

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1. Using the thalamic infarction model in dogs, 3 groups of animals with varying degrees of ischemia due to vascular occlusion were produced : severe ischemia (less than 40% of pre-occlusion levels), moderate ischemia (between 40% and 70% of pre-occlusion levels), and mild ischemia (greater than 70% of pre-occlusion levels). Temporary vascular occlusion was undertaken for 30 minutes, 1, 2, or 6 hours and changes in the CO₂ response at the center of the ischemic focus were measured during occlusion and for 4 hours of recirculation. The value of rCBF was measured by the hydrogen clearance method. The CO2 response was determined by PaCO₂ and rCBF measurements made during loading 5-10% CO₂ gas. The appearance of infarctic foci was investigated at autopsy.
2. In the animals with severe ischemia, the CO₂ response returned to normal following 30 minutes vascular occlusion, but in 8 of the 9 animals with 1 or more hours of occlusion, the CO₂ response was abnormal both during occlusion and recirculation. All 8 of these dogs showed infarctic foci.
3. Among the animals with moderate ischemia, many had abnormal CO₂ responses during occlusion but during recirculation there were some animals which recovered normal CO₂ responses and some which, did not. Among the 3 dogs which had abnormal CO₂ responses after 4 hours of recirculation, 2 showed histological signs of infarction and 4 of the 5 animals which maintained normal responses showed no signs of infarction.
4. Among the animals with mild ischemia, the CO₂ response was maintained in nearly all cases even during 6 hour vascular occlusion and recirculation. No infarction was found.

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In 1965, Fisher first reported the syndrome of pure sensory stroke (PSS) which involves face, arm and leg. In Japan, few clinical studies of this syndrome have been reported. We reported 8 cases which fitted the clinical syndrome of PSS and were studied by CT scan and sensory evoked potential (SEP) elicited by bilateral stimulation of the median nerve. All the patients had arterial hypertention. Two patients had diabetes mellitus, but no patient had atrial fibrillation. Stroke occured at rest in 6 cases and clinical signs progressed slowly over a few days. In 4 patients, the distribution of the dysesthetic and paresthetic sensations was in the entire side of the body, including the face, arm and leg, in the other 4 patients it was limited only the face and the distal portion of the extremity. CT scan revealed a small low density area in the lateral portion of the thalamus in 5 cases and in the posterior portion of the internal capsule in 3 cases. SEP study was done in 7 cases and revealed some abnormalities in all the cases. In the affected hemisphere, all the Ni, P2 and N2 waves were markedly reduced in 2 cases and one or more of these waves were absent in the other 5 cases.
These findings suggest that
1) PSS may be due to lacunar infarction of the lateral portion of the thalamus and/or sensory pathway through the internal capsule.
2) The thalamocortical fibers in the posterior limbs of the internal capsule at the supra-thalamic level was thought to be responsible for the occurence of the dysesthetic and paresthetic sensations.
3) SPE is a helpful diagnostic procedure in the patient with PSS.

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SLTA (Standard language test of aphasia), a battery of tests for speech impairments, has been widely used in Japan since 1974. The author analyzed SLTA profiles of 168 poststroke aphasic patients who were admitted to Nanasawa Hospital, Kanagawa Rihabilitation Center from 1975 to 1981.
Initial evaluations were obtained on admission (160 days, on the average, after the cerebrovascular accident) and reevaluations were obtained at discharge (192 days, on the average, after the admission). The employed statistical methods were multiple regression analysis and regression analysis with 3rd. order equation for each item.
In order to predict the recovery of patients based on the result of the 28 tests of SLTA on admission and the patients' background, multiple regression analysis with forward selection was performed. Considerably accurate prediction of the prognosis of speech impairments was obtained from three items of SLTA, together with patients' age and days after the onset of the disease, with a multiple correlation coefficient of 0.92.
According to the multiple regression analysis, the coefficients of patients' age and days after the onset of disease at admission were negative values, which suggested the recovery of speech was better as patients' age are young and as days after the onset of disease are short.

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The present report contains an unusual case with right mesial frontal lobe infarction, who demonstrated bilateral dressing apraxia.
A 71 year-old right handed man was admitted to our clinic because of inability of dressing. Sixteen days prior to ad-mission, he abruptly became unable to keep standing and fell down. According to his family's observation, he did not lose muscle power nor consciousness. Several hours later, he complained muscle weakness of the left side of the body, which reached to its maximum degree on the next day, and gradually improved thereafter. It was noted that, even after he became able to walk, he could not put on his clothes by himself, and that he was apt to disuse his left hand.
On admission, neurological examinations revealed characteristic symptom complex of motor neglect of the left upper limb and typical dressing apraxia, in addition to slight memory disturbances and diminution of initiative and spontaneity. He also showed left hemiparesis of mild degree but it was impossible to attribute dressing apraxia and motor, neglect to this mild hemiparesis. He did not show aphasia nor agnosia of any type and other deficits of integrative functions were not detected.
Routine laboratory studies were within normal limits. Computed tomograms of the brain on 6th day after onset revealed high density focus with surrounding low density area in the mesial side of the right superior frontal gyrus. Two weeks later, this lesion showed marked enhancement by contrast media. The diagnosis of hemorrhagic infarction was made.
Generally, dressing apraxia is considered to be a characteristic symptom of the parieto-temporo-occipital region of the non-dominant hemisphere, which embraces integrative functions concerning to recognition of the body schema, spatial relations as well as to praxis of constructional and/or ideomotor type.
Nowadays, though neuropsychological observations on the human frontal lobe are rather scanty, it has been suggested that one of deficits due to frontal lesion is dysintegration of the temporal ordering of events. Moreover, lesions of the left is said to produce an impairment on verbal tasks; lesion of the right, a deficits on nonverbal tasks.
Dressing apraxia observed in this case did not differ essentially from that in lesions of the parieto-temporo-occipital region. Thus, the present observation might be of significance, suggesting that the right mesial frontal lobe may play an important role in execution of dressing; a complex nonverbal task consisting of multifactorial argorithmic process. Several factors of this argorithmic process might be functions of the parieto-temporo-occipital region.

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Despite of common involvement of the carotid arteies cerebral infarction is relatively rare in aortic arch syndrome. Furthermore, amaurosis fugax as prodromal symptom of cerebral infarction in this syndrome has not been described. We reported a case of aortic arch syndrome with amaurosis fugax and cerebral infarction.
A 30-years old woman admitted with left hemiparesis. Two years before admission, she had experienced a transient blindness of righ eye during her second trimester of the pregnancy. Following the second attack of amaurosis fugax, left hemiparesis had suddenly developed in her puerperium. On admission, neurological examination revealed only mild left hemiparesis. The bruit was audible at the left supraclavicular fossa. The pulsation of the right common carotid artery and right radial artery were not palpable. Arch aortogram showed occlusions of the innominate artery and right common carotid artey with abundant collateral circulation. CT scan showed a well demarcated low density area in the right deep frontal region.
The cause of amaurosis fugax and cerebral infarction of this case is supposed to be embolism from the terminal portion of thrombus in the carotid artey.

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