PAPERS READ AT THE 1964 SCIENTIFIC MEETING 207 ROMANES, G. J. (Scotland) thought the answer to that was Yes. The grey matter was much more vascular in capillary veins than the white matter. WOLMAN, L. (England) said he was particularly interested in the difference between anterior and posterior horns, where they had the concentration of nerve cells. Did the capillary network correlate with the increased number of nerve cells? Was there any difference? ROMANES, G. J. (Scotland) replied that if one took the actual density of nerve cells the density would be in the anterior horn, in areas where there were big motor cells taking up a great deal of room. In the posterior horn the density of nerve cells was quite high. If one counted these they were higher in the posterior horn in the intermediate region than they were in the lateral part of the anterior horn in the lumbar enlargement. What was interesting was the fact that the tip of the posterior horn was supplied from the posterior spinal vessels, while one had the remainder of the grey matter supplied from the perforating branches of the anterior spinal artery but, where they joined, there was no evidence of junction; there must be anastomosis of capillary fields, because there was no break that one could see, and yet on injecting one vessel one filled one territory and on injecting the other one filled another territory. WOLMAN, L. (England). It looked the same in both anterior and posterior horn? ROMANES, G. J. (Scotland). Agreed. He had not done actual measurements of density. Horn Cragie had done quite a lot of this at one time, measuring the lengths of capillaries in a given volume of grey and white matter, but as far as he could recall the figures did not seem to show any difference. THE PATHOLOGY OF VASCULAR DISORDERS OF THE SPINAL CORD TREVOR HUGHES, M.D. By J. The Radcliffe Infirmary, Oxford THE spinal cord has one of the most complex blood supplies of any part of the body and it is necessary to understand some of its complexity before turning to the problem of its vascular disorders. At this meeting we have been fortunate in hear­ ing Professor Romanes' excellent account of the anatomy of the spinal cord vascular supply. Reflecting on the complicated pattern of blood supply I should like to pick out the features that have a special importance in the pathology of vascular disorders of the spinal cord: The multiplicity of feeding sources into the spinal arterial system. This I. forms a powerful reserve of arterial supply immune except to interruption at specially vulnerable places. 2. The dependence on a moderate number of tributary arteries of inconstant position and which are relatively so large that the other tributaries may be interrupted with impunity. The strict division into anterior and posterior spinal artery territories which 3. supply two-thirds and one-third of the cross-sectional area respectively. The absence of significant anastomosis between anterior and posterior 4. spinal artery circumferentially around the cord. (But the anterior spinal PARAPLEGIA 208 artery does make a good anastomosis with the posterior spinal arteries around the Cauda equina.) The overwhelming importance in the whole system of the single anterior 5. spinal artery. The reserve of venous drainage so that venous obstruction rarely damages 6. the spinal cord. The possible sites of obstruction to the vascular supply of the spinal cord may be grouped under seven headings. In group we have the aorta to which the sub­ clavian artery is added. The internal iliacs couldI be included but in this context are of no importance. Group 2 consists of the vertebral arteries whose peculiar anatomical situation merits separate consideration. In group are the paired aortic 3 branches such as the intercostals and the lumbar arteries and in group are the 4 radicular tributaries to the anterior and posterior spinal arteries, these tributaries accompanying the nerve roots through the intervertebral foramina. Group 5 comprises the anterior and posterior spinal arteries, and group 6 all the small spinal arteries arising from the anterior and posterior spinal arteries. In group 7 are the veins of the spinal cord. TABLE Vascular Disorders of the Spinal Cord (Analysis of 28 necropsies selected from a 2o-year period) 1----- Number Site of Lesion Cause I � a:��_ __ f C ' 1 I __ I '- --------- - -;�A�rta I Atheroma . 3 (5 cases) Dissecting aneurysm 1 I Trauma 1 I 2 Vertebrals Trauma 2 1 . (2 cases) Intercostals Thoraco-Iumbar sympathectomy 1 3· I (I case) 8 I 4. Radicular tributaries Malignant infiltration . I (10 cases) Tuberculosis (Psoas abscess) . 1 I ! I Herpes Zoster I I 5· Anterior spinal artery Thrombosis (Idiopathic) I I, (4 cases) Thrombosis (Cervical Spondylosis) I 2I Ischaemia (Cervical Spondylosis) I Small spinal arteries Tuberculosis meningitis 3 6. (4 cases) Syphilis (Erb's) . I Veins Foix-Alajouanine disease 2I 7. (2 cases) I I Total. 