EQUINE VETERINARY JOURNAL Equine vet. .I. (1977), 9 (l), 40-42
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Ataxia in a Welsh Cob Filly due to a Venous Malformation in the Thoracic Spinal Cord J. S . GILMOUR Animal Diseases Research Association, Moredun Institute, 408 Gilmerton Road, Edinburgh Eti 1 7 7JH J. A. FRASER Edinburgh University Veterinary Field Station, Bush Estate, Nr. Roslin, Midlothian
SUMMARY An 8-month old Welsh Cob filly had shown progressive ataxia of the hindquarters since about 3 months of age. Autopsy revealed a venous malformation resulting in malacia in the ninth thoracic segment of the spinal cord. It is proposed that the tissue destruction associated with this congenital lesion gave rise to the ataxia.
INTRODUCTION EQUINE ataxia resulting from a spinal vascular lesion is rare, although Palmer and Hickman (1960) described an angioma in the cervical spinal cord resulting in an ataxia affecting principally the forelimbs. This paper records a different type of vascular mass, found in the thoracic spinal cord and giving rise to a caudal ataxia. CLINICAL CASE A 6 month old Welsh cob filly was presented with a history of incoordination of the hind-limbs of 2 to 3 months duration. On examination, the filly was bright, alert, well grown and in good bodily condition. The most marked clinical feature was caudal ataxia, associated with excessive adduction and crossing-over of the hind legs and trailing of the toes. Staggering occurred when the filly was turned in a circle or backed. In contrast to the wobbler syndrome, excessive abduction of the hind limbs when turning was absent. The forelimb action was normal and no other nervous signs were observed. Haematological parameters were measured and found to be within the normal limits. The CSF cell count and protein level were normal, and bacteriological examination of the CSF was negative. On the basis of the foregoing, a lesion of the spinal cord in the thoracolumbar region was suspected. However, radiography of the vertebral column revealed no abnormalities. The filly was re-examined 2 months later and it was found that the ataxia had progressed. No further information was forthcoming from this latest examination and, 4-5 months after the onset of clinical signs, the owner requested euthanasia for the animal. AUTOPSY The filly was given a lethal dose of thiopentone sodium and autopsy with tissue collection was carried out immediately.
A heavy worm burden comprising mainly Strongylus species and Parascaris equorum was present and it was noted that the cranial mesenteric artery was affected with verminous arteritis. Examination of the cranial cavity, vertebral canal, brain, spinal cord and meninges revealed an abnormality in the 9th thoracic segment of the spinal cord (T9). On reflecting the dorsal dura mater over this area, a mass of tortuous blood vessels was observed on the surface and within the spinal cord, mainly on the right side (fig. 1). The dorsal longitudinal venous trunk was especially prominent and, with its tributaries, was distended for some distance cranial and caudal to the mass. Transverse slices through the lesion showed that a well-demarcated zone of the right side of the cord appeared black; it was abnormally firm. HISTOLOGICAL EXAMINATION The brain and spinal cord were fixed in 10 per cent formol saline. Blocks of the lesion, of forebrain, midbrain, cerebellum and medulla, and of spinal cord at cervical, thoracic, lumbar and sacral levels were cut, post-fixed in a saturated solution of mercuric chloride, dehydrated, and embedded in par,affin wax. Sections at 6 pm were stained with haematoxylin and eosin (HE), Lendrum’s acid picro-Mallory method and by Perl’s prussian blue reaction. In transverse sections through the lesion, the most prominent features were a large number of wide bore, thin walled blood vessels present in the pia mater and substance of the cord (fig. 2), and an accompanying copious haemorrhage into adjacent white matter. This lesion obliterated large parts of the right dorsal, lateral and ventral white matter columns of the spinal cord, and adjacent nerve tracts were malacic. The walls of most of the blood vessels which formed the mass consisted only of a single layer of endothelial cells, but in some there was also an outer thin layer of connective tissue. Among the cells fforming these walls,
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Fig. 1 . Dorsal aspect of formol-fixed spinal cord (T9) with dura mater reflected and a block of spinal cord removed. This demonstrates the mass of tortuous blood-vessels associated with rhe dorsal longitudinal trunk and penetrating the right side of the cord.
mitotic figures were rarely encountered. Additional features included a small number of fibrin thrombi and infiltration of the affected white matter by eosinophils, polymorphs and haemosiderin-laden macrophages. In the centre of the lesion a small area was undergoing liquefactive necrosis. The right horns of grey matter were not obscured although capillaries in the ventral horn were dilated and a small number of neurones in the ventral horn were necrotic. Changes were observed cranially only as far as the 7th thoracic segment where loss of nerve fibres was evident in the right lateral columns. Caudally, similar changes, as well as neuronal alteration in the nucleus dorsalis and the ventral horn on both sides, extended as far as the upper lumbar segments. The neuronal alterations consisted of absent or reduced Nissl substance. No other changes were observed in the CNS.
