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Secondary Prevention After Cerebral Ischaemia of Presumed Arterial J Neurol Neurosurg Psychiatry 1999;67:827–834 827 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.67.6.832a on 1 December 1999. Downloaded from On physical examination, blood pressure was secondary to thrombosis of the inferior vena 110 over 75 mm Hg. Heart, lungs, and cava has not been reported previously. LETTERS TO abdomen were normal. Peripheral arterial pul- The mechanism by which the neurological sations were present. Both legs were slightly symptoms and signs were produced is prob- THE EDITOR swollen and coloured red to purple and livido ably twofold. Firstly, there is compression of reticularis was present. On catheterisation of cauda equina nerve roots in the spinal canal the bladder, there was no urine retention. and foramen by the dilated anterior internal Neurological examination showed weakness of vertebral veins. Secondly, the symptoms and both legs with proximal strength Medical signs may be due to ischaemia of the cauda Acute cauda equina syndrome caused Research Council (MRC) grade 2–3 and distal equina caused by stasis of the blood flow in by thrombosis of the inferior vena cava MRC grade 1–2. There was bilateral sensory the radicular veins. The mentioned anterior loss in the dermatomesL1toS1.Tendon internal vertebral veins and radicular veins are Deep venous thrombosis of the lower limbs is reflexes of the legs were absent. Plantar part of the spinal venous plexus. This valveless the most common vascular disorder in hospi- responses were both indiVerent. The patient plexus is connected by the intervertebral veins tal. Although the clinical features are not spe- was diagnosed as having an acute cauda equina to the ascending lumbar veins which drain to cific, the most important symptoms are syndrome with possibly deep venous thrombo- the inferior caval vein (fig 2). The ascending oedema, local tenderness, and pain. Well sis of both legs, and an immediate MRI of the lumbar veins, however, also communicate known complications of deep venous throm- thoracic and lumbar spine was performed. This with the azygos system and the occipital and bosis are pulmonary embolism and chronic MRI disclosed a strongly dilated anterior basilar sinuses. After occlusion of the inferior venous insuYciency. Neurological complica- epidural venous plexus with compression of the vena cava, this vertebrolumbar collateral tions are uncommon after deep venous cauda equina and nerve roots in the foramina pathway can function as an alternative route thrombosis. (fig 1 A–C). Signal intensity of the thoracic spi- for venous blood from the lower limbs. Due to We report on a patient who presented with nal cord was normal. Ultrasound examination this bypass eVect running parallel to the infe- an acute cauda equina syndrome, which of the lower abdomen and legs showed throm- rior caval vein, the anterior epidural veins are turned out to be caused by thrombosis of the bosis of the inferior caval vein. Abdominal CT dilated by increased blood flow. In our case, inferior vena cava. confirmed the presence of thrombosis of the the dilated veins have probably compressed A 58 year old previously healthy white man inferior caval vein (just below the insertion of the cauda equina and certainly compressed presented at the emergency department of the renal veins) extending into the iliac veins. spinal roots in the intervertebral foramina, as our hospital with acute severe low back pain No other abnormalities that could have caused can be seen on the MRI. irradiating to both legs. The pain in the legs the inferior vena cava thrombosis were seen on Vascular spinal neurological complications was severe and was located from the lower CT. Routine laboratory investigations (includ- are also known in spinal arteriovenous half of the upper legs down to the feet. He ing coagulability testing) were unremarkable, malformations (AVMs) and spinal angiomas. also had noted decreased strength as well as except for slight increase in erythrocyte More than half of the patients with AVMs sensory disturbances of both legs. Spontane- sedimentation rate. have bladder dysfunction, paresis, and sen- ous micturition was not possible. The patient was diagnosed as having an sory change caused by the ischaemic eVect of acute cauda equina syndrome due to dilated venous hypertension. In patients with spinal anterior epidural veins secondary to thrombo- AVMs, an apoplectiform onset of clinical sis of the inferior vena cava. He was treated presentation, as presented in our patient, is with intravenous heparin and acenocoumarol described in 30%-50% due to thrombosis or copyright. to prevent spread of thrombosis. In the next haemorrhage.1 Neurological signs are also few days, the neurological disturbances known as a related phenomena to spinal gradually diminished. Despite exhaustive test- angiomas. Although ischaemia of the cord in ing, no cause of the thrombosis was found. these angiomas is mostly caused by stealing We report on a patient with an acute cauda blood through a significant arteriovenous equina syndrome due to thrombosis of the shunt, spinal