coarctation of the aorta refers to a congenital narrowing of the aortic lumen and occurs in approximately 3.2 of 10,000 live births . the overall incidence has been reported to be between 5 and 8% of all congenital heart defects . aortic coarctation can be either pre - ductal ( 10% ) or post - ductal ( 90% ) , depending upon the relation of the point of narrowing with the embryological ductus arteriosus ( or ligamentum arteriosum ) and the origin of the left subclavian artery . while the former presents with severe heart failure , mostly within the first week of life , the latter form has a relatively late presentation with incidental hypertension noted during evaluation of acute associated ailments or non - specific pathologies like life - threatening intracranial hemorrhage . the obstruction of blood flow through the aortic arch provokes the development of collateral vessels that would allow blood to flow from high - pressure to low - pressure areas . collateral vessels most frequently emerge from the branches of the subclavian arteries above the obstruction and supply blood to the tissues below the obstruction . the collateral pathways that develop most commonly in proximal thoracic aortic stenosis are as follows : ( 1 ) subclavian artery - internal mammary artery ( also called internal thoracic artery)-intercostal arteries ( retrograde flow)-postcoarctation descending thoracic aorta ; ( 2 ) subclavian artery - thyrocervical and costocervical trunks - thoracoacromial and descending scapular arteries - postcoarctation descending thoracic aorta ; and ( 3 ) subclavian artery - vertebral artery - anterior spinal artery - intercostal arteries - postcoarctation descending thoracic aorta . these abnormal vessels , rarely if ever , appear due to compression of adjacent vital structures or hemorrhages . only few reports were encountered in the contemporary literature where intraspinal collaterals and a hypertrophied anterior spinal artery had a causative role toward compressive myelopathy in a case of aortic coarctation , as in the present case , with the maximum documented age of a patient being 30 years as against an advanced age of 57 years in this case . further , none of these patients had an associated epidural hematoma , which was seen in this case and was an important cause of cord compression probably due to rupture of one of these abnormal vessels . a 57-year - old female patient presented to the emergency department of our hospital with sudden - onset symmetric paralysis of bilateral lower limbs . the patient had no other contributory history including that of fever , acute bouts of cough , coagulopathy , or any other chronic medical or surgical co - morbidity . she was referred for magnetic resonance imaging ( mri ) of the spinal cord to evaluate the cause of paraplegia on a 1.5 tesla whole body magnet ( siemens medical systems , erlangen , germany ) . an examination was performed on a 1.5 t scanner [ figure 1 ] which revealed a mixed intensity complex multilobulated lesion in the anterior epidural space with convex posterior margin , adjacent to the c7-d2 vertebral bodies . the lesion was seen to cause gross compression and displacement of the spinal cord in the region with altered cord signal intensity ( extending from c3 to d3 levels ) suggestive of cord edema . this raised a suspicion of small anterior epidural hematoma which , however , could not explain the gross compression of cord along with the length of the edematous cord segment . the mri also showed multiple dilated tortuous vascular channels in the epidural space along with the hematoma , as well as in the paravertebral space . this prompted a computed tomography ( ct ) angiography [ figure 2 ] which confirmed the presen ce of extensive epidural , paravertebral , and chest wall collateral vessels , along with a hypertrophied anterior spinal artery compressing the spinal cord in the cervicodorsal region . the imaging was performed on a 64 slice mdr ct scanner ( ge medical systems , milwaukee , usa ) . the collaterals were connected to bilateral internal thoracic , vertebral , and anterior spinal arteries . in addition , the long segment cord edema was probably due to vascular congestive state in the region as a result of slow flow and compression of perimedullary veins by the intraspinal space - occupying lesion hence formed . an interesting finding emerging at this stage was severe post - ductal coarctation of aorta , which could explain the genesis of all above features . the patient was referred for further management to the cardiovascular surgery unit , where she was counseled for a possible shunt surgery , in the event of a cardiac emergency . surgical therapy is associated with a low risk of restenosis and recurrence , whereas endovascular therapy , consisting of percutaneous balloon angioplasty and endovascular stent repair , has much higher incidence of restenosis , but is a safe and acceptable modality in poor surgical candidates . as for the present episode , she was managed conservatively with supportive hospital care and showed satisfactory improvement in grade of power , sensations and gait . sagittal t1w ( a ) and t2w ( b ) images showing the multilobulated intraspinal extradural space - occupying lesion ( white arrow ) grossly compressing and displacing the spinal cord . the cord ( black arrow ) appears hyperintense on t2w images over a long segment suggesting edema ( myelopathy ) . note the flow voids ( dark areas on both t1w and t2w ) and areas of organized blood ( bright areas on t1w ) on the images , which raise a suspicion of abnormal vessels with small epidural hematoma ct scan of the patient performed during clinical workup , ( a - c ) volume - rendered , and ( d - f ) multiplanner thick maximum intensity projection images . note the stenosed aortic segment ( straight white arrows ) , as described in text , associated with extensive collaterals in all areas including the paravertebral and epidural space ( hollow arrows ) . the anterior spinal artery appears quite dilated ( curved arrow ) , especially in the compressed segment of the cord collateral shunting of blood , in a case of post - ductal aortic coarctation , develops to decompress the high - pressure proximal segment to the low - pressure distal segment , usually via dilated intercostal and internal mammary arteries . the same remains a slowly evolving process , hence the patient may present in second or early third decade with systemic hypertension . aortic coarctation is not uncommonly diagnosed during evaluation of such  incidental hypertension ,  unless the patient presents due to associated complex cardiac anomalies . as the pressure of the proximal segment increases , certain pre - existing embryologic vessels also hypertrophy , along the body wall , as was seen in the present case . all these vessels , however , remain asymptomatic per se , serving as the tell - tale sign of the inciting pathology . under rare circumstances , collaterals develop inside the spinal canal as well , along with hypertrophy of the spinal cord vasculature . when present , these vessels can be potentially dangerous , mainly due to chances of hemorrhage associated with rupture of these channels . in exceptionally rare cases , these vessels may contribute toward spinal cord compression , as was noted in our patient . although these vessels rarely attain aneurysmal dimensions , the compression is probably a result of constant pulsation under pressure in a closed space . further , increased intraspinal canal pressure can lead to lymphovenous congestion which can result in chronic myelopathy . the patient described in the present report represents one such situation where a sub - acute process of cord edema and sub - clinical myelopathy was unmasked by an acute episode of epidural hematoma , which led to presentation above the clinical horizon . other uncommon causes of primary compressive myelopathy in a case of aortic coarctation are spinal artery aneurysm , compression due to radicular artery aneurysm , aortic steal mechanism , dislodgement of microthrombi from dilated collaterals , and spontaneous bleed from dilated weak collaterals . however , all these complications have been described within the age window of first to third decades , unlike the present patient where the presentation was delayed to the late sixth decade . from an imaging perspective , on one hand , this case emphasizes the importance of thorough evaluation of the vascular system in all cases of spinal epidural hematomas , while on other hand it warns one to be wary of making a blind diagnosis of spinal arteriovenous malformations without such investigation .