The purpose of this paper is to describe the pattern of arteries supplying the spinal cord in the cat and to present the results of experimental occlusion of certain tributaries of the ventral spinal artery.Despite the extensive use of the cat in neurological research, surprisingly little has been written about the circulation through the spinal cord in this animal and the original description by Tauber and Langworthy (1935) made no mention of the relative size or importance of the various segmental anastomoses. Subsequent studies in man by Suh and Alexander (1939), in the monkey by Yoss (1950), and in the rat by Woollam and Millen (1955)
Vascular accidents involving the spinal cord, in contrast to the brain, are extremely rare. Damage to the spinal cord from verified emboli seems to be an even greater rarity and no examples were found by Blackwood (1958) in a series of 3,737 postmortem reports from the National Hospital, Queen Square, London. Embolic myelomalacia has been reported in bacterial endocarditis and other forms of heart disease such as mitral stenosis and coronary occlusion. When caisson disease and air embolism are excluded, the paucity of the literature on the subject indicates that spinal embolism is very uncommon, and in some reports confirmation of the emboli and the site of their impaction has been lacking. The purpose of this paper is to record two further examples of the syndrome and to present details of the nature and origin of the emboli and the lesions produced. CASE REPORTS CASE 1 T.D., a man aged 59, early in March, 1966, noticed progressive weakness first of the right and, a few days later, of the left lower limb. The disability was slight until six weeks later when he awoke with paralysis of both lower limbs and numbness up to the waist. The following morning he was unable to pass urine. He had suffered from a cough dating from bronchitis 20 years previously but otherwise the past and family histories contributed nothing. On May 2, he was admitted to hospital elsewhere and transferred to the neurological department on 26 May 1966.On examination the spine, cranial nerves, and special senses were intact. Inconspicuous but coarse fasciculation was observed over the shoulder girdles and arms, but the upper limbs were otherwise normal. There was flaccid paralysis of both lower limbs. The deep tendon reflexes were normal in the upper and depressed in the lower limbs, the abdominal responses were absent and both plantars were extensor. Vibration sense was absent below and including the pelvis and joint position sense was absent in the toes and defective in the ankles. There was a cutaneous sensory impairment to pin prick, temperature and touch below the second dorsal segment and including the sacral area on both sides. There was retention of urine which necessitated the use of an indwelling catheter and numerous deep pressure sores over the sacrum, buttocks, and legs. General examination was unremarkable and the blood pressure was 190/90 mm. Hg.A plain radiograph of the chest revealed evidence of an old right basal pleurisy. Radiographs of cervical and dorsal spines were normal. A full blood count was normal but the erythrocyte sedimentation rate (E.S.R.) was 50 mm./hr. The lumbar cerebrospinal fluid pressure and manometric observations were normal and the fluid contained no white cells, 7 red cells/c.mm., protein 35 mg./100 ml.; Lange no change. The Wassermann reaction (W.R.) was negative in the blood and cerebrospinal fluid. A myelogram showed no abnormality between the lumbar sac and the foramen magnum.In view of the negative results of investigation, it was thought that the patient was probably suffering from the effects ...
SYNOPSIS The clinical features of 49 patients who had sustained small strokes in the internal carotid artery territory, who were normotensive, free from cardiac or other relevant disease, and who each had a normal appropriate single vessel angiogram are presented. These were randomized into two groups: group A, 25 patients, who received only supportive treatment; group B, 24 patients, who were treated with anticoagulants for an average period of 18 months. There was a reduced incidence of neurological episodes during the administration of anticoagulant therapy but, after treatment was discontinued, there was no significant difference between the two groups. In view of the relatively benign prognosis for this syndrome, unless special facilities exist for the personal control of anticoagulant treatment, the dangers may outweigh the benefits.In a previous study of small strokes in the territory of the internal carotid artery, Bradshaw and Gumpert (1972) reported that appropriate single vessel angiography was normal in 50 of 69 consecutive patients. Thirty-five of the 50 who had normal arteriograms were normotensive and, when followed up for between six months and six years, it was found that three patients had died of related disease, three had been disabled by further stroke, and 29 were normal. Further, it was noted that all nine patients who had received long-term anticoagulant treatment had remained well. However, the benign nature of the syndrome and the paucity of patients treated with anticoagulants made evaluation of such treatment impossible. This paper is an extension of the previous study and presents a series of patients who had sustained small strokes in the internal carotid territory, were normotensive, without evidence of any cardiac source of emboli, and who had normal appropriate single vessel angiography. Twenty-four of these were treated with anticoagulant therapy and 25 received only supportive treatment.
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