28 _____L ----�--- --� The series of cases that I now wish to present to you has been gathered from the material of our neuropathology department at Oxford and comprises 28 necropsied cases drawn from a twenty-year period. The table shows these 28 cases divided into the groups that I have enumerated. I propose to deal with each group in turn but have selected one case from each group for detailed description. PAPERS READ AT THE 1964 SCIENTIFIC MEETING 209 Group Aortic Cases. Aortic atheroma is very common, but it is rare for the clinical workerI. to attribute spinal cord ischaemia to this cause. In three cases severe aortic atheroma had caused ischaemic areas in the spinal cord, the clinical course being an ill-defined chronic paraparesis. The commonest aortic cause of acute spinal cord ischaemia is probably dissecting aneurysm, in which the dissection of the tunica media by a haematoma compresses the origins of the intercostal or lumbar arteries. In these cases the clinical signs of neurological involvement are often slight and scrutiny of the spinal cord shows only trivial findings. But when an important intercostal or lumbar artery is blocked extensive spinal cord infarction can occur. The case I now wish to describe was most unusual in being caused by aortic trauma. It has been described in more detail elsewhere (Hughes, 1964a). A 62-year-old housewife crashed her car into a shop, sufferinginjuries to herCase chest Report. and a lacerated chin. Although momentarily unconscious she was able to walk away from her car and an ambulance took her to hospital. On admission she was found to have fractures of the 2nd, 3rd and 4th ribs anteriorly with a progressive left haemothorax necessitating a thoracotomy the following day. Removal of two litres of blood from the left hemithorax disclosed a 2·s-cm. tear in the pleura over the aorta just above the diaphragm, and extensive mediastinal bruising. With massive blood trans­ fusion her general condition was restored but on the 4th post-operative day impaired movement of the legs was noticed and a full neurological examination the following morn­ ing showed complete paralysis of the legs and absence of all sensation up to the level of T3. Plain X-rays of the spine showed no fracture and a myelogram did not demonstrate any evidence of spinal block. On the 6th post-operative day the patient's blood pressure suddenly collapsed and IS minutes later she died. At necropsy the thoracic aorta showed a transverse intimal tear almost encircling the aorta at a level 4 cm. below the origin of the left subclavian artery. The tear was plugged with thrombus continous with a large mural haematoma in the damaged tunica media and adventitia. At their origin the 2nd, 3rd, 4th and Sth intercostal arteries were surrounded and compressed by the mural haematoma. The spinal cord showed extensive infarction from T3 to T7 (not examined caudal to T7) the whole diameter of the cord being involved. Neurones were absent and the myelin and axons broken up with a perivascular polymorph reaction but few lipid phagocytes. A round infarcted area was present in the posterior columns of C7 and minor ischaemic changes in C7, C8, TI and T2. Group Vertebral Artery Cases. My experience with obstruction of the vertebral artery2. (Hughes, 1964b) is confined to two almost identical cases one of which I shall describe. A S2-year-old factory worker was knocked down by a car, being momentarilyCase Report. unconscious and having scalp lacerations, fractures of the left humerus and right clavicle and intra-abdominal bleeding from a ruptured spleen. With splenectomy and massive transfusion his general condition improved but the following day it was clear he had a partial cord transection causing a quadriparesis. Initially affecting the lower cervical cord segments it then spread upwards causing respiratory difficulty resulting in his death on the third day after his accident. The most interesting necropsy findings were in the cervical spine. The prevertebral muscles were infiltrated with haematoma which covered a tear through the CS-6 intervertebral disc. The spine was mobile due to this and to loosening of the capsular ligament around the intervertebral joints. No fractures could be seen and the spinal canal was not otherwise abnormal. When the vertebral arteries were exposed they were seen to be kinked as they passed through the region of the disc tear. The left vertebral artery was partially torn and embedded in blood clot. The 210 PARAPLEGIA spinal cord externally showed slight swelling and a bloodless anterior spinal artery from C4 to C7. The sections showed ischaemic changes from CI to C3 then frank infarction from C4 to C6. Group Intercostal Arteries.