DISCUSSION It is considered that the lesion and the associated malacia adequately explain the ataxia. The lesion is very similar in gross and histological appearance to that classified as a venous malformation within the broader group of blood-vessel hamartomas, and is
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said to be the commonest vascular abnormality of the spinal cord and its meninges in man (Russell and Rubinstein, 1963). The long-standing nature of the vascular lesion is indicated by the infrequency of mitosis in the vessel walls of the mass. The presence of haemosiderin-laden macrophages as well as extra-venous erythrocytes suggests that haemorrhage was intermittent. A remarkable feature of the case was the appearance of clinical signs at a very early age. The history suggests that the malformation was already present at about 3 months of age. In man, although the diagnosis of such lesions is not achieved generally until adulthood, vascular hamartomas are thought to be congenital abnormalities (Russell and Rubinstein, 1963). However, in a 9 year old Thoroughbred, Palmer and Hickman (1960) described a venous angioma sited in the 6-7th cervical segment of the spinal cord. This also differed from the present case in that the vessels were small with fibrous, thickened walls, and in that no haemorrhage was present. Alternatively, the presence of fibrin thrombi and eosinophils in this lesion, together with the heavy, but not unusual, worm burden and associated cranial mesenteric verminous arteritis, might suggest that a nematode larval migration into this section of the cord may have been involved. In our experience, however, vascular proliferation does not result from such migration, and in any case there was no evidence of active proliferation in the lesion. There were, furthermore, no nematode larvae in the lesion, nor other evidence of parasite migration in the CNS. It is intriguing that the lesion appeared to be unilateral when the clinical signs suggested a bilateral affliction. Precise knowledge of spinal pathways in the lower animals is sparse, but proprioceptive information from the hind limbs is almost certainly carried in both dorsal and ventral spino-cerebellar tracts(Palmer,’1965). If these pathways in the horse are similar to those in the human, then each ventral spino-cerebellar tract arises from neurones of the dorsal and intermediate grey columns on both sides, and the dorsal spino-cerebellar tract arises from neurones in the ipsilateral and perhaps also the contralateral nucleus dorsalis (Ranson and Clark, 1959). Thus a lesion interfering with both spino-cerebellar tracts on one side of the cord could interrupt passage of proprioceptive information from both hind limbs. It is of interest to note that in this horse, some neurones of the nucleus dorsalis were altered on both sides of the cord in the upper lumbar area, although the tract changes were unilateral. ACKNOWLEDGEMENTS The authors gratefully acknowledge the contribution of Mr. J. Bowie B.SC., M.R.c.v.s.,who drew their attention to this case; Dr. R. M. Barlow, for expert advice; and Messrs. J. Cairns, G . Newlands, Jr. and J. Wight for skilled technical assistance.
Fig. 2. Transverse section of spinal cord at T9, showing mass of blood-filled veins, asrociated haemorrhage and adjacent malacia (arrow). H E x 4.
REFERENCES Palmer, A. C. (1965). Introduction to Animal Neurology, p. 29. Oxford, Blackwell Scientific Publications. Palmer, A. C. and Hickman, J. (1960). Ataxia in a Horse due to an Angioma of the Spinal Cord. Vet. Rec. 72, 611-613. Ranson, S. W. and Clark, S. L. (1959). The Anatomy of the Nervorrs System, 10th edition, pp. 188-189. Philadelphia and London. W. B. Saunders C o . Russell, D. S. and Rubinstein, L. J. (1963). Pathologyof Tumours ojthe Nervous System, 2nd edition, pp. 71,78 and 88. London, Edward Arnold.
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RESUME Une pouliche Cob Welsh agCe de huit mois montrait depuis 1’8ge de trois mois des signes d’une ataxie progressive posttrieure. L‘autopsie mit en Cvidence une malformation veineuse avec dCgCnCrescence du 96 segment thoracique de la moelle Cpinibre. On pense qu’il en rtsulta l’ataxie constatCe.
ZUSAMMENFASSUNG Bei einem 8 Monate alten Welsh Cob Stutfohlen wurde eine seit 5 Monaten bestehende, progressive Ataxie der Nachhand beobachtet. Die Autopsie zeigte eine Venenmissbildung mit resultierender Malazie im 9. Thorakalsegment des Ruckenmarks. Es wird vermutet, dass die Gewebszerstorung auf diese kongmitale Missbildung zuriickzufiihren ist und Anlass zu Ataxie gegeben hat.
Accepted for publication 21.10.76