compression by very large inferior vena cava. An acute cauda equina draining veins is also important in some syndrome is usually caused by a prolapsed patients.2 Besides cauda equina compression, intervertebral disc and less often by a dilated veins secondary to thrombosis of the tumour, trauma, or epidural bleeding. inferior vena cava can also lead to destruction Well known complications of deep venous of pedicles of lumbar vertebral bodies and thrombosis are pulmonary embolism and partial obstruction of the ureter.34In conclu- chronic venous insuYciency. To our knowl- sion, an acute cauda equina syndrome may be edge, an acute cauda equina syndrome rarely caused by a dilated venous spinal http://jnnp.bmj.com/ plexus secondary to thrombosis of the 3 7 2 5 1 on September 27, 2021 by guest. Protected 6 4 8 10 9 Figure 2 Diagram of lumbar vertebral veins.5 (1) Lateral anterior internal vertebral vein (AIVV); (2) medial AIVV; (3) posterior internal vertebral venous plexus; (4) Figure 1 Lumbar spine MRI. Strongly dilated epidural and foraminal veins as black tubular basivertebral vein; (5) intervertebral vein structures due to signal loss, consistent with increased speed of flow. (A) Axial T1 weighted cut at (IVV); (6) ascending lumbar vein (ALV);(7) L4–5; Anterior epidural plexus indicated by arrows. (B) Mid-sagittal proton density weighted cut posterior external vertebral venous plexus; (8) showing compression of dural sac at L5 and S1 levels. (C) Lateral sagittal T1 weighted cut anterior external vertebral venous plexus; (9) showing dilated foraminal veins. left lumbar vein; (10) inferior caval vein. 828 J Neurol Neurosurg Psychiatry 1999;67 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.67.6.832a on 1 December 1999. Downloaded from inferior vena cava. The list of causes of the drosis. Routine laboratory blood tests, screening thetic pericarotid lesions after infrequent bilat- cauda equina syndromes5 should therefore for cardiovascular diseases, and Doppler sonog- eral internal carotid artery dissections whereas also include inferior vena cava thrombosis. raphy were all normal. Cranial magnetic reso- unilateral dissections may cause only a mild 1 JELLE DE KRUIJK nance angiography and cerebral digital subtrac- and clinically often inapparent irritation. ARTHUR KORTEN tion angiography showed bilateral dissection of Cusimano and Sekhar described a syn- JELIS BOITEN the internal carotid artery with dissecting aneu- drome they termed “pseudocerebrospinal Department of Neurology rysms on both sides (figure A-D). fluid rhinorrhoea” with ipsilateral nasal hy- Anticoagulation with heparin and then persecretion and nasal stuYness after surgery JAN WILMINK 4 Department of Radiology, University Hospital dicumarole was initiated and the patient’s of the cranial base. In these patients, the Maastricht, The Netherlands symptoms gradually improved. On follow up pericarotid sympathetic plexus, the petrous Correspondence to: Dr JR de Kruijk, Department examination 6 months and 14 months later, he or cavernous carotid artery parts, and the of Neurology, University Hospital, Maastricht, P showed marginal ptosis and a slightly smaller greater petrosal nerve had been removed or Debeylaan 25, NL 6229 HX, Maastricht, The pupil (2 mm) in the dark on the left side, but dissected. Experimental selective parasympa- Netherlands. Fax 0031 43 3877055; email no headaches, rhinorrhoea, or tinnitus. Cer- thetic nerve activation in the nasal mucosa of [email protected] ebral magnetic resonance angiography of the the cat leads to an increase in nasal secretion left internal carotid artery was now normal but and vascular congestion.5 Lung found nasal 1 Byrne T, Waxman S. Neoplastic causes of spinal cord compression: intradural-extramedullary the dissecting aneurysm of the right internal congestion to be related to a withdrawal of and intramedullary tumors. In: Plum F, ed. carotid artery was unchanged. Therefore anti- sympathetic discharge rather than to an over- Contempory neurology. Spinal cord compression: coagulation was continued. activity of the parasympathetic nerves.6 Thus diagnosis and principles of management. Philadel- We suggest that in our patient bilateral the nasal hypersecretion and stu ness in our phia: FA Davis, 1990. (Series 33.) Y 2 Friedman A, Sprayregen S, Appelman R. Partial carotid artery dissection led to a lesion and patient is in agreement with the assumption obstruction of the ureter by venous collaterals dysfunction of the sympathetic pericarotid of a lesion of pericarotid sympathetic nerve in inferior vena cava thrombosis. Angiology plexus leading to a parasympathomimetic state fibres after carotid artery dissection. 1978;29:925–8. 3 Singson R, Dee G, Quader M. Case report 265. with nasal hypersecretion and congestion of In the diVerential diagnosis, cluster head- Skeletal Radiol 1984;11:293–5. nasal vessels. This condition was reversible ache and paroxysmal hemicrania have to be 4 Djindjian R. Angiomas of the spinal cord. In: after recanalisation of the left internal carotid considered. Our patient’s symptoms diVered Vinken P, Bruyn G. Handbook of clinical neurol- artery.
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